All Skin Disorders

Here is the full list of pages on skin-disorders.phoolish.org

2008-07-18T20:39:00.001-07:00

Here is the full list of pages on skin-disorders.phoolish.org

43. Clearing Pus From the Ear
42. All About Genital warts
41. All About Blisters
40. All About Erythroderma
39. All About Erysipelas
38. All About Epidermolysis bullosa
37. All About Diaper rash
36. All About Dermatofibroma
35. All About Dandruff
34. All About Cutaneous larva migrans (Creeping Eruption)
33. All About Herpes simplex (cold sores)
32. All About Chloracne
31. All About Cellulitis
30. All About Carbuncles
29. All About Aphthous ulcers (Canker Sores)
28. All About Bullous pemphigoid
27. All About Bowen's disease
26. All About Boils
25. All About Behçet's disease
24. All About Bedsores
23. All About Basal cell carcinoma
22. All About Urushiol-induced contact dermatitis
21. All About Autoeczematization
20. All ABout Neurodermatitis
19. All ABout Stasis dermatitis
18. All ABout Nummular dermatitis
17. All About Dyshidrosis
16. All About Seborrhoeic dermatitis
15. All About Xerotic eczema
14. All About Contact dermatitis
13. All About Eczema
12. All About Atopic dermatitis - eczema
11. All About Dermatitis herpetiformis
10. All About Swimmer's itch
09. All About Dermatitis
08. All About Aquagenic pruritus
07. All About Athlete's foot
06. All About Spider angioma
05. All About Cherry angioma
04. All About Angioma
03. All About Actinic keratosis
02. All About Acne (Acne Vulgaris)
01. All About Dermatology

Clearing Pus From the Ear

2007-06-03T00:42:00.000-07:00

male evacuates pus filled earlobe; warning - extremely graphic.

All About Genital warts

2007-04-02T18:26:00.034-07:00

Genital warts (or condyloma, condylomata acuminata, or venereal warts) is a highly contagious sexually transmitted infection. Caused by some sub-types of the human papillomavirus (HPV) genital warts are spread through direct skin-to-skin contact during oral, genital, or anal sex with an infected partner. Genital warts are the most easily recognized sign of genital HPV infection. Of the multiple strains of genital HPV, strains 6, 11, 30, 42, 43, 44, 45, 51, 52, and 54 can cause genital warts; types 6 and 11 are the most common.[1] Most people who acquire those strains never develop warts or any other symptoms. HPV is also responsible for over 90% of all cases of cervical cancer. (However, the HPV strains responsible for cervical cancer differ from the strains that cause genital warts.)

Genital warts often occur in clusters and can be very tiny or can spread into large masses in the genital or anal area. In women the warts occur on the outside and inside of the vagina, on the opening (cervix) to the womb (uterus), or around the anus. While genital warts are approximately as prevalent in men, the symptoms of the disease may be less obvious. When present, they usually are seen on the tip of the penis. They also may be found on the shaft of the penis, on the scrotum, or around the anus. Rarely, genital warts also can develop in the mouth or throat of a person who has had oral sex with an infected person.

Treatment

Genital warts often disappear even without treatment. In other cases, they eventually may develop a fleshy, small raised growth. There is no way to predict whether the warts will grow or disappear.

Depending on factors such as the size and location of the genital warts, a doctor will offer one of several ways to treat them.

* Imiquimod, (Aldara®) a topical immune response cream which can be applied to the affected area
* A 20% podophyllin anti-mitotic solution, which can be applied to the affected area and later washed off
* A 0.5% podofilox solution, applied to the affected area but should not be washed off
* A 5% 5-fluorouracil (5-FU) cream
* Trichloroacetic acid (TCA)
* Pulsed dye laser
* Liquid nitrogen cryosurgery
* Electric or Laser cauterization

With pregnancy, podophyllin or podofilox should not be used as they are absorbed by the skin and may cause birth defects in the fetus. In addition, 5-fluorouracil cream should not be used while trying to become pregnant or if there is a possibility of pregnancy.

In case of small warts, they can be removed by freezing (cryosurgery), burning (electrocautery), or laser treatment. Surgery is occasionally used to remove large warts that have not responded to other treatment.

Some doctors use the antiviral drug interferon-alpha, which they inject directly into the warts, to treat warts that have returned after removal by traditional means. The drug is expensive, however, and does not reduce the rate that the genital warts return.

Although treatments can get rid of the warts, they do not get rid of the HPV virus, so warts can recur after treatment. The body's immune system typically clears the virus anywhere from 8 to 13 months, but it occasionally remains in the body for a lifetime.[2] The state of the immune system determines the chances of ridding the virus entirely and can be affected by factors such as HIV infection, certain medications, stress, or illness.[3] There is even some suggestion that effective treatment of the wart may aid the body's immune response[citation needed].

Prevention

The virus that causes genital warts is spread by skin-skin contact. Condoms do not adequately protect against genital warts, because the infected spot may not be covered by a condom. The only reliable prevention is to have no skin contact with potentially infected tissue.

Gardasil, an HPV vaccine, protects women from the strains of HPV that cause 70% of all cervical cancers and 90% of all genital warts and has been approved by the Food and Drug Administration.[4] The license allows prescription to females between the ages of 9-26. This vaccine is most effective when administered before the girl has contacted any of the HPV strains which the virus protects. For this reason, the vaccine should be preferably administered before a girl becomes sexually active. This vaccine is currently being tested for males. Gardasil does not contains the preservative thimerosal.[5]

Hirsuties papillaris genitalis

It is a common misconception among men that hirsuties papillaris genitalis are in fact genital warts. Hirsuties papillaris genitalis is not contagious and no treatment for the condition is necessary. Some may deem it unsightly and there are various methods of ridding the penis of the condition such as carbon dioxide laser treatment.

Fordyce's spots

Genital warts should not be confused with Fordyce's spots, which are considered benign.

Pregnancy and childbirth

Genital warts may cause a number of problems during pregnancy. Sometimes the warts get larger during pregnancy, making it difficult to urinate. If the warts are in the vagina, they can make the vagina less elastic and cause obstruction during child birth.

Rarely, infants born to women with genital warts develop warts in their throats (laryngeal papillomatosis). Although uncommon, it is a potentially life-threatening condition for the child, requiring frequent laser surgery to prevent obstruction of the breathing passages. Research on the use of interferon therapy in combination with laser surgery indicates that this drug may show promise in slowing the course of the disease.

References

1. ^ eMedicine med/1037
2. ^ What is HPV? at plannedparenthood.org
3. ^ Learn about HPV > Myths and Misconceptions at American Social Health Association
4. ^ FDA Licenses New Vaccine for Prevention of Cervical Cancer and Other Diseases in Females Caused by Human Papillomavirus
5. ^ GARDASIL® Questions and Answers. CBER - Quadrivalent Human Papillomavirus (Types 6, 11, 16, 18) Recombinant Vaccine. Retrieved on 2007-03-19.

All About Blisters

2007-04-02T18:26:00.033-07:00

A blister or bulla is a defense mechanism of the human body. When the outer (epidermis) layer of the skin separates from the fibre layer (dermis), a pool of lymph and other bodily fluids collect between these layers while the skin re-grows from underneath. Blisters can be caused by chemical or physical injury. An example of chemical injury would be an allergic reaction. Physical injury can be caused by heat, frostbite, or friction.

Treatment

Unless infection occurs, blisters usually heal quickly without additional treatment. If a blister is punctured, it forms an open wound so it is a good idea to bandage it when one is working around unsanitary conditions. If the blister has 'popped,' the excess skin should not be removed, unless it is dirty or torn. Removing the excess skin often makes the wound more prone to further infection (Kaiser Permanente, 2001). As with all wounds, it is a good idea to keep blisters clean.

Variations

If a blister is associated with sub-dermal bleeding it will partially fill with blood, forming a blood blister. Certain autoimmune diseases feature extensive blistering as one of their symptoms. These include pemphigus and pemphigoid. Blistering also occurs as part of foodborne illness with Vibrio vulnificus (seafood). The class of chemical weapons known as vesicants acts by causing blisters (often within the respiratory tract). Mustard gas and lewisite are examples of such agents.

See also

* Buboe
* Dracunculiasis
* Herpangina
* Herpes zoster
* Ulcer

All About Erythroderma

2007-04-02T18:26:00.032-07:00

Erythroderma is defined as a generalized skin disorder characterized by reddening and scaling of 100% of the skin. It is also known as erythrodermatitis, generalized exfoliative dermatitis, and red man syndrome. There may also be normal areas of skin present.

Causes

Erythroderma is produced by several skin diseases, such as psoriasis, contact dermatitis, drug reactions, and mycosis fungoides (a cutaneous lymphoma). A dermatologist must first diagnose the cause, usually with a skin biopsy, a blood smear examined by a pathologist and patch testing (if the eruption can be temporarily cleared).

Treatment

The treatment is dependent on the cause.

See also

* List of skin diseases
* Eczema

All About Erysipelas

2007-04-02T18:26:00.031-07:00

Erysipelas (Greek ερυσίπελας - red skin) is an acute streptococcus bacterial skin infection, resulting in inflammation and characteristically extending into underlying fat tissue.

(Erysipelas is also the name given to an infection in animals caused by the bacterium Erysipelothrix rhusiopathiae. Infection by Erysipelothrix rhusiopathiae in humans is known as erysipeloid.)

Risk factors

This disease is most common among the elderly, infants, and children. People with immune deficiency, diabetes, alcoholism, skin ulceration, fungal infections and impaired lymphatic drainage (e.g., after mastectomy, pelvic surgery, bypass grafting) are also at increased risk.

Signs and symptoms

Patients typically develop symptoms including high fevers, shaking, chills, fatigue, headaches, vomiting, and general illness within 48 hours of the initial infection. The erythematous skin lesion enlarges rapidly and has a sharply demarcated raised edge. It appears as a red, swollen, warm, hardened and painful rash, similar in consistency to an orange peel. More severe infections can result in vesicles, bullae, and petechiae, with possible skin necrosis. Lymph nodes may be swollen, and lymphedema may occur. Occasionally, a red streak extending to the lymph node can be seen.

The infection may occur on any part of the skin including the face, arms, fingers, legs and toes, but it tends to favor the extremities. Fat tissue is most susceptible to infection, and facial areas are typically around the eyes, ears, and cheeks. Repeated infection of the extremities can lead to chronic swelling (lymphadenitis).

Etiology

Most cases of erysipelas are due to Streptococcus pyogenes (also known as group A streptococci), although non-group A streptococci can also be the causative agent. Historically, the face was most affected; today the legs are affected most often. [1]

Erysipelas infections can enter the skin through minor trauma, eczema, surgical incisions and ulcers, and often originate from strep bacteria in the subject's own nasal passages.

Diagnosis

This disease is mainly diagnosed by the appearance of the rash and its characteristics. Blood cultures are unreliable for diagnosis of the disease, but may be used to test for sepsis. Erypsipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, and diffuse inflammatory carcinoma of the breast.

Erysipelas can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevaiton of the antistreptolysin O titre occurs after around 10 days of illness.

Treatment

Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal.

Complications

* Spread of infection to other areas of body through the bloodstream (bacteremia), including septic arthritis and infective endocarditis (heart valves).
* Septic shock.
* Recurrence of infection – Erysipelas can recur in 18-30% of cases even after antibiotic treatment.
* Lymphatic damage
* Necrotizing fasciitis -- AKA "the flesh-eating bug." A potentially-deadly exacerbation of the infection if it spreads to deeper tissue.

All About Epidermolysis bullosa

2007-04-02T18:26:00.030-07:00

In medicine (dermatology) Epidermolysis bullosa (EB) is a rare genetic disease characterized by the presence of extremely fragile skin and recurrent blister formation, resulting from minor mechanical friction or trauma. The condition was brought to public attention in the UK through the Channel 4 documentary The Boy Whose Skin Fell Off, chronicling the life and death of English sufferer Jonny Kennedy.

Forms

There are three main forms of inherited EB. These different subtypes are defined by the depth of blister location within the skin layers, and the location of the dissolution of the skin.

EB Simplex (EBS) -- ABOVE the basement membrane

See main article at Epidermolysis bullosa simplex.

Blister formation of EB simplex is within the basal keratinocyte of the epidermis. Sometimes EB simplex is called epidermolytic. There are four subtypes of EBS:

1. EBS - Weber-Cockayne (EBS-WC)
2. EBS - Koebner (EBS-K)
3. EBS - Dowling-Meara (EBS-DM) -- caused by missense mutation in KRT5 (E477K) or one of two missense mutations in KRT14 (R125C and R125H)
4. EBS - Mottled Pigmentation (EBS-MP) - caused by one missense mutation in KRT5 (I161S) or by missense mutations in the plectin gene (Koss-Harnes et al., 1997;Koss-Harnes et al., 2002).

Junctional EB (JEB) -- THROUGH the basement membrane

Condition characterized by spontaneous blistering of the skin and mucous membranes at the level of the lamina lucida within the basement membrane zone. Condition is caused by defects in the structures of laminin 5 or laminin 6, proteins that contribute to the cohesion of the dermis and epidermis A severe form of the disease, JEB gravis is often fatal early in life. Death occurs as a result of epithelial blistering of the respiratory, digestive and genitourinary systems.

Dystrophic EB (DEB) -- UNDER the basement membrane

Dystrophic EB (DEB) forms which can lead to scarring occur in a deeper tissue level; the sub-lamina densa region (the beneath the lamina densa) within the upper dermis. The disease DEB is caused by genetic defects (or mutations) within the molecule type VII collagen (collagen VII). Collagen VII is a very large molecule (780 nm) that dimerizes to forms a semicircular looping structure: the anchoring fibril. Anchoring fibrils are thought to form a structural link between the epidermal basement membrane and the fibrillar collagens in the upper dermis.

Collagen VII is also present in the epithelial tissue of the esophagus, which leads to chronic scarring, webbing, and obstruction. Affected individuals are often severely malnourished due to trauma to the oral and esophageal mucosa and require feeding tubes for nutrition. They also suffer from iron-deficiency anemia of uncertain origin, which leads to chronic fatigue.

Open wounds on the skin heal slowly or not at all, often scarring extensively, and are particularly susceptible to infection. Many individuals bathe in a bleach and water mixture to fight off these infections.

The chronic inflammation leads to errors in the DNA of the affected skin cells, which in turn causes squamous cell carcinoma (SCC). The majority of these patients die before the age of 30, either of SCC or complications related to DEB.

Laymen's Terms

The skin has two layers; the outer layer is called the epidermis and the inner layer the dermis. In normal individuals there are "anchors" between the two layers that prevent them from moving independently from one another. In people born with EB the two skin layers lack the anchors that hold them together, and any action that creates friction between the layers (like rubbing or pressure) will create blisters and painful sores. Sufferers of EB have compared the sores to third-degree burns.[1]

Epidemiology

An estimated 50 in 1 million live births are diagnosed with EB, and 9 in 1 million are in population. Of these cases, approximately 92% are EBS, 5% are DEB, 1% are JEB, and 2% are unclassified. Carrier frequency ranges from 1 in 333 for Junctional, to 1 in 450 for Dystrophic. Carrier frequency for Simplex is not indicated in this article, but is presumed to be much higher than JEB or DEB.

The disorder occurs in every racial and ethnic group throughout the world and affects both genders. [2]]

All About Diaper rash

2007-04-02T18:26:00.029-07:00

Diaper rash (U.S.) or nappy rash (UK), is a generic term applied to skin rashes in the diaper area that are caused by a various skin disorders and/or irritants.

Generic rash or irritant diaper dermatitis (IDD) is characterized by joined patches of erythema and scaling mainly seen on the convex surfaces, with the skin folds spared.

Diaper dermatitis with secondary bacterial or fungal involvement tends to spread to concave surfaces (i.e. skin folds), as well as convex surfaces, and often exhibits a central red, beefy erythema with satellite pustules around the border (Hockenberry, 2003).

Differential diagnosis

Other rashes that occur in the diaper area include Seborrheic dermatitis and Atopic dermatitis. Both Seborrheic and Atopic dermatitis require individualized treatment; they are not the subject of this article.

* Seborrheic dermatitis, typified by oily, thick yellowish scales, is most commonly seen on the scalp (cradle cap) but can also appear in the inguinal folds.
* Atopic dermatitis, or eczema, is associated with allergic reaction, often hereditary. This class of rashes may appear anywhere on the body and is characterized by intense itchiness.

Causes

Irritant diaper dermatitis develops when skin is exposed to prolonged wetness, increased skin pH caused by urine and feces, and resulting breakdown of the stratum corneum, or outermost layer of the skin. In adults, the stratum corneum is composed of 25 to 30 layers of flattened dead keratinocytes, which are continuously shed and replaced from below. These dead cells are interlay with lipids secreted by the stratum granulosum just underneath, which help to make this layer of the skin a waterproof barrier. The stratum corneum's function is to reduce water loss, repel water, protect deeper layers of the skin from injury and to repel microbial invasion of the skin (Tortora and Grabowski, 2003). In infants, this layer of the skin is much thinner and more easily disrupted.

Urine's effects

Although wetness alone macerates the skin, softening the stratum corneum and greatly increasing susceptibility to friction injury, urine has an additional impact on skin integrity because of its effect on skin pH. While studies show that ammonia alone is only a mild skin irritant, when urea breaks down in the presence of fecal urease it increases skin pH, which in turn promotes the activity of fecal enzymes such as protease and lipase (Atherton, 2004; Wolf, Wolf, Tuzun and Tuzun, 2001). These fecal enzymes increase the skin's permeability to bile salts and act as irritants in and of themselves.

Diet's effects

The interaction between fecal enzyme activity and IDD explains the observation that infant diet and diaper rash are linked, since fecal enzymes are in turn affected by diet. Breast-fed babies, for example, have a lower incidence of diaper rash, possibly because their stools have lower pH and lower enzymatic activity (Hockenberry, 2003). Diaper rash is also most likely to be diagnosed in infants 8–12 months old, perhaps in response to an increase in eating solid foods and dietary changes around that age that affect fecal composition. Any time an infant’s diet undergoes a significant change (i.e. from breast milk to formula or from milk to solids) there appears to be an increased likelihood of diaper rash (Atherton and Mills, 2004).

The link between feces and IDD is also apparent in the observation that infants are more susceptible to developing diaper rash after treatment with antibiotics, which affect the intestinal microflora (Borkowski, 2004; Gupta & Skinner, 2004). Also, there is an increased incidence of diaper rash in infants who have suffered from diarrhea in the previous 48 hours, which may be due to the fact that fecal enzymes such as lipase and protease are more active in feces which have passed rapidly through the gastrointestinal tract (Atherton, 2004).

Secondary infections

The significance of secondary infection in IDD remains controversial. Atherton contends that, “Candida albicans can only be isolated from a minority of IDD cases; in many cases this is a reflection of antibiotic therapy. It has also been established that bacterial infection does not play a substantial part in the development of IDD.”(Atherton, 2004, p. 646).

However, there is little argument that once the stratum corneum has been damaged by a combination of physical and chemical factors, the skin is necessarily more vulnerable to secondary infections by bacteria and fungi. In analyzing swab samples at the perianal, inguinal and oral areas of 76 infants, Ferrazzini et al. (2003) found that colonization with Candida albicans was significantly more likely in children with symptomatic diaper rash than without. Staphylococcus aureus was also present more frequently in symptomatic than in healthy infants, but the difference was not statistically significant. A wide variety of other infections has been reported on occasion, including Proteus mirabilis, enterococci and Pseudomonas aeruginosa, but it appears that Candida is the most common opportunistic invader in diaper areas (Ferrazzini et al., 2003; Ward et al., 2000).

Although apparently healthy infants sometimes culture positive for Candida and other organisms without exhibiting any symptoms, there does seem to be a positive correlation between the severity of the diaper rash noted and the likelihood of secondary involvement (Ferrazzini et al., 2003; Gupta & Skinner, 2004; Wolf et al., 2001).

Treatments

The most effective treatment, although not always the most practical one, is to discontinue use of diapers, allowing the affected skin to air out. Other commonly recommended remedies include oil-based protectants, often using various over-the-counter "diaper creams", but sometimes people use petroleum jelly and shark liver oil or cod liver oil; zinc oxide based ointments, and, in extreme cases, anti-fungal cremes. Low concentration hydrocortisone creams are also sometimes used to treat the symptoms of diaper rash, although they do little to clear up the rash itself.

References

* Atherton, D.J. (2001) The aetiology and management of irritant diaper dermatitis. Journal of the European Academy of Dermatology and Venereology 15 (Supplement 1), p. 1-4.

* Atherton, D.J. (2004) A review of the pathophysiology, prevention and treatment of irritant diaper dermatitis. Current Medical Research and Opinion, 20(5), p. 645-649.

* Atherton, D.J. & Mills, K. (2004) What can be done to keep babies’ skin healthy? RCM Midwives Journal, 7(7), p. 288-290.

* Borkowski, S. (2004) Diaper rash care and management. Pediatric Nursing, 30 (6) p. 467-470.

* Concannon P, Gisoldi E, Phillips S, Grossman R. (2001) Diaper dermatitis: a therapeutic dilemma. Results of a double-blind placebo controlled trial of miconazole nitrate 0.25%. Pediatric Dermatology, 18(2) p.149-55.

* Ferrazzini, G., Kaiser, R.R., Hirsig Cheng, S.K., Wehrli, M., Della Casa, V., Pohlig, G., Gonser, S., Graf, F. & Jorg, W. (2003) Microbiological aspects of diaper dermatitis. Dermatology, 206, p. 136-141.

* Gupta, A.K., Skinner, A.R. (2004) Management of diaper dermatitis. International Journal of Dermatology, 43 p. 830-834.

* Hockenberry, M.J. (2003) Wong’s Nursing Care of Infants and Children. St. Louis, MO; Mosby, Inc.

* Tortora, G.J & Grabowski, S.R. (2003) Principles of Anatomy and Physiology, Tenth Edition; New York, NY; John Wiley & Sons, Inc.

* Ward, D.B, Fleischer, A.B., Feldman, S.R., & Krowchuk, D.P. (2000). Characterization of diaper dermatitis in the United States. Archives of Pediatrics & Adolescent Medicine, 154 (9), p. 943-946.

* Wolf, R., Wolf, D., Tuzun, B. & Tuzun, Y. (2001) Diaper Dermatitis. Clinics in Dermatology, 18, p. 657-660.

All About Dermatofibroma

2007-04-02T18:26:00.028-07:00

Dermatofibromas are harmless benign skin growths, found especially on the legs, that range in size from about 0.5 to 1 cm. They are hard papules (rounded bumps) that may appear in a variety of colors, usually brownish to tan. Typical dermatofibromas cause little or no discomfort, although itching and tenderness can occur. Some physicians and researchers believe dermatofibromas form as a reaction to previous injuries such as insect bites or thorn pricks. They are composed of disordered collagen laid down by fibroblasts. Rarely, basal cell carcinoma may develop in a dermatofibroma.

Dermatofibromas occur most often in women: the male to female ratio is about 1:4. Most physicians will advocate treatment only if the lesion is in the way of shaving, or is becoming irritated by clothing. Removal can be done surgically with local anesthesia, but since much of the growth extends beneath the surface of the skin, the scar may be larger and more noticeable than the original tumor. Cryosurgery may also be used to remove a dermatofibroma.

See also

* Dermatology
* Seborrheic keratosis

All About Dandruff

2007-04-02T18:26:00.027-07:00

Dandruff (also called scurf and historically termed Pityriasis capitis) is due to the excessive shedding of dead skin cells from the scalp. As it is normal for skin cells to die and flake off, a small amount of flaking is normal and in fact quite common. Some people, however, either chronically or as a result of certain triggers, experience an unusually large amount of flaking, which can also be accompanied by redness and irritation. Most cases of dandruff can be easily treated with specialized shampoos. Simple dandruff does not cause hair loss.

Excessive flaking can also be a symptom of seborrhoeic dermatitis, psoriasis, fungal infection or excoriation associated with infestation of head lice. Dandruff is a global phenomenon and many people find that dandruff can cause social or self-esteem problems. Treatment may be important purely for psychological reasons.

Causes

As the epidermal layer continually replaces itself, cells are pushed outward where they eventually die and flake off. In most people, these flakes of skin are too small to be visible. However, certain conditions cause cell turnover to be unusually rapid, especially in the scalp. For people with dandruff, skin cells may mature and be shed in 2 - 7 days, as opposed to around a month in people without dandruff. The result is that dead skin cells are shed in large, oily clumps, which appear as white or grayish patches on the scalp and clothes.

Dandruff has been shown to be the result of three required factors:

1. Skin oil commonly referred to as sebum or sebaceous secretions;
2. The metabolic by-products of skin micro-organisms (most specifically Malassezia yeasts);
3. An individual susceptibility.
4. Due to stress

Common older literature cites the fungus Malassezia furfur (previously known as Pityrosporum ovale) as the cause of dandruff. While this fungus is found naturally on the skin surface of both healthy people and those with dandruff, it has recently been shown that a scalp specific fungus, Malassezi Globosa, is the responsible agent. This fungus metabolizes triglycerides present in sebum by the expression of lipase, resulting in a lipid byproduct oleic acid (OA). Penetration by OA of the top layer of the epidermis, the stratum corneum, results in an inflammatory response which disturbs homeostasis and results in erratic cleavage of stratum corneum cells.

Rarely, dandruff can be a manifestation of an allergic reaction to chemicals in hair gels/sprays, hair oils, or sometimes even dandruff medications like Ketoconazole.

There is no convincing evidence that food (such as sugar or yeast), excessive perspiration, or climate have any role in the pathogenesis of dandruff.

There have been many strategies for the control of dandruff. Simply increasing shampooing will remove flakes. However, elimination of the fungus results in dramatic improvement. Regular shampooing with an anti-fungal product will not only treat but prevent recurrence.

Seborrheic dermatitis

Flaking is a symptom of seborrheic dermatitis. Joseph Bark notes that "Redness and itching is actually seborrheic dermatitis, and it frequently occurs around the folds of the nose and the eyebrow areas, not just the scalp." Dry, thick, well-defined lesions consisting of large, silvery scales may be traced to the less common psoriasis of the scalp.

Seasonal changes, stress, and immuno-suppression seem to affect seborrheic dermatitis.

Treatment

* Head & Shoulders anti-dandruff shampoo containing active ingredient Zinc pyrithione. [1]
* Nizoral Shampoo anti-fungal/anti-dandruff shampoo containing active ingredient Ketoconazole.
* Selsun Blue anti-dandruff shampoo containing active ingredient Selenium sulfide.
* The antifungal properties of tea tree oil have been reported as useful in the treatment of dandruff. [2]
* Tar containing shampoos are also used for treatment of dandruff. [3]

Misconceptions

* Dandruff is sometimes confused with dried shampoo. This usually occurs when hair isn't rinsed properly.
* Dandruff is not an organism like lice; it is just dead skin that accumulates in the scalp.
* Dandruff is unlikely to be the cause of hair loss, although excess sebum which is linked to dandruff contains DHT, the primary agent in alopecia.

References

* Dandruff Health Article. Retrieved on 2007-03-28.
* Mayo Clinic page on dandruff. Retrieved on 2007-03-28.

All About Cutaneous larva migrans (Creeping Eruption)

2007-04-02T18:26:00.026-07:00

Cutaneous larva migrans ("CLM") is a skin disease in humans, caused by the larvae of various nematode parasites, the most common of which is Ancylostoma braziliense.

Sometimes referred to as "creeping eruption" or "ground itch", in some parts of the Southern USA this condition is also referred to as "sandworms."

Cause

These parasites are found in dog and cat feces and although they are able to infect the deeper tissues of these animals (through to the lungs and then the intestinal tract), in humans they are only able to penetrate the outer layers of the skin and thus create the typical wormlike burrows visible underneath the skin. The parasites apparently lack the collagenase enzymes required to penetrate through the basement membrane deeper into the skin.

Presentation

The infection causes a red, intense itching eruption. The itching can become very painful and if scratched may allow a secondary bacterial infection to develop.

Treatment

CLM can be treated a number of different ways:

* Systemic (oral) agents include albendazole (trade name Albenza) and ivermectin (trade name Stromectol).

* Another agent which can be applied either topically or taken by mouth is thiabendazole (trade name Mintezol).

* Topical freezing agents, such as ethyl chloride or liquid nitrogen, applied locally can freeze and kill the larvae (but is often a hit-or-miss proposition).

[edit] See also

* Dermatology
* Intestinal parasite
* Visceral larval migrans

All About Herpes simplex (cold sores)

2007-04-02T18:26:00.025-07:00

Herpes simplex is a viral infection caused by one of two Herpes Simplex Viruses (HSV), members of the Herpesviridae family. Manifestations of herpes infections vary significantly between individuals. Most cases of genital herpes are caused by HSV-2. It is widespread, affecting an estimated 1 in 4 females and 1 in 5 males in the United States. Although certain therapies can prevent outbreaks or reduce the risk of transmission to partners, no cure is yet available.[1]

HSV disease

There are two types of Herpes Simplex Virus: HSV Type 1 and HSV Type 2. The ways in which herpes infections manifest themselves vary tremendously among individuals. The following are general descriptions of the courses outbreaks may take in the oral and genital regions.
Infectious fluid-filled blister on lower lip (herpes labialis)
Infectious fluid-filled blister on lower lip (herpes labialis)

Herpes is also formed on the tongue as bumps or white dots

Orofacial infection (generally HSV-1)

1. Prodromal symptoms
2. Skin appears irritated
3. Sore or cluster of fluid-filled blisters appear
4. Lesion begins to heal, usually without scarring

It is estimated that 50% of adults in the United Kingdom are carriers of the Herpes Simplex Virus,[2] many of which will never exibit any symptoms of infection. Similarly, 50% of Americans have HSV-1 antibodies in their blood by the time they're teenagers or young adults and 80-90% of Americans have HSV-1 antibodies by the time they are over age 50.[3] It is also possible for the virus to be transmitted across the skin in the absence of a coldsore. Oral herpes lesions typically occur on the lips, but can occur almost anywhere on the face. They can also occur on the fixed mucosa inside the mouth, including the hard palate (roof of the mouth), and gingiva (gums). Oral herpes and cold sores can sometimes be confused with canker sores. Only a medical physician can provide adequate diagnosis.

Genital infection (generally HSV-2)

1. Prodromal symptoms
2. Itching in affected area
3. Sore appears
4. Lesion begins to heal, usually without scarring

In males, the lesions may occur on the shaft of the penis, in the genital region, on the inner thigh, buttocks, or anus. In females, lesions may occur on or near the pubis, labia, clitoris, vulva, buttocks, or anus. This may require a very careful examination; for example, during delivery, examination by use of a flashlight may be necessary. Symptoms can be confused with that of chlamydia or gonorrhea, so careful observation by a doctor is important.

The appearance of herpes lesions and the experience of outbreaks in these areas varies tremendously among individuals. Herpes lesions on/near the genitals may look like cold sores. An outbreak may look like a paper cut, or chafing, or appear to be a yeast infection. Symptoms of a genital outbreak may include aches and pains in the area, discharge from the penis or vagina, and severe discomfort and burning when urinating.

Initial outbreaks are usually more severe than subsequent ones, and generally also involve flu-like symptoms and swollen glands for a week or so. Subsequent outbreaks tend to be periodic or episodic, typically occur four to five times a year, and can be triggered by stress, illness, fatigue, menstruation, and other changes. The virus sequesters in the nerve ganglia that serve the infected dermatome during non-eruptive periods, where it cannot be conventionally eliminated by the body's immune system.

Herpes simplex encephalitis (generally HSV-1)
Herpesviral encephalitis
Classification & external resources ICD-10 B00.4, G05.1
ICD-9 054.3

Herpes simplex encephalitis is a very serious disorder, thought to be caused by the retrograde transmission of the virus from a peripheral site to the central nervous system along a nerve axon. It is known that the virus lies dormant in the ganglion of the trigeminal or fifth cranial nerve. The reason for reactivation remains unclear. It has also been proposed that the olfactory nerve may be involved.[4] Without treatment, it results in rapid death in around 70% of cases. Even with the best modern treatment, it is fatal in around 20% of cases, and causes serious long-term neurological damage in over half the survivors. Again, for unknown reasons the virus seems to target the temporal lobes of the brain. A small population of survivors, perhaps 20%, show little long-term damage. It is most common in children and middle-aged adults. Although herpes simplex is by no means the most common cause of viral encephalitis (accounting for about 10% of cases in the US), because of the high risk associated with it if it is not treated as well as being one of the few encephalitis to which definitive treatment is available, patients presenting with encephalitis symptoms are likely to be treated against this disorder without waiting for a positive diagnosis. A positive diagnosis can be obtained by CSF PCR for herpes simplex DNA, CSF viral culture or a rising titre for antibodies. The fact that the Electroencephalogram is abnormal in >90% of the patients with Herpes Simplex Encephalitis further aids the diagnosis.

The virus usually infects through the mouth and enters the nucleus during the first 7 days, and will remain latent for 10 days to 100 years, and will then reactivate from common stress, fever, or a sunburn. The virus will soon be contagious through more cold sores, and the disease will start to attack the brain.

Neonatal herpes simplex
Congenital herpesviral (herpes simplex) infection
Classification & external resources ICD-10 P35.2
ICD-9 771.2
HSV at newborn child.
HSV at newborn child.

Neonatal HSV disease is a rare, but serious, consequence of vertical HSV transmission from mother to newborn child. Prospective active surveillance data indicate an incidence rate of 3.61 per 100,000 live births in Australia, with similar rates in the UK; but much lower than the USA. [5][6] Preliminary studies indicate the epidemiology in Canada is closer to Europe than to the United States. The mortality rate from neonatal HSV disease is high (up to 25%) despite current interventions with antiviral therapies. Death results from disseminated HSV disease and/or HSV encephalitis in the newborn children.

Ocular herpes

Ocular herpes (generally HSV-1) is a special case of herpes infection (herpes viral keratitis) that affects the nerves serving the cornea of the eye. It usually manifests as small white itchy lesions on the surface of the cornea, known as dendritic ulcers because they show a branching pattern. Additional symptoms include dull pain deep inside the eye, mild to acute dryness and sinusitis. Most first infections resolve spontaneously in a few weeks or with the use of oral and topical antivirals. However, the virus continues to inhabit the neurons of the eye and to multiply. Subsequent symptoms (with or without visible lesions) include chronic dry eye, low grade intermittent conjunctivitis or chronic unexplained sinusitis. When the patient is immunocompromised or the concentration of viral DNA reaches a critical limit, the presence of the virus can trigger a massive autoimmune response in the eye, resulting in the patient's own system destroying the corneal stroma. This usually results in loss of vision due to opacification of the cornea. Treatment with corneal transplants may be ineffective, as reinfection of the transplant is common; however, with concurrent use of antivirals the chance of graft acceptance is higher. Research is ongoing for a vaccine against ocular herpes.[citation needed]

Ocular herpes is the leading cause of infectious blindness in the developed world.[citation needed] As with orofacial or genital herpes, trauma to the eye increases the chance of a recurrence. Thus herpes viral keratitis can produce complications in the case of patients undergoing radial keratotomy by laser (lasik) to correct vision defects, and patients undergoing this procedure should be carefully screened.

A common cause of infection of the eye is the handling of contact lenses with hands infected by active sores at other sites, notably the mouth; thus the common practice of wetting lenses with saliva when no proprietary solution is available (such as for reinsertion after accidental dislodging) is extremely dangerous and should always be avoided.[citation needed]

Outbreak Triggers

Oral herpes

Physical or psychological stress can trigger an outbreak. Local injury to the face, lips, eyes or mouth, as through trauma, surgery, or sunburns are well established triggers of recurrent orolabial herpes due to herpes simplex virus type 1 (HSV-1). Similarly, intercurrent infections, such as upper respiratory viral infections or other febrile diseases, can cause outbreaks, hence the historic terms "cold sore" and "fever blister". Generalized psychological stress and anxiety are also triggers.

Genital herpes

Controversy exists about triggers of recurrent outbreaks of genital herpes, typically due to HSV-2. It is often stated that stress, menstruation, diet (such as foods high in arginine, like chocolate, peanuts and walnuts) or sexual activity may increase the chance and severity of outbreaks.[citation needed] However, no scientific studies have clearly documented such triggers, and the objective data available suggest that outbreaks are not influenced by stressful events, anxiety, depression, or similar influences. The clinical experience of most experts involved in clinical care is that attempts by infected persons to modify external triggers is virtually never effective in controlling symptomatic oubreaks of genital herpes. Similarly, neither objective data nor biololgical plausibility support the notion that excessive usage of antibiotics affect the immune system's ability to keep the disease within the nerve ganglia (particularly as antibiotics are useless against viruses of any type) or otherwise affect herpes recurrences, nor the occasional assertion that "chronic" genital herpes is in any way related to low-level food allergy.

Symptoms

Herpes infections, whether initial or recurring, are usually first felt as a tingling and/or itching sensation in the affected location. These initial feelings are usually followed, depending on how severe the infection is, by the emergence of a raised or swollen area on the skin. This swollen area then becomes painful in general, but acutely sore when touched, stretched or moved. Eventually the sore area will abscess, and emit a virus laden clear fluid for several days before scabbing over. Once scabbed over the lesion will usually heal completely within a period of a week to ten days. In immuno-compromised individuals this cycle can be significantly protracted.

From the onset of infection/outbreak, many patients experience headaches, fatigue (sometimes extreme), and peculiar twitching sensations in the nerves that lead to the area of the outbreak. The fatigue associated with herpes infections can concatenate with depression brought on by the cosmetic or sexually compromising nature of the infection, to yield a deeply gloomy overall mental state that some believe can contribute to increasing the length and severity of an infection.

Transmission

Herpes is contracted through direct skin contact (not necessarily in the genital area) with an infected person, and less frequently by indirect contact (for instance, by sharing lip balm or a virus infested shared towel). The virus travels through tiny breaks in the skin (or mucous membranes in the mouth and genital areas), so, healthy skin and mucous membranes are normally an effective barrier to infection. However, in the case of mucous membranes, even microscopic abrasions are sufficient to expose the nerve endings into which the virus splices itself. This is why most herpes transmission happens in mucous membranes, or in areas of the body where mucous membranes and normal skin merge (e.g., the corners of the mouth).

Symptoms may not appear for up to a month or more after infection.[citation needed]

Transmission was thought to be most common during an active outbreak; however, in the early 1980s, it was found that the virus can be shed from the skin, saliva and genital secretions in the absence of symptoms.

Recurrence

Herpes recurs only at a site of previous infection. The periodicity (frequency) and amplitude (severity) of recurrence varies greatly depending on the individual and various environmental factors including stress (both physical and mental). Often, for a given site, the infection will recur only two or three times, with severity attenuating (decreasing) each time. The mechanism by which the body seems to gain the upper-hand for a given recurrence site is poorly understood by the medical community.

Self Reinfection

Self reinfection, known medically as autoinoculation, is more likely during intensely virulent initial infection with either HSV-1 or HSV-2 in a given infection site. The most common manifestations are herpetic whitlow, a pustular lesion typically of a finger, and herpes of the eye (keratitis, keratoconjunctivitis).

General hygiene principles suggest that persons with recurrent oral or genital herpes should avoid direct contact with active lesions and should wash their hands immediately after using the toilet or touching the area of an oral lesion, to further limit the low risk of autoinoculation.

In cases where herpes is present in an area where the dermis is subject to high abrasive forces (such as the often irritated shaved beard region, or the surfaces of the penis and vagina during vigorous sexual activity), it is quite common to spread an initial lesion to other sites, which then become highly virulent initial infections, and so on. The medical community has failed to make this very obvious fact clear to patients and this has resulted in great amplification of their general misery, not to mention the much higher likelihood that a person infected in multiple sites (whether genital, or otherwise) will spread this disease to friends, family and sexual partners.

Asymptomatic Shedding

HSV asymptomatic shedding is believed to occur on 2.9% of days while on antiviral therapy, versus 10.8% of days without. Shedding is known to be more frequent within the first 12 months of acquiring HSV-2, and concurrent infection with HIV also increases the frequency and duration of asymptomatic shedding.[7] There are some indications that some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified. Sex should always be avoided in the presence of symptomic lesions. Oral sex performed by someone with oral lesions or other symptoms should be avoided, to avoid transmission of HSV-1 to the partner's genitals. Even without symptoms it is possible for transmission to occur. Many people still believe Herpes cannot be transmitted through oral sex. This is a dangerous myth.

Women are more susceptible to acquiring genital HSV-2 than men; in the US, 11% of men and 23% of women carry HSV-2.[8] On an annual basis, without the use of antivirals or condoms, the transmission risk from infected male to female is approximately 8-10%. This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is approximately 4-5% annually. Suppressive antiviral therapy reduces these risks by 50%. Antivirals also help prevent the development of symptomatic HSV in infection scenarios by about 50%, meaning the infected partner will be seropositive but symptom free. Condom use also reduces the transmission risk by 50%. Condom use is much more effective at preventing male to female transmission than vice-versa. [9] The effects of combining antiviral and condom use is roughly additive, thus resulting in approximately a 75% combined reduction in annual transmission risk. These figures reflect experiences with subjects having frequently-recurring genital herpes (>6 recurrences per year). Subjects with low recurrence rates and those with no clinical manifestations were excluded from these studies.

Prevention

For genital herpes, condoms are a highly recommended way to limit transmission of herpes simplex infection, as demonstrated in research. [9][10] However, condoms are by no means completely effective. The effectiveness of this method is somewhat limited on a public health scale by the limited use of condoms in the community [11]; and on an individual scale because some blisters may not be covered by the condom, or free virus in female vaginal fluid may enable infection around the base of the penis or testicles not covered by the condom.

Condoms do not prevent the condom wearer from spreading the infection to new sites either on himself through abrasion (if he is already infected and suffering an outbreak), or on the female partner if she is suffering from an outbreak and the sexual activity spreads this infection from one site to another on her own body (see "Self Reinfection" above).

The use of condoms or dental dams can limit the transmission of Herpes from the genitals of one partner to the mouth of the other (or vice versa) during oral sex.

When one partner has herpes simplex infection and the other does not, the use of valaciclovir, in conjunction with a condom, has been demonstrated to decrease further the chances of transmission to the uninfected partner, and the Food and Drug Administration (FDA) approved this as a new indication for the drug in August 2003.

Vaccines for HSV are currently undergoing trials. Once developed, they may be used to help with prevention or minimize initial infections as well as treatment for existing infections. [12]

Other measures that have been suggested include:

* Avoidance of cross-infecting new sites on the body if HSV blisters are present
* Gentle and well lubricated as opposed to vigorous, abrasive sex
* Thorough washing of the genitals after sex
* Not ejaculating inside a partner during sex (if herpes lesions have appeared inside the urethra)
* Management of stress
* Adequate sleep and nutrition
* Use of a lip protectant or lip gloss to avoid cracks and abrasions through which the virus may infect
* Treatment using ascorbate-Cu(II) [13]

Future vaccines

The National Institutes of Health (NIH) in the United States is currently in the midst of phase III trials of a vaccine against HSV-2. The vaccine has only been shown to be effective for women who have never been exposed to HSV-1. Overall, the vaccine is approximately 48% effective in preventing HSV-2 seropositivity and about 78% effective in preventing symptomatic HSV-2. Assuming FDA approval, a commercial version of the vaccine is estimated to become available around 2008. During initial trials, the vaccine did not exhibit any evidence in preventing HSV-2 in males. Additionally, the vaccine only reduced the acquisition of HSV-2 and symptoms due to newly acquired HSV-2 among women who did not have HSV-1 infection at the time they got the vaccine. Because about 50% of persons in the United States have HSV-1 infection, this further reduces the population for whom this vaccine might be appropriate. The candidate vaccine is called Herpevac, and individuals who might be interested in learning about the study can easily find information at Herpevac Trial for Women

Treatment

Currently, there is no cure for herpes. There is no treatment that can eradicate herpes virus from the body at reactivations of the virus. Non-prescription analgesics can reduce pain and fever during initial outbreaks.

Anti-viral Medication

There are several prescription antiviral medications for controlling herpes outbreaks, including aciclovir (Zovirax), valaciclovir (Valtrex), famciclovir (Famvir), and penciclovir. Aciclovir was the original and prototypical member of this class and generic brands are now available at a greatly reduced cost. Some prescription drugs to treat herpes can cause diarrohea several times a day so patients are advised to take non prescribed diarrohea tablets as required in these cases along with the medication. It has been claimed that the evidence for the effectiveness of topically applied cream for recurrent labial outbreaks is weak.[14] Likewise oral therapy for episodes is inappropriate for most non-immunocompromised patients, whilst there is evidence for oral prophylactic role in preventing recurrences.[15]

Valaciclovir and famciclovir are prodrugs of aciclovir and penciclovir respectively, with improved oral bioavailability (55% vs 20% and 75% vs 5% respectively). These antiviral medications work by interfering with viral replication, effectively slowing the replication rate of the virus and providing a greater opportunity for the immune response to intervene. All drugs in this class depend on the activity of the viral thymidine kinase to convert the drug to a monophosphate form and subsequently interfere with viral DNA replication. Penciclovir's primary advantage over aciclovir is that it has a far longer cellular half-life – 10 hours (HSV-1)/20 hours (HSV-2) for penciclovir versus 3 hours (HSV-1/2) for aciclovir.

Aciclovir is the recommended antiviral for suppressive therapy to prevent transmission of herpes simplex to the neonate. The use of valaciclovir and famciclovir, while potentially improving treatment compliance and efficacy, are still undergoing safety evaluation in this context. [16] There is evidence in mice that treatment with famciclovir, rather than aciclovir, during an initial outbreak can help lower the incidence of future outbreaks by reducing the amount of latent virus in the neural ganglia. This potential effect on latency over aciclovir drops to zero a few months post-infection. [17]

Other drugs exhibiting anti-viral activity

Docosanol (Abreva) is another treatment that may be effective. Docosanol works by preventing the virus from fusing to cell membranes, thus barring entry into the cell for the virus. This may keep an outbreak contained to a smaller area than would otherwise be observed.

Zilactin is an early relief cold sore/fever blister gel that works by applying the gel, which when dry forms a "shield" to prevent the sore from increasing in size and prevents spreading by breakage or oozing during the healing process.

Tromantadine is another antiviral drug effective against herpes.

Other drugs

Cimetidine, a common component of heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances, and offered some relief from herpes simplex [18] [19] [20] . This is an off-label use of the drug.

It and probenecid have been shown to reduce the renal clearance of aciclovir. [21] The study showed these compounds reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir. Renal clearance of aciclovir was reduced by approximately 24% and 33% respectively. In addition, respective increases in the peak plasma concentration of acyclovir of 8% and 22% were observed. The authors concluded that these effects were "not expected to have clinical consequences regarding the safety of valaciclovir". Due to the tendency of aciclovir to precipitate in renal tubules, combining these drugs should only occur under the supervision of a physician.

Availability of non-generic prescriptions

* Valaciclovir (GlaxoSmithKline) is protected under U.S. Patent 4957924 protection expiring June 2009
* Famciclovir (Novartis) is protected under U.S. Patent 5246937 protection expiring Sept 2010
* Penciclovir (GlaxoSmithKline) is protected under U.S. Patent 5075445 protection expiring Sept 2010
* Docosanol (Avanir) is protected under U.S. Patent 4874794 protection expiring April 2014

[edit] Availability of generic prescriptions

* Acyclovir is no longer under US patent protection, available in generic form

[edit] Drugs in development

* BAY 57-1293, a helicase-primase inhibitor researched by Bayer AG scientist Gerald Kleymann's team in Wuppertal, Germany. [22][23]

* BILS 179 BS, BILS 45 BS, BILS 22 BS, also inhibitors of helicase-primase enzyme, researched in Ridgefield, Connecticut, by James Crute's team at Boehringer Ingelheim Pharmaceuticals. [24][25]

* Roscovitine is an inhibitor of cellular cyclin-dependent kinase and seems to prevent transcription of viral genomes. Roscovitine has entered clinical trials for HIV infection. [26][27][28]

Natural compounds

Lysine

Lysine supplementation has been proposed as a complementary therapy for the prophylaxis and treatment of herpes simplex. Lysine supplementation is highly dose-dependent, with beneficial effects apparent only at doses exceeding 1000 mg per day. A small randomised controlled trial indicated a decrease in recurrence rates in nonimmunocompromised patients at a dose of 1248 mg of lysine monohydrochloride, but no effect at 624 mg daily. This study did not show any evidence of shortening the healing time compared to placebo. [29] Another small randomised controlled trial indicated the benefit of 3000 mg lysine daily for the reduction of occurrence, severity and healing time for recurrent HSV infection. [30]

Tissue culture studies have shown the suppression of viral replication when the lysine to arginine ratio in vitro favours lysine. The therapeutic consequence of this finding is unclear, but dietary arginine may affect the effectiveness of lysine supplementation. [31]

Lysine intake may be supplemented by varying the diet. Dairy products offer the highest ratio of lysine to arginine amino-acid content. Contrarily, nuts (and peanuts, even though they aren't true nuts), deliver a large dose of arginine. To help forestall outbreaks, you might avoid nuts during stressful periods, and eat cheese any time you do eat nuts. During an outbreak, eating cheese may slow the spread of lesions, and reduce virus shedding and self-reinfection. Eating 100g (~4oz) of Parmesan cheese supplies 3.3g of lysine, vs. 1.3g of arginine. The same amount of almonds provides 0.7g of lysine, but 2.4g of arginine. (Cf. the Danish Food Composition Databank, http://www.foodcomp.dk/fcdb_alphlist.asp)

High doses of lysine (greater than 10 grams daily) are known to cause gastrointestinal adverse effects. Dyspepsia was reported in 3 of 114 subjects treated with L-lysine in one study. [30] Prolonged and/or very high lysine doses may also have adverse effects on renal function, indeed lysine is contraindicated in lysine hypersensitivity and kidney or liver disease. (Anon., 2005) One patient, with a history of risk factors for renal impairment, developed tubulointerstitial nephritis (Fanconi's Syndrome) after taking lysine 3000 mg daily for approximately 5 years. [32]

Polysaccharides

Carrageenans, linear sulphated polysaccharides extracted from red seaweeds, have been shown to have antiviral effects in HSV-infected cells.

* There are indications that a carrageenan based gel may offer some protection against HSV-2 transmission by binding to the receptors on the herpes virus thus preventing the virus from binding to cells. Researchers have shown that a carrageenan-based gel effectively prevented HSV-2 infection at a rate of 85% in a mouse model.[33] There is an ongoing large-scale trial of the efficacy of a similar formulation on humans results are expected to be published in 2007.
* The natural carrageenans 1T1, 1C1, 1C3 isolated from Gigartina skottsbergii seaweed inhibited the replication activity of HSV-1 and HSV-2 in infected mouse astrocyte nerve cells and vero cells.[34]

Lactoferrin

Lactoferrin, a component of whey protein, has been shown to have a synergistic effect with aciclovir against HSV in vitro.[35] The concentration of lactoferrin which achieved 50% of maximum effectiveness observed (that is, the EC50) also acted in synergy with aciclovir; the concentration required to achieve EC50 for each substance was reduced "two- to seven-fold."

Resveratrol

Resveratrol, a compound in red wine, has been shown by researchers to prevent HSV replication in vitro by inhibiting a protein needed by the virus to replicate. Resveratrol alone was not considered potent enough by the researchers to be an effective treatment.[36] A more recent in vivo study in mice showed the efficacy of topical resveratrol cream in preventing cutaneous HSV lesion formation.[37] Research on a much more potent derivative of resveratol, named stil-5, is ongoing. There is no evidence that red wine consumption provides any similar benefits.

Unproven

Limited evidence suggests that low dose aspirin (125 mg daily) might be beneficial in patients with recurrent HSV infections. A small study of 21 volunteers with recurrent HSV indicated a significant reduction in duration of active HSV infections, milder symptoms, and longer symptom-free periods as compared to a control group. [38] A recent animal study found that aspirin inhibited thermal stress-induced ocular viral shedding of HSV-1, and a possible benefit in reducing recurrences. [39] Aspirin is not recommended in persons under 18 years of age with herpes simplex due to the increased risk of Reye's syndrome. Long term daily doses of aspirin have a side effect of reduced blood coagulation, facilitating bruising. A single 81 mg "daily dose" aspirin is a safer regimen given that there are no studies of the correlation between dosage and anti-viral effects of aspirin.

Other

The evidence for the effectiveness of zinc and Vitamin C supplementation is poor. [40] Other supplements with anecdotal evidence of benefits include monolaurin, vitamin A, vitamin B12, garlic, and echinacea. Daily multivitamin intake may be beneficial through maintenance of immune system health. High doses of vitamin A should not be taken in early pregnancy due to linkage with birth defects. In addition, some anecdotal reports indicate that placing ice in contact with an emerging cold sore for 5-10 minutes throughout the day can help shorten the duration of the outbreak, or prevent it from developing further.

Butylated Hydroxytoluene (BHT), commonly available as a food preservative, has been shown in in-vitro laboratory studies to inactivate the herpes virus.[41] In-vivo studies in animals confirmed the anti-viral activity of BHT against genital herpes.[42] However BHT has not been clinically tested and approved to treat herpes infections in humans.

Latent infection and biology

The herpes virus is a double-stranded DNA (dsDNA)-type virus. Herpes establishes a latent infection in cells of the nervous system. Double-stranded DNA is incorporated into the cell physiology by infection of the cell nucleus, where a loop of dsDNA is maintained. During inactive, or latent, periods of the infection, a subset of the Herpes genome termed LAT or Latency Associated Transcript is active and may be involved in maintenance of latency.

Long-term effects

The long-term effects of herpes are not well known, but the blisters may leave scars, and historically it was thought to contribute to the risk of cervical cancer in women. Subsequently, another virus, human papillomavirus (HPV), has been shown to be a primary cause of cervical cancer in women. Additionally, people with herpes are at a higher risk of HIV transmission because of open blisters. In newborns, however, herpes can cause serious damage: death, neurological damage, mental retardation, and blindness.

The immune system is able to destroy active herpes virus particles but the herpes virus has the ability to hide from the immune system in an inactive (or latent) state. Current research suggests that this ability to hide may be achieved via modification to cellular enzyme histone deacetylases (HDACs), namely HDAC1 and HDAC2. [43] Hypothetically, by interfering with the HDAC enzymes' effectiveness, it may be possible to block the virus's ability to hide from the immune system, leading to a complete elimination of the virus by the immune system. Studies on the impact of HDAC inhibitors on viral latency are ongoing in the HIV arena.

Obstetric / Neonatal risks

Recurrent genital herpes has very significant obstetrical/neonatal risks associated with it, and probably may merit treatment with acyclovir as an independent problem. [44]

Viral Meningitis

It is reasonably well-established in the last few years that herpes simplex virus 2 (HSV-2) is the most common cause of recurrent viral meningitis (Mollaret's meningitis). [45]

Psychological and social effects

Herpes can have a dramatic effect on an individual's mental well-being and sexual behaviour.

Quality of life issues

Upon diagnosis of genital herpes, people can experience a number of negative feelings related to the condition. Though these feelings lessen over time, they can include:[46]

* depression 81%
* fear of rejection 75%
* feeling of isolation 69%
* fear of being found out 55%
* self-destructive feelings 28%

The impact of genital herpes included:

* partial or complete cessation of sexual activity
* total or partial loss of interest in sex
* decreased sexual pleasure
* sex life more inhibited and less spontaneous
* anxiety related to sexual desirability
* increased depression

In order to improve the well-being of people with herpes, a number of support groups [47], communities [48] and dating sites [49][50] have formed a presence on the Internet.

Media portrayal

Media portrayals of genital herpes - which might help to destigmatise the condition - remain few and, when they occur, are often negative.[51]

Examples of such portrayals in the main types of media include:

* in the mainstream press, a 1982 article in Time magazine called “Herpes: Today’s Scarlet Letter”; [52]

* on television, a 1983 telefilm called “Intimate Agony”;[53]

* in music, a 1993 Marilyn Manson song called “Herpes”;[54]

* in the cinema, a 2005 film called “Merry Christmas… I Got You Herpes”;[55]

* in literature, a 2006 novel called “Stigma”;[56]

Disclosure to new partners

People with genital herpes are often hesitant to divulge to other people that they have the virus, including friends and family but especially new or potential sexual partners. People may be less likely to inform what they consider to be 'casual' partners.[57] In addition, the perception of the likely reaction is sometimes taken into account before making a decision about whether to inform new partners. An event such as a couple moving in together was found to be the point when some people disclosed their status. Reactions by sexual partners may not always be negative, and individuals often use various strategies to mitigate the impact of disclosure such as keeping the issue "low key," choosing a relaxed environment and suggesting the couple being tested jointly for a range of sexually transmitted infections.

Legal redress

Whether the law can help a person who catches herpes depends on the jurisdiction where it was contracted as legal jurisdictions define their own rules regarding the transmission of STIs such as herpes.[58] There can be both criminal and civil possibilities. For example, in the criminal case of R. v. Sullivan heard in England and Wales, a man was prosecuted for sexual assault after his partner experienced a primary outbreak of genital herpes, on the basis that he had failed to reveal the fact that he had herpes. Ultimately, the man was discharged due to an inability to prove prior knowledge. Civil claims for transmission of herpes are, for their part, usually based on negligence if transmission was accidental and battery if deliberate. The first successful case to allow such a claim in the United States was Kathleen K. v. Robert B., decided by the California Court of Appeals.

Myths

Some common misconceptions about herpes are:

* that it is fatal. Fact: This is only true for newborns, which is rare, but it is fatal in 25% of all such cases. It can also possibly kill an adult if it infects the brain causing encephalitis, or infects the meninges causing meningitis.
* that it only affects the genital areas. Fact: It can affect any part of the body. If you touch a genital herpes sore and then touch another part of your body, you can potentially spread the virus.
* that condoms are completely effective in preventing the spread of this disease. Fact: They do greatly improve protection but are imperfect only preventing transmission 50% of the time.
* that it is only transmittable in the presence of symptoms. Fact: There is more viral shedding during an outbreak but it's possible to transmit any time.
* that it can make you sterile Fact: Genital Herpes cannot make you sterile.
* that Pap smears detect herpes Fact PAP smears are not designed to detect herpes simplex virus infections. Type-specific serology tests and viral cultures are used to diagnose genital herpes and are not normally conducted during a woman's annual gynecological examination.
* that it can not be transmitted between the genitals and the mouth. Fact: Even the use of a condom will not prevent transmission between genital and oral regions.
* that only promiscuous people get it. Fact: It is so common that anyone can contract it. The more sexual partners an individual has, however, the more likely they are to contract the disease.[59]

There is a basis in fact that herpes could be transmitted via an inanimate object such as a toilet seat or wet towel but the conditions required for this kind of transmission (high heat, high moisture, and a vulnerable exposure site) make it extremely unlikely. Although there are no confirmed cases of this type of transmission, sharing a towel with somebody with active lesions should be avoided. Likewise, sharing lip or mouth products (toothbrushes, lipstick, lip balm, or similar) with somebody with active lesions should also be avoided.

Footnotes

1. ^ Center for Disease Control (CDC) - Herpes Fact Sheet Accessed February 7, 2007.
2. ^ U.K Herpes Viruses Association - [1] Accessed March 15, 2007.
3. ^ "Herpes Online: Exploring the "H" Community", American Social Health Association, 1996, pp. 1-4. Retrieved on 2007-03-29. (in English)
4. ^ Dinn J (1980). "Transolfactory spread of virus in herpes simplex encephalitis.". Br Med J 281 (6252): 1392. PMID 7437807.
5. ^ Elliott E, Rose D. (2003). "Australian Paediatric Surveillance Unit. Reporting of communicable disease conditions under surveillance by the APSU, 1 January to 30 September 2003". Commun. Dis. Intell. 28 (1): 90-91. PMID 15072162.
6. ^ Jones CA (2004). "Vaccines to prevent neonatal herpes simplex virus infection". Expert Rev. Vaccines 3 (4): 363-364. PMID 15270635.
7. ^ Kim H, Meier A, Huang M, Kuntz S, Selke S, Celum C, Corey L, Wald A (2006). "Oral herpes simplex virus type 2 reactivation in HIV-positive and -negative men.". J Infect Dis 194 (4): 420-7. PMID 16845624.
8. ^ Carla K. Johnson. "Percentage of people with herpes drops", Associated Press, Aug 23, 2006.
9. ^ a b Wald A, Langenberg AG, Link K, Izu AE, Ashley R, Warren T, Tyring S, Douglas JM Jr, Corey L. (2001). "Effect of condoms on reducing the transmission of herpes simplex virus type 2 from men to women". JAMA 285 (24): 3100-3106. PMID 11427138.
10. ^ Casper C, Wald A. (2002). "Condom use and the prevention of genital herpes acquisition.". Herpes 9 (1): 10-14. PMID 11916494.
11. ^ de Visser RO, Smith AM, Rissel CE, Richters J, Grulich AE. (2003). "Sex in Australia: safer sex and condom use among a representative sample of adults". Aust. N. Z. J. Public Health. 27 (2): 223-229. PMID 14696715.
12. ^ Seppa, Nathan. "One-Two Punch: Vaccine fights herpes with antibodies, T cells", Science News, 2005-01-05, pp. 5. Retrieved on 2007-03-29. (in English)
13. ^ Betanzos-, G; CabreraRamirez FJ, Munoz JL, Barron BL, Maldonado R. (2004-09-15). "Inactivation of HSV-2 by ascorbate-Cu(II) and its protecting evaluation in CF-1 mice against encephalitis.". Journal of virological methods 120 (2): 161-165. DOI:2004-09-15. 15288958. Retrieved on 2007-03-29.
14. ^ Graham Worrall (6 Jul 1996). "Evidence for efficacy of topical acyclovir in recurrent herpes labialis is weak". BMJ 313: 46. - Letter
15. ^ Graham Worrall (6 Jan 1996). "Acyclovir in recurrent herpes labialis". BMJ 312: 6. - Editorial
16. ^ Leung DT, Sacks SL. (2003). "Current treatment options to prevent perinatal transmission of herpes simplex virus". Expert Opin. Pharmacother. 4 (10): 1809-1819. PMID 14521490.
17. ^ Thackray AM, Field HJ. (1996). "Differential effects of famciclovir and valaciclovir on the pathogenesis of herpes simplex virus in a murine infection model including reactivation from latency". J. Infect. Dis. 173 (2): 291-299. PMID 8568288.
18. ^ Kapinska-Mrowiecka M, Toruwski G (1996.). "Efficacy of cimetidine in treatment of herpes zoster in the first 5 days from the moment of disease manifestation.". Pol Tyg Lek. 51 (23-26): 338-339. PMID 9273526.
19. ^ Hayne ST, Mercer JB (1983). "Herpes zoster:treatment with cemetidine.". Can Med Assoc J 129 (12): 1284-1285. PMID 6652595.
20. ^ Komlos L, Notmann J, Arieli J, et.al. (1994). "In vitro cell-mediated immune reactions in herpes zoster patients treated with cimetidine.". Asian Pac J Allelrgy Immunol 12 (1): 51-58. PMID 7872992.
21. ^ De Bony F, Tod M, Bidault R, On NT, Posner J, Rolan P. (2002). "Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite acyclovir". Antimicrob. Agents Chemother. 46 (2): 458-463. PMID 11796358.
22. ^ Winstead ER.. Two new anti-herpes drugs tested. Genome News Network. Retrieved on 2006-03-20.
23. ^ Kleymann G, Fischer R, Betz UA, Hendrix M, Bender W, Schneider U, Handke G, Eckenberg P, Hewlett G, Pevzner V, Baumeister J, Weber O, Henninger K, Keldenich J, Jensen A, Kolb J, Bach U, Popp A, Maben J, Frappa I, Haebich D, Lockhoff O, Rubsamen-Waigmann H. (2002). "New helicase-primase inhibitors as drug candidates for the treatment of herpes simplex disease". Nat. Med. 8 (4): 392-398. PMID 11927946.
24. ^ Crute JJ, Grygon CA, Hargrave KD, Simoneau B, Faucher AM, Bolger G, Kibler P, Liuzzi M, Cordingley MG. (2002). "Herpes simplex virus helicase-primase inhibitors are active in animal models of human disease". Nat. Med. 8 (4): 386-391. PMID 11927945.
25. ^ Liuzzi M, Kibler P, Bousquet C, Harji F, Bolger G, Garneau M, Lapeyre N, McCollum RS, Faucher AM, Simoneau B, Cordingley MG. (2004). "Isolation and characterization of herpes simplex virus type 1 resistant to aminothiazolylphenyl-based inhibitors of the viral helicase-primase". Antiviral Res. 64 (3): 161-170. PMID 15550269.
26. ^ Schang LM, Coccaro E, Lacasse JJ. (2005). "Cdk inhibitory nucleoside analogs prevent transcription from viral genomes.". Nucleosides Nucleotides Nucleic Acids. 24 (5-7): 829-837. PMID 16248044.
27. ^ Diwan P, Lacasse JJ, Schang LM. (2004). "Roscovitine inhibits activation of promoters in herpes simplex virus type 1 genomes independently of promoter-specific factors". J. Virol. 78 (17): 9352-9365. PMID 15308730.
28. ^ Schang LM. (2005). "Advances on cyclin-dependent kinases (CDKs) as novel targets for antiviral drugs". Curr. Drug Targets Infect. Disord. 5 (1): 29-37. PMID 15777196.
29. ^ McCune MA, Perry HO, Muller SA, O'Fallon WM. (2005). "Treatment of recurrent herpes simplex infections with L-lysine monohydrochloride". Cutis. 34 (4): 366-373. PMID 6435961.
30. ^ a b Griffith RS, Walsh DE, Myrmel KH, Thompson RW, Behforooz A. (1987). "Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis". Dermatologica. 175 (4): 183-190. PMID 3115841.
31. ^ Griffith RS, Norins AL, Kagan C. (1978). "A multicentered study of lysine therapy in Herpes simplex infection". Dermatologica. 156 (5): 257-267. PMID 640102.
32. ^ Lo JC, Chertow GM, Rennke H, Seifter JL. (1996). "Fanconi's syndrome and tubulointerstitial nephritis in association with L-lysine ingestion.". Am. J. Kidney Dis. 28 (4): 614-617. PMID 8840955.
33. ^ Zacharopoulos VR, Phillips DM. (1997). "Vaginal formulations of carrageenan protect mice from herpes simplex virus infection". Clin. Diagn. Lab. Immunol. 4 (4): 465-468. PMID 9220165.
34. ^ Carlucci MJ, Scolaro LA, Damonte EB. (1999). "Inhibitory action of natural carrageenans on Herpes simplex virus infection of mouse astrocytes". Chemotherapy 45 (6): 429-436. PMID 10567773.
35. ^ Andersen JH, Jenssen H, Gutteberg TJ. (2003). "Lactoferrin and lactoferricin inhibit Herpes simplex 1 and 2 infection and exhibit synergy when combined with acyclovir". Antiviral Res. 58 (3): 209-215. PMID 12767468.
36. ^ Docherty JJ, Fu MM, Stiffler BS, Limperos RJ, Pokabla CM, DeLucia AL. (1999). "Resveratrol inhibition of herpes simplex virus replication". Antiviral Res. 43 (3): 145-155. PMID 10551373.
37. ^ Docherty JJ, Smith JS, Fu MM, Stoner T, Booth T. (2004). "Effect of topically applied resveratrol on cutaneous herpes simplex virus infections in hairless mice". Antiviral Res. 61 (1): 19-26. PMID 14670590.
38. ^ Karadi I, Karpati S, Romics L. (1998). "Aspirin in the management of recurrent herpes simplex virus infection". Ann. Intern. Med. 128 (8): 696-697. PMID 9537952.
39. ^ Gebhardt BM, Varnell ED, Kaufman HE. (2004). "Acetylsalicylic acid reduces viral shedding induced by thermal stress". Curr. Eye Res. 29 (2-3): 119-125. PMID 15512958.
40. ^ Unknown (2005). "Herpes simplex virus oral", in Klasco RK (ed.): AltMedDex System. Greenwood Village, CO: Thomson Micromedex.
41. ^ Snipes W, Person S, Keith A, Cupp J. "Butylated hydroxytoluene inactivates lipid-containing viruses" Science. 1975;188(4183):64-6
42. ^ Richards JT, Katz ME, Kern ER. "Topical butylated hydroxytoluene treatment of genital herpes simplex virus infections of guinea pigs" Antiviral Res 1985;5(5):281-90
43. ^ Poon AP, Liang Y, Roizman B. (2003). "Herpes simplex virus 1 gene expression is accelerated by inhibitors of histone deacetylases in rabbit skin cells infected with a mutant carrying a cDNA copy of the infected-cell protein no. 0". J. Virol. 77 (23): 12671-12678. PMID 14610189.
44. ^ Brocklehurst P, Kinghorn GA et al.. "randomised placebo controlled trial of suppressive acyclovir in late pregnancy in women with recurrent genital herpes infection" 105 (3): 275-80.
45. ^ Recurring viral meningitis & herpes II. Med Help International. Retrieved on 2006-11-21.
46. ^ Vezina C, Steben M. (2001). "Genital Herpes: Psychosexual Impacts and Counselling". The Canadian Journal of CME (June): 125-134.
47. ^ Herpes Support Groups & Clinics
48. ^ Herpes message forum with over 4000 members
49. ^ H-Date, a dating site for persons with either or both of HSV-1 or HSV-2
50. ^ MPwH - Meeting People with Herpes, a dating site with over 65000 members
51. ^ Webpage on social aspects of genital herpes
52. ^ Time Magazine archives
53. ^ Film Database description of Intimate Agony
54. ^ Wikipedia article including reference to the song Herpes
55. ^ Film Database description of Merry Christmas...
56. ^ Description of novel Stigma
57. ^ Green J, Ferrier S, Kocsis A, Shadrick J, Ukoumunne OC, Murphy S, Hetherton J. (2003). "Determinants of disclosure of genital herpes to partners.". Sex. Transm. Infect. 79 (1): 42-44. PMID 12576613.
58. ^ Webpage on social aspects of genital herpes
59. ^ Myths and Facts about Genital Herpes. Famciclovir (2007). Retrieved on 2007-01-31.

All About Chloracne

2007-04-02T18:26:00.024-07:00

Chloracne is an acne-like eruption of blackheads, cysts, and pustules associated with over-exposure to certain halogenic aromatic hydrocarbons, such as chlorinated dioxins and dibenzofurans. The lesions are most frequently found on the cheeks, behind the ears, in the armpits and groin region.

The condition was first described in German industrial workers in 1897 by Von Bettman, and was initially believed to be caused by exposure to toxic chlorine (hence the name "chloracne"). It was only in the mid-1950s that chloracne was associated with aromatic hydrocarbons[1]. The substances that may cause chloracne are now collectively known as "chloracnegens".

Chloracne is particularly linked to toxic exposure to dioxins (byproducts of many chemical processes, including the manufacture of herbicides such as Agent Orange) — so much so that it is considered a clinical sign of dioxin exposure. The severity and onset of chloracne may follow a typical asymptotic dose response curve.

Etiology and progression

Chloracne normally results from direct skin contact with chloracnegens, although ingestion and inhalation are also possible causative routes.

Chloracnegens are fat-soluble, meaning they persist in the body fat for a very long period following exposure. Chloracne is a chronic inflammatory condition that results from this persistence, in combination with the toxin's chemical properties. It is believed, at least from rodent models, that the toxin activates a series of receptors promoting macrophage proliferation, inducing neutrophilia and leading to a generalised inflammatory response in the skin. This process may also be augmented by induction of excess tumor necrosis factor in the blood serum.

The inflammatory processes lead to the formation of keratinous plugs in skin pores, forming yellowish cysts and dark pustules. The skin lesions occur mainly in the face, but in more severe cases they involve the shoulders and chest, the back, and the abdomen. In advanced cases, the lesions appear also on the arms, thighs, legs, hands and feet.

In some instances, chloracne may not appear for three to four weeks after toxic exposure; however in other cases - particularly in events of massive exposure - the symptoms may appear within days [1][2].

Treatment

Once chloracne has been identified, the primary action is to remove the patient and all other individuals from the source of contamination. Further treatment is symptomatic.

Severe or persistent lesions may be treated with oral antibiotics or isotretinoin. However, chloracne may be highly resistant to any treatment.

The course of the disease is highly variable. In some cases the lesions may resolve within two years or so; however, in other cases the lesions may be effectively permanent (mean duration of lesions in one 1984 study was 26 years, with some workers remaining disfigured over three decades after exposure [3]).

Recent research by groups at University of Cincinnati School of Medicine in Ohio and the University of Western Australia indicated that PCB poisoning, including chloracne symptoms, can be treated with fat substitute olestra.

Related conditions

Chloracne is very often seen in combination with hyperhidrosis (clammy, sweaty skin) and porphyria cutanea tarda (a skin condition of increased pigmentation, hair coarsening and blistering).

Notable cases

* 193 cases of chloracne occurred in Seveso, Italy in 1976 following the Seveso disaster in which several kilograms of TCDD were released into the atmosphere.

* Hundreds of individuals suffered chloracne after chronic exposure to PCBs and PCDFs in central Taiwan in 1979.

* Ukrainian President Viktor Yushchenko suffered from extremely prominent facial chloracne after being diagnosed with dioxin poisoning in late 2004. His diagnosis of chloracne was put forth by prominent toxicologist John Henry.

See also

* Dioxin
* Neal Stephenson's novel Zodiac discusses the effects of chloracne.

References

1. ^ a b Williams, D.E.; Wolfe, W.H.; Lustik, M.B. et al. (1995). An Epidemiologic Investigation of Health Effects in Air Force Personnel Following Exposure to Herbicides. Vol. 4.
2. ^ De Marchia, B, and Ravetzb, J.R. (1999). Risk management and governance: a post-normal science approach. Futures 31:743–757.
3. ^ Moses, M. et al. (1984). American Journal of Industrial Medicine 5(3):161-82.

All About Cellulitis

2007-04-02T18:26:00.023-07:00

Cellulitis is an inflammation of the connective tissue underlying the skin, that can be caused by a bacterial infection. Cellulitis can be caused by normal skin flora or by exogenous bacteria, and often occurs where the skin has previously been broken: cracks in the skin, cuts, burns, insect bites, surgical wounds, or sites of intravenous catheter insertion. The mainstay of therapy remains treatment with appropriate antibiotics. Skin on the face or lower legs is most commonly affected by this infection, though cellulitis can occur on any part of the body. Cellulitis may be superficial — affecting only the surface of the skin — but cellulitis may also affect the tissues underlying the skin and can spread to the lymph nodes and bloodstream.

It is unrelated to cellulite, a cosmetic condition featuring dimpling of the skin.

Forms of cellulitis

A few of the forms of cellulitis are as follows: periorbital cellulitis (an infection of the eye socket), erysipelas, clostridial cellulitis, nonclostridial cellulitis, and synergistic necrotizing cellulitis (Pankey, 1992). A few forms of cellulitis do not have some of the symptoms most commonly listed (for example, clostridial and nonclostridial cellulitis do not cause the skin to turn red [Pankey, 1992]), but the majority do. Necrotizing fasciitis can be mistaken for cellulitis but is notable for involvement of the deeper tissue structures, the fascia, and can be limb and life threatening.
Infected left knee
Infected left knee

Symptoms

Cellulitis is characterized by redness, swelling, warmth, and pain or tenderness. Cellulitis frequently occurs on exposed areas of the body such as the arms, legs, and face. Other symptoms can include fever or chills and headaches. In advanced cases of cellulitis, red streaks (sometimes described as ‘fingers’) may be seen traveling up the affected area. The swelling can spread rapidly.
Cellulitis in a Limb showing typical red streaks and swelling

Causes

Cellulitis is caused by a type of bacteria entering by way of a break in the skin. This break need not be visible. Group A streptococcus and staphylococcus are the most common of these bacteria, which are part of the normal flora of the skin but cause no actual infection until the skin is broken. Predisposing conditions for cellulitis include insect bite, animal bite, pruritic skin rash, recent surgery, athlete's foot, dry skin, eczema, burns & boils, though there is debate as to whether minor foot lesions contribute.

The appearance of your skin will help your doctor make a diagnosis. Your doctor may also suggest blood tests, a wound culture or other tests to help rule out a blood clot deep in the veins of your legs. Cellulitis in the lower leg is characterized by signs and symptoms that may be similar to those of a clot occurring deep in the veins, such as warmth, pain and swelling.

This reddened skin or rash may signal a deeper, more serious infection of the inner layers of skin. Once below the skin, the bacteria can spread rapidly, entering the lymph nodes and the bloodstream and spreading throughout your body.

In rare cases, the infection can spread to the deep layer of tissue called the fascial lining. Necrotizing fasciitis, also called by the media "flesh-eating bacteria", is an example of a deep-layer infection. It represents an extreme medical emergency.
Infected left knee in comparison to knee with no sign of symptoms
Infected left knee in comparison to knee with no sign of symptoms

Risk factors

The elderly and those with weakened immune systems are especially vulnerable to contracting cellulitis. Diabetics are more prone to cellulitis than the general population because of impairment of the immune system; they are especially prone to cellulitis in the feet because their disease causes impairment of blood circulation in their legs leading to their having foot ulcers that commonly become infected. Cellulitis is also a common complication of Obesity.

Immunosuppressive drugs, HIV, and other illnesses or infections that weaken the immune system are also factors that make infection more likely. In addition, chickenpox and shingles often result in blisters which break, providing a gap in the skin through which bacteria can enter. Lymphedema, which causes swelling on the arms and/or legs, can also put an individual at risk.

Diseases that affect blood circulation in the legs and feet, such as chronic venous insufficiency and varicose veins, are also risk factors for cellulitis.

Cellulitis is also extremely prevalent amongst dense populations sharing hygiene facilities and common living quarters. Military installations which require communal showers provide such an environment, as it is prevalent among many recruits going through boot camp.

Diagnosis

Cellulitis is most often a clinical diagnosis, and local cultures do not always identify the causative organism. Blood cultures usually are positive only if the patient develops generalised sepsis. Conditions that may resemble cellulitis include deep vein thrombosis, which can be diagnosed with a compression leg ultrasound, and stasis dermatitis, which is inflammation of the skin from poor blood flow.

Incubation

Cellulitis can develop in as little as twenty-four hours, or can take days to develop.

Duration

In many cases, cellulitis takes less than a week to disappear with antibiotic therapy. However, it can take months to resolve completely in more serious cases, and can result in severe debility or even death if untreated.

Treatment

Antibiotics - typically a combination of intravenous and oral antibiotics are administered. Bed rest and elevation of affected limbs is also recommended.

Prevention

Good hygiene and good wound care lower the risk of cellulitis. Any wounds should be cleaned and dressed appropriately. Changing bandages daily or when they become wet or dirty will reduce the risk of contracting cellulitis. Medical advice should be sought for any wounds which are deep, dirty or if there is concern about retained foreign bodies.

References

* MFMER. 'Cellulitis'. 3 July 2002. Mayo Foundation for Medical Education and Research. 30 Oct. 2003 [1].
* NLM. 'Group A streptococcal infections'. 2002. National Library of Medicine. 30 Oct. 2003 > .
* Pankey, George A. "Approach to rashes and infections of the skin and subcutaneous tissues." Textbook of internal medicine. 2nd ed. 2 vols. Philadelphia: J. B. Lippincott Company, 1992.
* Cellulitis Overview (with picture).
* Cellulitis

All About Carbuncles

2007-04-02T18:26:00.022-07:00

A carbuncle is an abscess larger than a boil, usually with one or more openings draining pus onto the skin. It is usually caused by bacterial infection. It is treated by drainage of the carbuncle, once it begins to "point" (begin to open to the surface), along with administration of antibiotics.

All About Aphthous ulcers (Canker Sores)

2007-04-02T18:26:00.021-07:00

An aphthous ulcer or canker sore is a type of mouth ulcer which presents as a painful open sore inside the mouth caused by a break in the mucous membrane. The condition is also called aphthous stomatitis, also known as "Sutton's Disease", especially if there are multiple or recurring mouth ulcers.

The term aphtha means ulcer; it has been used for many years to describe areas of ulceration on mucous membranes. Aphthous stomatitis is a condition which is characterized by recurrent discrete areas of ulceration which are almost always painful. Recurrent aphthous stomatitis (RAS) can be distinguished from other diseases with similar appearing oral lesions, such as certain viral exanthems, by their tendency to recur, their multiplicity, and chronicity. Recurrent aphthous stomatitis is one of the most common oral conditions. At least 10% of the population suffers from it. Women are more often affected than men. About 30–40% of patients with recurrent aphthae report a family history.[1]

Presentations of aphthous stomatitis

Aphthous ulcers are classified according to the diameter of the lesion.

Recurrent Aphthous Stomatitis

Recurrent Aphthous Stomatitis, often referred to as canker sores, is a T-cell mediated localized destruction of oral mucosa associated with an increased relative ratio of CD8+ T-cells to CD4+ T-cells.

Minor aphthous ulcerations

This is the most common and least severe form of the disease. Aphthous ulcers develop in childhood and adolescence, and continue sporadically throughout life. Aphthous ulcers occur exclusively on non-keratinized, moveable mucosa, such as buccal (cheeks) and lingual mucosa, the floor of the mouth, and the soft palate. It is characterized as a yellow-gray ulcer surrounded by an erythematous halo less than 10 mm in diameter. They tend to heal without scarring in 7–10 days. Typical treatment is with topical steroids, although treatment is not necessary for healing to occur.

Major aphthous ulcerations

Major aphthous ulcers have the same appearance as minor ulcerations, but are greater than 10 mm in diameter and are extremely painful. They usually take more than a month to heal, and frequently leave a scar. These typically develop after puberty with frequent recurrences. They occur on moveable non-keratinizing oral surfaces, but the ulcer borders may extend onto keratinized surfaces. The lesions heal with scarring and cause severe pain and discomfort.

Herpetiform aphthous ulcerations

This is the most severe form. It occurs more frequently in females, and onset is often in adulthood. It is characterized by small, numerous, 1–3 mm lesions that form clusters. They typically heal in less than a month without scarring. Palliative treatment is almost always necessary.[2]

Symptoms

Aphthous ulcers often begin with a tingling or burning sensation at the site of the future mouth ulcer. In a few days, they often progress to form a red spot or bump, followed by an open ulcer.

The aphthous ulcer appears as a white or yellow oval with an inflamed red border. Sometimes a white circle or halo around the lesion can be observed. The grey-, white-, or yellow-colored area within the red boundary is due to the formation of layers of fibrin, a protein involved in the clotting of blood. The ulcer, which itself is often extremely painful, especially when agitated, may be accompanied by a painful swelling of the lymph nodes below the jaw, which can be mistaken for toothache.

Causes

The exact cause of aphthous ulcers is unknown. In some cases they are thought to be caused by an overreaction by the body's own immune system. Factors that appear to provoke them include stress, fatigue, illness, injury from accidental biting, hormonal changes, menstruation, sudden weight loss, food allergies, the foaming agent in toothpaste: SLS, and deficiencies in vitamin B12, iron, and folic acid.[3] Some drugs, such as nicorandil, have been linked with mouth ulcers. A well-known cause for ulcers in the mouth is when the skin inside the mouth is opened up, a common cause of this is biting one's lip or any tissue within the mouth.

Aphthous ulcers are thought to form when the body becomes aware of and attacks chemicals which it does not recognize.[citation needed] The presence of the unrecognized molecules garners a reaction by the lymphocytes, which trigger a reaction that causes the damage of a mouth ulcer.

Trauma to the mouth is a common cause of aphthous ulcers.[citation needed] Physical trauma, such as toothbrush abrasion, poking with sharp food, accidental biting (this can be particularly common with sharp canine teeth), or dental braces can cause mouth ulcers by breaking the mucous membrane. Other factors, such as chemical irritants or thermal injury, may also lead to the development of ulcers. However, in many cases the cause is unknown.

There appears to be a commonly held belief that another cause of aphthous ulcers is gluten intolerance (Coeliac disease), whereby consumption of wheat, rye, barley and sometimes oats can result in chronic mouth ulcers. However, two small studies of patients with Coeliac disease have demonstrated no link between the disease and aphthous ulcers.[4][5] If patients with aphthous ulcers do happen to have gluten intolerance, they may experience benefit in eliminating breads, pastas, cakes, pies, cookies, scones, biscuits, beers and so on from their diet and substituting gluten-free varieties where available.[4]

Artificial sugars, such as those found in diet cola and sugarless gum, have been reported as causes of aphthous ulcers as well. They can also be linked to an increased intake of acids such as ascorbic acid (one form of Vitamin C) or citric acid. In this case the sores disappear after intake decreases (for example, by substituting ascorbate salts for ascorbic acid).

Another possible cause of aphthous ulcers may be opportunistic activity by combinations of otherwise normal bacterial flora, such as aerobic streptococci, Neisseria, Actinomyces, spirochetes, and bacteroides.[citation needed] According to small-scale experiments by one patent applicant Hau, (6,248,718 ), topical preparations of high doses of penicillin resulted in accelerated healing of mouth ulcers.

Repeat episodes of aphthous ulcers can be indicative of an immunodeficiency, signalling low levels of immunoglobulin in the mucous membrane of the mouth.[citation needed] Certain types of chemotherapy cause mouth ulcers as a side effect.[6] Mouth ulcers may also be symptoms or complications of several diseases listed in the following section. The treatment depends on the believed cause.

The large majority of toothpastes sold in the U.S. contain Sodium lauryl sulfate (SLS), which is known to cause aphthous ulcers in certain individuals. Using a toothpaste without SLS will reduce the frequency of aphthous ulcers in persons who experience aphthous ulcers caused by SLS.[7][8][9] However, some studies find no connection between SLS in toothpaste and mouth ulcers.[10]

A common urban myth is that aphthous ulcers are directly connected to the onset of the herpes simplex virus. In reality, ulcers associated with herpes (or cold sores) are of an entirely different nature from mouth ulcers, which are not contagious.

Pain relief and healing
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Any mouth sore that does not heal after two weeks should be looked at by a dentist or an oral surgeon as it could be a sign of a more serious condition such as oral cancer.

Aphthous ulcers normally heal without treatment within 1 to 2 weeks. Good oral hygiene should be maintained, and spicy, acidic, and salty foods and drinks are best avoided, as they may irritate existing ulcers.

Pain can be treated with several pain-relieving gels, such as Anbesol, Bonjela, Campho-Phenique, Orabase B, Zilactin, or Kanka, available in drugstores. Some people claim that such gels also accelerate the healing of their ulcers.

A dental laser can be used to treat an aphthous ulcer. Immediate and lasting pain relief is achieved, and the ulcer will heal in a few days.[citation needed]

Use of a hydrogen peroxide antiseptic mouthwash can help to significantly reduce pain from irritation caused by debris and bacteria that accumulate in an ulcer, reducing complications associated with its presence. This treatment is widely available at pharmacies from companies such as Colgate, whose product is called Peroxyl. Diluting 3 percent food grade hydrogen peroxide (commonly available in drug stores) with equal parts water can be as effective and less expensive.

Another purported remedy is the use of the prescription steroid Dexaltin Oral Paste (Dexamethasone 1–mg/g).[citation needed]

Triamcinolone Acetonide dental paste can be very effective; the steroid reduces the immune system's response in the area of the ulcer. It is available by prescription only.

A recent study of the Oral-B product Amosan suggests that it may reduce anaerobic bacteria, such as those found in oral wounds. The study did not, however, demonstrate the efficacy of the product in treating mouth ulcers.[11]

Tincture of benzoin can be used as a protectant for recurring aphthous ulcers, by forming a layer over the sore and protecting it from further irritation.

Early treatment

The timing of treatment can be critical for a significant reduction of the length of time of the pain caused by the ulcer. If repeated antiseptic mouthwash treatments are applied as early as possible, preferably within 12 hours of the initial symptoms, i.e. the onset of tingling or burning sensations, then the subsequent intense pain will only last 1–2 days, instead of the usual 7 to 10 days.[citation needed] Although the ulcer will continue its normal course of healing within 7 to 10 days, an early treatment limits the pain to just the first couple of days.

Since this type of ulcer is highly recurrent, people suffering from it can usually recognize the telltale signs of another imminent onset, and therefore the chance of reducing or even eliminating the pain associated is good if treated early. Unfortunately, if treatment is delayed until 24 hours after the start of intense pain, only temporary relief of up to several hours can be achieved per treatment.

Home remedies

The most popular home remedies for canker sores include the following:

* Rinse the mouth with salt water— 1 teaspoon of salt dissolved in 1 cup (250 ml) of warm water (a.k.a. a saline solution).
* Eat 8 ounces per day of yogurt with active Lactobacillus acidophilus cultures.
* Swab mouth ulcers with sea-buckthorn fruit oil.
* Rinse regularly with ginger, lemon and honey tea. All 3 ingredients have strong anti-bacterial properties. This has been found very effective by some people, with white caps disappearing within 24 hrs.
* Rinse the mouth with an antiseptic mouthwash (e.g., Listerine), which can relieve pain for a few hours. This effect has been known to diminish over time in some individuals after prolonged usage[citation needed]
* Apply Carbamide peroxide (Gly-Oxide®) directly to the ulcers, and swish around mouth.
* Take Lysine-L supplements.[12]
* Rinse mouth and especially the affected area with sage tea 3 times a day. The improvement can be seen as early as within 24 hours.[citation needed]
* Paint half-strength gentian violet solution on the ulcer.[1]
* Gargle a mouthful of warm vinegar with a half-tablespoon of salt for about 30 seconds, 3 times per day; this may be extremely painful, immediate removal of white viscous cap on the sore, providing pain relief after rinsing quite quickly, but healing can be seen in as early as 2 days.[citation needed]
* Some have applied anise directly on the ulcer.
* Hold moderately concentrated alcohol in the mouth over the area of the ulcer, possibly because of alcohol's diuretic effect (although there is no direct evidence to support this). Alcohol may also be useful due to its antiseptic properties.
* Similarly the direct application of a small layer of salt to the canker sore, while extremely painful for the first 10 seconds or so, will numb the area for about 30 minutes to an hour.
* Bee propolis may speed healing and provide pain relief due to its anesthetic and anti-bacterial properties.
* Licorice Root (Glycyrrhiza) may help heal canker sores if the medicated disks are applied early on.[citation needed]

Antacid techniques suggested include the following:

* Swab the ulcers with Milk of Magnesia.[2]
* Apply powdered alum, a spice used in canning, dry directly to the ulcers— available in the spice aisle at grocery[citation needed]stores; this can be very painful at first, and then sore will be numbed.
* Make a paste of baking soda and water; apply directly to the ulcers.[3]
* Rinse the mouth with a baking soda-water mix—1 teaspoon of baking soda dissolved in 1 cup (250 ml) of warm water.[citation needed]
* Make a paste of crushed Tums (antacid) and water—apply directly to the ulcers.[citation needed]
* Avoid acidic foods such as tomato, citrus, soft drinks, and vinaigrette salad dressings.[citation needed]
* Apply a yeast-based spread such as Vegemite, Marmite, or Cenovis directly to the ulcer. The salt helps kill any bacteria and dry out the wound, while the vitamin B facilitates healing.[citation needed]
* Make a mix of half Mylanta and half Benadryl, and hold in the mouth for up to 3 minutes.[citation needed]
* Dab the ulcer with Vanilla extract.
* Keeping the ulcer dry by exposing the ulcer to the air and keeping saliva out of the ulcer for periods up to 30 minutes once or twice a day sometimes has a dramatic effect on the ulcer in as little as 24 hours.[citation needed]

Combination therapies recommend the use of the antiseptic before the antacid; that is, swab mouth ulcers with hydrogen peroxide and then swab them with Milk of Magnesia.

A good temporary remedy for the pain of the mouth ulcer is to numb the affected area with ice. Although this may cause intense pain in the beginning, it is highly effective and lasts for about half an hour,[citation needed] depending on the number of ice cubes used and the time spent using the ice cubes.[citation needed]

Treatment for severe cases

Treatments based on antibiotics and steroids such as Dexamethasone Elixir are reserved for severe cases, and should be used only under medical supervision. Tetracycline suspension is a common antibiotic prescribed for mouth ulcers. Some doctors may also prescribe a local anesthetic, such as lidocaine, for cases of multiple or severe aphthous ulcers. If it does not heal within a week, a doctor or dentist may cauterize it using a laser to burn off the ulcer, causing it to completely disappear within a few hours or two to three days.[citation needed]

In very severe cases, a doctor may prescribe a steroid treatment. One such steroid is methylprednisolone (usually in a dose-pack), taken orally for a period of 7 days. Alternatively, the doctor may directly inject a steroid into the site of the ulcer (this treatment is performed with kenalog. Between 0.2 and 0.4 ml of kenalog is injected into the site of the ulcer, which will usually be completely healed 72 to 96 hours after the injection).

Patients in whom ulcers do not respond to local treatment may benefit from a short course of pulsed prednisone.

Some dentists recommend a sulfuric acid solution for treating mouth ulcers, such as debacterol.

Thalidomide has been effective in unresponsive aphthous stomatitis. Thalidomide has been used successfully generally to treat various inflammatory conditions characterized by tissue infiltration with polymorphonuclear leukocytes (PMNLs). Therapeutic benefit has been attributed to depression of PMNL chemotaxis and, possibly, PMNL phagocytosis. However, adverse effects can be both problematic and clinically significant.

Another chemical treatment option is the application of silver nitrate to cauterize the sore. In clinical trials it was found that this treatment reduced pain in patients by 70% with one application but had no effect on healing compared to placebo.[13]

Another choice doctors have is to prescribe Aphthasol, the only Food and Drug Administration (FDA) approved treatment specifically indicated for Aphthous ulcers.

Controversial therapies include levamisole, colchicine, gamma-globulin, dapsone, estrogen replacement, MAOIs, and tetracycline. [4]

Some evidence supports treatment with tetracycline. Tetracycline oral mouth rinse (ie, swish orally and swallow) decreases healing time and pain severity and duration. Whether this benefit is due to a direct antimicrobial effect or to an inhibitory effect on chemotaxis and chemotoxicity is not known.

The miracle cures that are advertised should be viewed with skepticism. However, aqueous sulphuric acid products as listed above can provide significant pain relief, if not treating the underlying causes.

Prevention

Oral and dental measures

* Regular use of mouthwash may help prevent or reduce the frequency of the sores.[14]

* In some cases, switching toothpastes can prevent mouth ulcers from occurring with research looking at the role of sodium dodecyl sulfate (sometimes called sodium lauryl sulfate, or simply SLS), a detergent found in most toothpastes. Using toothpaste free of this compound has been found in several studies to help reduce the amount, size and recurrence of ulcers,[15][16] but not in all studies.[17]

* A few individuals have noticed that switching to a toothpaste with baking soda prevented recurrence of mouth ulcers.[citation needed]

* Some people have reported that the frequency of mouth ulcer occurrences decreased greatly after a particularly large amalgam tooth filling was replaced by some other kind of dental restoration.[citation needed] However, the connection between amalgam fillings and mouth ulcers is not universally accepted, and such replacement can be costly.

* Dental braces are a common physical trauma that can lead to mouth ulcers and can be treated with wax to reduce abrasion of the mucosa. Avoidance of other types of physical and chemical trauma will prevent some ulcers, but since such trauma is usually accidental, this type of prevention is not usually practical.

Nutritional therapy

* Zinc deficiency has been reported in people with recurrent mouth ulcers.[18]The few small studies looking into the role of zinc supplementation have mostly reported positive results particularly for those people with deficiency,[19][20]although some research has found no therapeutic effect.[21]

* Julian Whitaker, M.D., founder and president of the Whitaker Wellness Center in Newport Beach, California, says that eating at least four tablespoons of yogurt daily can prevent outbreaks.[22] He notes that the yogurt must contain active Lactobacillus acidophilus cultures. (If the yogurt contains these cultures, it will say so on the label.)

* Many people have found that taking Lysine-L supplements can help to reduce the frequency of mouth ulcer appearances and speed the healing of those that do occur.[citation needed]

* Likewise, abstaining from arginine (lysine's counterpart), which is found in chocolate and nuts, can prevent an outbreak.[citation needed]

* The presence of bacterially infected ulcers could be a symptom of intestinal bacterial imbalance.[citation needed] Probiotic supplements or 'good bacteria' found in food like yoghurt will treat this condition.[citation needed]

Alternative medicine

Chinese medicine points to one's diet or emotions as potential causes of such symptoms of 'heat in the mouth.'[citation needed]

Greasy/fried foods or 'energetically hot' food (for example: spicy food, alcohol, potato chips) may also trigger mouth ulcers. Some claim that certain emotions, such as anger, frustration, resentment, or stress, can also impede the proper flow of one's energy and create 'heat' in the body, with such manifestations as mouth ulcers, red eyes, sore throats, insomnia, or constipation. In order to neutralize this 'hot energy' certain 'energetically cool' foods such as herbal teas and certain fruits and vegetables must be consumed. Some other examples of such 'cooling' foods include coconut juice (surprisingly the kernel is opposite and is classified 'hot'), mung bean soup, and ginseng tea.[citation needed]

See also

* Mouth ulcer
* Herpes simplex

Footnotes

1. ^ Young, Stephen K.. Canker Sores & Cold Sores: What's the Difference. Continuing Education. University of Oklahoma College of Dentistry. Retrieved on 2006-08-22.
2. ^ Bruce A, Rogers R (2003). "Acute oral ulcers.". Dermatol Clin 21 (1): 1–15. PMID 12622264.
3. ^ Wray D, Ferguson M, Hutcheon W, Dagg J (1978). "Nutritional deficiencies in recurrent aphthae". J Oral Pathol 7 (6): 418–23. PMID 105102.
4. ^ a b Bucci P, Carile F, Sangianantoni A, D'Angio F, Santarelli A, Lo Muzio L. (2006). "Oral aphthous ulcers and dental enamel defects in children with coeliac disease.". Acta Paediatrica 95 (2): 203–7. PMID 16449028.
5. ^ Sedghizadeh PP, Shuler CF, Allen CM, Beck FM, Kalmar JR. (2002). "Celiac disease and recurrent aphthous stomatitis: a report and review of the literature.". Oral Surgery Oral Medicine Oral Pathology Oral Radiology & Endodontics 94 (4): 474–8. PMID 12374923.
6. ^ Non Hodgkin's Lymphoma Cyberfamily — Side effects. NHL Cyberfamily. Retrieved on 2006-08-10.
7. ^ Herlofson B, Barkvoll P (1994). "Sodium lauryl sulfate and recurrent aphthous ulcers. A preliminary study." (PDF). Acta Odontol Scand 52 (5): 257–9. PMID 7825393.
8. ^ Herlofson B, Barkvoll P (1996). "The effect of two toothpaste detergents on the frequency of recurrent aphthous ulcers.". Acta Odontol Scand 54 (3): 150–3. PMID 8811135.
9. ^ Chahine L, Sempson N, Wagoner C (1997). "The effect of sodium lauryl sulfate on recurrent aphthous ulcers: a clinical study.". Compend Contin Educ Dent 18 (12): 1238–40. PMID 9656847.
10. ^ Healy C, Paterson M, Joyston-Bechal S, Williams D, Thornhill M (1999). "The effect of a sodium lauryl sulfate-free dentifrice on patients with recurrent oral ulceration.". Oral Dis 5 (1): 39–43. PMID 10218040.
11. ^ Wennström J, Lindhe J (1979). "Effect of hydrogen peroxide on developing plaque and gingivitis in man.". J Clin Periodontol 6 (2): 115–30. PMID 379049.
12. ^ Canker Sores: What Are They and What Can You Do About Them? (American Academy of Family Physicians)
13. ^ Alidaee M, Taheri A, Mansoori P and Ghodsi S (September 2005). "Silver nitrate cautery in aphthous stomatitis: a randomized controlled trial". Br J Derm 153 (3): 521. DOI:10.1111/j.1365-2133.2005.06490.x.
14. ^ Studies mostly agree that antiseptic mouthwashes can help prevent recurrences:
* Meiller TF, Kutcher MJ, Overholser CD, Niehaus C, DePaola LG, Siegel MA. (Oct 1991). "Effect of an antimicrobial mouthrinse on recurrent aphthous ulcerations.". Oral Surg Oral Med Oral Pathol. 72 (4): 425–9. PMID 1923440.
* Skaare AB, Herlofson BB, Barkvoll P. (Aug 1996). "Mouthrinses containing triclosan reduce the incidence of recurrent aphthous ulcers (RAU)". J Clin Periodontol 23 (8): 778–81. PMID 8877665.
But this is not accepted by all reports:
* Barrons RW. (Jan 1 2001). "Treatment strategies for recurrent oral aphthous ulcers.". Am J Health Syst Pharm. 58 (1): 41–50. PMID 11194135.
15. ^ Herlofson BB, Barkvoll P. (Jun 1996). "The effect of two toothpaste detergents on the frequency of recurrent aphthous ulcers.". Acta Odontol Scand. 54 (3): 150–3. PMID 8811135.
16. ^ Chahine L, Sempson N, Wagoner C. (Dec 1997). "The effect of sodium lauryl sulfate on recurrent aphthous ulcers: a clinical study.". Compend Contin Educ Dent. 18 (12): 1238–40. PMID 9656847.
17. ^ Healy CM, Paterson M, Joyston-Bechal S, Williams DM, Thornhill MH. (Jan 1999). "The effect of a sodium lauryl sulfate-free dentifrice on patients with recurrent oral ulceration.". Oral Dis. 5 (1): 39–43. PMID 10218040.
18. ^ Wang SW, Li HK, He JS, Yin TA (1986). "[The trace element zinc and aphthosis. The determination of plasma zinc and the treatment of aphthosis with zinc]" (in French). Rev Stomatol Chir Maxillofac. 87 (5): 339–43. PMID 3467416.
19. ^ Merchant HW, Gangarosa LP, Glassman AB, Sobel RE (May 1977). "Zinc sulfate supplementation for treatment of recurring oral ulcers". South Med J. 70 (5): 559–61. PMID 870981.
20. ^ Orbak R, Cicek Y, Tezel A, Dogru Y (Mar 2003). "Effects of zinc treatment in patients with recurrent aphthous stomatitis". Dent Mater J. 22 (1): 21–9. PMID 12790293.
21. ^ Wray D (May 1982). "A double-blind trial of systemic zinc sulfate in recurrent aphthous stomatitis". Oral Surg Oral Med Oral Pathol 53 (5): 469–72. PMID 7048184.
22. ^ Preventions Healing with Vitamins Canker Sores

All About Bullous pemphigoid

2007-04-02T18:26:00.020-07:00

Bullous pemphigoid, also referred to as BP, is a chronic autoimmune skin disease, involving the formation of blisters below the surface of the skin and antibodies against collagen XVII. It can also (albeit only rarely) involve the mucous membranes, and has been shown to afflict dogs, cats, pigs, and horses, as well as humans.

See also

* pemphigoid
* pemphigus

All About Bowen's disease

2007-04-02T18:26:00.019-07:00

In medicine (dermatology), Bowen's disease (BD) is a sunlight-induced skin disease, considered either as an early stage or intraepidermal form of squamous cell carcinoma. It was named after Dr John T. Bowen, the doctor who first described it in 1912.

Causes

Causes of BD include solar damage, arsenic, immunosuppression (including AIDS), viral infection (human papillomavirus or HPV) and chronic skin injury and dermatoses.
Bowen's disease as seen under a microscope
Bowen's disease as seen under a microscope

Signs and symptoms

Bowen's disease typically presents as a gradually enlarging, well demarcated erythematous plaque with an irregular border and surface crusting or scaling. BD may occur at any age in adults but is rare before the age of 30 years - most patients are aged over 60. Any site may be affected, although involvement of palms or soles is uncommon. BD occurs predominantly in women (70-85% of cases); about three-quarters of patients have lesions on the lower leg (60-85%), usually in previously or presently sun-exposed areas of skin.
Histology

The cells in Bowen's are extremely unusual or atypical under the microscope and in many cases look worse under the microscope than the cells of many outright and invading squamous-cell carcinomas. The degree of atypia (strangeness, unusualness) seen under the microscope best tells how cells may behave should they invade another portion of the body.

Treatment

Cryotherapy (freezing) or local chemotherapy (with 5-fluorouracil) are favored by some clinicians over excision.

All About Boils

2007-04-02T18:26:00.018-07:00

Boil or furuncle is a skin disease caused by the inflammation of hair follicles, thus resulting in the localized accumulation of pus and dead tissues. Individual boils can cluster together and form an interconnected network of boils called carbuncles. In severe cases, boils may develop to form abscesses.

Symptoms

The symptoms of boils are red, pus-filled lumps that are tender, warm, and/or painful. A yellow or white point at the center of the lump can be seen when the boil is ready to drain or discharge pus. In a severe infection, multiple boils may develop and the patient may experience fever and swollen lymph nodes. A recurring boil is called chronic furunculosis.

In some people, itching may develop before the lumps begin to develop. Boils are most often found on the back, underarms, shoulders, face, lip, thighs and buttocks, but may be found elsewhere. Boils on the ear tend to be more painful, and can create shooting pain in the entire ear when touched.

Sometimes boils will emit an unpleasant smell, particularly when drained or when discharge is present, due to the presence of bacteria in the discharge.

Causes

Boils are generally caused by an infection of the hair follicles by Staphylococcus aureus or staph, a strain of bacteria that normally lives on the skin surface. It is thought that a tiny cut of the skin allows this bacterium to enter the follicles and cause an infection. This can happen during bathing or while using a razor.

People with immune system disorders, diabetes, poor hygiene or malnutrition (Vitamin A or E deficiency) are particularly susceptible to getting boils; however, they may also occur in healthy, hygienic individuals.

Hidradenitis suppurativa causes frequent boils.

Boils in the armpits can sometimes be caused by anti-perspirant deodorants.

Treatments

Most boils run their course within 4 to 10 days. For most people, self-care by applying a warm compress or soaking the boil in warm water can help alleviate the pain and hasten draining of the pus (colloquially referred to as "bringing the boil to a head"). Fire cupping can be utilised to facilitate this procedure. Once the boil drains, the area should be washed with antibacterial soap or antibacterial herbs (chickweed poultice) and bandaged well.

For recurring cases, sufferers may benefit from diet supplements of Vitamin A and E.

In serious cases, prescription oral antibiotics such as dicloxacillin (Dynapen) or cephalexin (Keflex), or topical antibiotics, are commonly used. For patients allergic to penicillin-based drugs, erythromycin (E-base, Erycin) may also be used.

However, some boils are caused by a superbug known as community-acquired Methicillin-resistant Staphylococcus aureus, or CA-MRSA. Bactrim or other sulfa drugs must be prescribed relatively soon after boil has started to form. MRSA tends to increase the speed of growth of the infection.

Magnesium sulfate paste applied to the affected area can prevent the growth of bacteria and reduce boils by absorbing pus and drying up the lesion.

Prognosis

For most cases, there are no serious complications and a full recovery is expected.

All About Behçet's disease

2007-04-02T18:26:00.017-07:00

Behçet's disease, is a chronic condition due to disturbances in the body’s immune system. This system, which normally protects the body against infections through controlled inflammation, becomes overactive and produces unpredictable outbreaks of exaggerated inflammation. This extra inflammation affects blood vessels, usually the small ones. As a result, symptoms occur wherever there is a patch of inflammation, and can be anywhere where there is a blood supply.

Synonyms

Behçet's syndrome, Morbus Behçet, silk road disease.

History

Behçet's disease is named after Hulusi Behçet (1889-1948), the Turkish dermatologist and scientist who first recognized the syndrome in one of his patients in 1924 and reported his research on the disease in Journal of Skin and Veneral Diseases in 1936. The name (Morbus Behçet) was formally adopted at the International Congress of Dermatology in Geneva in September 1947.

The disease was probably first described by Hippocrates in the 5th century BC, in his 3rd Epidemion-book. [1]

Pronunciation note

Because it contains a cedilla, "Behçet" is frequently wrongly assumed to be French in origin and pronounced with a sibilant "s" sound (as in "satsuma") or soft "ch" (as in "shoe"), with the "t" incorrectly silenced: "Beshay". Because Hulusi Behçet was Turkish, the correct pronunciation is with a hard "ch", as in "choice", and with the terminal "t" sounded: "Beh-chet". Also, because Behçet was a physician and never had the disease himself, this should actually be referred to as "Behçet Disease," rather than "Behçet's Disease."

Pathology

The symptoms of Behçet's disease are believed to be caused by an over-active immune system which, without any apparent infections, produces recurrent outbreaks of inflammation in small blood vessels. Common symptoms include mouth ulcers, sore genitals and eye inflammation, and arthritis in older patients, mostly painful but not life-threatening conditions. However, some patients may be unable to work because of the pain and the impaired vision and mobility. In some severe cases, uncontrolled inflammation may lead to blindness, intestinal complications, stroke, and even meningitis, which can be fatal.

This disease usually first strikes patients in their 20s and 30s. It then becomes a fluctuating lifelong disorder with a series of remissions and exacerbations which can be from days to months. Complete remission is rare.

Diagnosis

There is no specific pathological test for Behçet disease at present. It is diagnosed clinically by specific patterns of symptoms and repeated outbreaks. Other causes for these symptoms have to be ruled out before making the diagnosis. The symptoms do not have to occur together, but can have happened at any time.

There are three levels of certainty for diagnosis:

1. International Study Group diagnostic guidelines (very strict for research purposes)
2. Practical clinical diagnosis (generally agreed pattern but not so strict)
3. 'Suspected' or 'Possible' diagnosis (incomplete pattern of symptoms)

International Study Group diagnostic guidelines

Must have

* mouth ulcers (any shape, size or number at least 3 times in any 12 months),

along with 2 out of the next 4 "hallmark" symptoms:

* genital ulcers (including anal ulcers and spots in the genital region and swollen testicles or epididymitis in men),
* skin lesions (papulo-pustules, folliculitis, erythema nodosum, acne in post-adolescents not on corticosteroids),
* eye inflammation (iritis, uveitis, retinal vasculitis, cells in the vitreous),
* pathergy reaction (papule >2 mm dia. 24-48 hrs or more after needle-prick).

Practical clinical diagnosis

Must have

* mouth ulcers,

along with 1 of the 4 hallmark symptoms above and with 2 of the symptoms below:

* arthritis/arthralgia,
* nervous system symptoms,
* stomach and/or bowel inflammation,
* deep vein thrombosis,
* superficial thrombophlebitis,
* cardio-vascular problems of inflammatory origin,
* inflammatory problems in chest and lungs,
* problems with hearing and/or balance,
* extreme exhaustion,
* changes of personality, psychoses,
* any other members of the family with a diagnosis of Behcet’s disease.

'Suspected' or 'Possible' diagnosis

Usually given when someone does not have mouth ulcers or has mouth ulcers but does not have 1 of the 4 hallmark symptoms but has other symptoms and signs of inflammation and other causes for these have been ruled out.

Causes

No one knows why the immune system starts to behave this way in Behcet’s disease. It is not because of any known infections, it is not hereditary, it does not have to do with ethnic origin, gender, life-style, or age, where someone has lived or where they have been on holiday. It is not associated with cancer, and links with tissue-types (which are under investigation) are not certain. It does not follow the usual pattern for autoimmune diseases.

Treatment

Current treatment is aimed at easing the symptoms, reducing inflammation, and controlling the immune system. Anti-TNF therapy such as infliximab has shown promise in treating the uveitis associated with the disease (Sfikakis et al, 2001; Sfikakis, 2002). Another Anti-TNF agent, Etanercept, may be useful in patients with mainly skin and mucosal symptoms (Melikoglu, 2005).

Interferon alfa-2a may also be an effective alternative treatment, particularly for the genital and oral ulcers (Alpsoy, 2002) as well as ocular lesions (Kotter, 2003). Azathioprine, when used in combination with interferon alfa-2b also shows promise (Hamuryudan, 2002), and Colchicine can be useful for treating some genital ulcers, erythema nodosum, and arthritis in women, and arthritis in men (Yurdakul et al, 2001).

Thalidomide has also been used due to its immune-modifying effect (Hamuryudan et al, 1998). Dapsone and rebamipide have been shown, in small studies, to have beneficial results for mucocutaneous lesions (Matsuda et al, 2003;Sharquie et al, 2002).

Epidemiology

Behçet's disease is considered more prevalent in the areas surrounding the old silk trading routes in the Middle East and in Central Asia. Thus, it is sometimes known as Silk Road Disease. However, this disease is not restricted to people from these regions.

An estimated 15,000 to 20,000 Americans have been diagnosed with this disease. In the UK, it is estimated to have about 2 cases for every 100,000 people.

Globally, males are affected more frequently than females. In the United States, more females are affected than males.

References

* Alpsoy E, Durusoy C, Yilmaz E, Ozgurel Y, Ermis O, Yazar S, Basaran E (2002). "Interferon alfa-2a in the treatment of Behcet disease: a randomized placebo-controlled and double-blind study". Arch Dermatol 138 (4): 467-71. PMID 11939808.
* Hamuryudan V, Mat C, Saip S, Ozyazgan Y, Siva A, Yurdakul S, Zwingenberger K, Yazici H (1998). "Thalidomide in the treatment of the mucocutaneous lesions of the Behcet syndrome. A randomized, double-blind, placebo-controlled trial". Ann Intern Med 128 (6): 443-50. PMID 9499327.
* Hamuryudan V, Ozyazgan Y, Fresko Y, Mat C, Yurdakul S, Yazici H (2002). "Interferon alfa combined with azathioprine for the uveitis of Behcet's disease: an open study". Isr Med Assoc J 4 (11 Suppl): 928-30. PMID 12455182.
* Kotter I, Zierhut M, Eckstein AK, Vonthein R, Ness T, Gunaydin I, Grimbacher B, Blaschke S, Meyer-Riemann W, Peter HH, Stubiger N (2003). "Human recombinant interferon alfa-2a for the treatment of Behcet's disease with sight threatening posterior or panuveitis". Br J Ophthalmol 87 (4): 423-31. PMID 12642304.
* Matsuda T, Ohno S, Hirohata S, Miyanaga Y, Ujihara H, Inaba G, Nakamura S, Tanaka S, Kogure M, Mizushima Y (2003). "Efficacy of rebamipide as adjunctive therapy in the treatment of recurrent oral aphthous ulcers in patients with Behcet's disease: a randomised, double-blind, placebo-controlled study". Drugs R D 4 (1): 19-28. PMID 12568631.
* Melikoglu M, Fresko I, Mat C, Ozyazgan Y, Gogus F, Yurdakul S, Hamuryudan V, Yazici H (2005). "Short-term trial of etanercept in Behcet's disease: a double blind, placebo controlled study". J Rheumatol 32 (1): 98-105. PMID 15630733.
* Sfikakis PP (2002). "Behcet's disease: a new target for anti-tumour necrosis factor treatment". Ann Rheum Dis 61 Suppl 2: ii51-3. PMID 12379622.
* Sfikakis PP, Theodossiadis PG, Katsiari CG, Kaklamanis P, Markomichelakis NN (2001). "Effect of infliximab on sight-threatening panuveitis in Behcet's disease". Lancet 358 (9278): 295-6. PMID 11498218.
* Sharquie KE, Najim RA, Abu-Raghif AR (2002). "Dapsone in Behcet's disease: a double-blind, placebo-controlled, cross-over study". J Dermatol 29 (5): 267-79. PMID 12081158.
* Yurdakul S, Mat C, Tuzun Y, Ozyazgan Y, Hamuryudan V, Uysal O, Senocak M, Yazici H (2001). "A double-blind trial of colchicine in Behcet's syndrome". Arthritis Rheum 44 (11): 2686-92. PMID 11710724.

All About Bedsores

2007-04-02T18:26:00.016-07:00

Bedsores, more properly known as pressure ulcers or decubitus, are lesions caused by unrelieved pressure to any part of the body, especially portions over bony or cartilaginous areas. Although completely treatable if found early, without medical attention, bedsores can become life-threatening.

Classification

The definitions of the four pressure ulcer stages are revised periodically by the National Pressure Ulcer Advisory Panel (NPUAP) in the United States. Briefly, however, they are as follows:

* Stage I is the most superficial, indicated by redness that does not subside after pressure is relieved. The skin may be hotter or cooler than normal, have an odd texture, or perhaps be painful to the patient. Although easy to identify on a light-skinned patient, ulcers on darker-skinned individuals may show up as shades of purple or blue in comparison to lighter skin tones.
* Stage II is damage to the epidermis extending into, but no deeper than, the dermis. In this stage, the ulcer may be referred to as a blister or abrasion.
* Stage III involves the full thickness of the skin, extending into, but not through, the subcutaneous tissue layer. This layer has a relatively poor blood supply and can be difficult to heal. At this stage, there may be undermining that makes the wound much larger than it may seem on the surface.
* Stage IV is the deepest, extending into the muscle, tendon or even bone.
* Unstageable pressure ulcers are covered with dead cells and wound exudate, so the depth cannot be determined.

With higher stages, healing time is prolonged. While about 75% of Stage II ulcers heal within eight weeks, only 62% of Stage IV pressure ulcers ever heal, and only 52% heal within one year.[1] It is important to note that pressure ulcers do not regress in stage as they heal. A pressure ulcer that is becoming shallower with healing is described in terms of its original deepest depth (e.g., healing Stage II pressure ulcer).

Etiology

Bedsores are accepted to be caused by three different tissue forces:

Pressure, or the compression of tissues. In most cases, this compression is caused by the force of bone against a surface. After an extended amount of time with decreased tissue perfusion, ischemia occurs and can lead to tissue necrosis if left untreated in an immunocompromised patient.

Shear force, or a force created when the skin of a patient stays in one place as the deep fascia and skeletal muscle slide down with gravity. This can also cause the pinching off of blood vessels which may lead to ischemia and tissue necrosis.

Friction, or a force resisting the shearing of skin. This may cause excess shedding through layers of epidermis.

Aggravating the situation may be other conditions such as excess moisture from incontinence, perspiration or exudate. Over time, this excess moisture may cause the bonds between epithelial cells to weaken thus resulting in the maceration of the epidermis. Other factors in the development of bedsores include age, nutrition, vascular disease, diabetes mellitus, and smoking, amongst others.

There are currently two major theories about the development of pressure ulcers. The first and most accepted is the deep tissue injury theory which claims that the ulcers begin at the deepest level, around the bone, and move outward until they reach the epidermis. The second, less popular theory is the top-to-bottom model which says that skin first begins to deteriorate at the surface and then proceeds inward.[2]

Pathophysiology

Pressure ulcers may be caused by inadequate blood supply and resulting reperfusion injury when blood re-enters tissue. A simple example of a mild pressure sore may be experienced by healthy individuals while sitting in the same position for extended periods of time: the dull ache experienced is indicative of impeded blood flow to affected areas. Within hours, this shortage of blood supply, called ischemia, may lead to tissue damage and cell death. The sore will initially start as a red, painful area, which eventually turns purple. Left untreated, the skin may break open and become infected. Moist skin is more sensitive to tissue ischemia and necrosis and is also more likely to get infected.

Epidemiology

Within acute care, the incidence of bedsores is 0.4% to 38%; within long-term care, 2.2% to 23.9%; and in home care, 0% to 17%. There is the same wide variation in prevalence: 10% to 18% in acute care, 2.3% to 28% in long-term care, and 0% to 29% in home care. There is a much higher rate of bedsores in intensive care units because of immunocompromised individuals, with 8% to 40% of ICU patients developing bedsores.[3]

The risk of developing bedsores can be determined by using the Braden Scale for Predicting Pressure Ulcer Risk. This scale is divided into six risk categories:

1. sensory perception
2. moisture
3. activity
4. mobility
5. nutrition
6. friction and shear

The best possible interpretation is a score of 23 whilst the worst is a 6. If the total score is below 11, the patient is at risk for developing bedsores.[4]

Treatment

The most important thing to keep in mind about the treatment of bedsores is that the most optimal outcomes find their roots in a multidisciplinary approach; by using a team of specialists, there is a better chance that all bases will be covered in treatment.

There are six major contributors to healing.

Debridement

The removal of necrotic tissue is an absolute must in the treatment of pressure sores. Because dead tissue is an ideal area for bacteria growth, it has the ability to greatly compromise wound healing. There are at least seven ways to excise necrotic tissue.[5]

1. Autolytic debridement is the use of moist dressings to promote autolysis with the body's own enzymes. It is a slow process, but mostly painless.
2. Biological debridement, or maggot debridement therapy, is the use of medical maggots to feed on necrotic tissue and therefore clean the wound of excess bacteria. Although this fell out of favour for many years, in January 2004, the FDA approved maggots as a live medical device.[6]
3. Chemical debridement, or enzymatic debridement, is the use of prescribed enzymes that promote the removal of necrotic tissue.
4. Mechanical debridement is the use of outside force to remove dead tissue. A quite painful method, this involves the packing of a wound with wet dressings that are allowed to dry and then are removed. This in also unpopular because it has the ability to remove healthy tissue in addition to dead tissue. Lastly, with Stage IV ulcers, there is the chance that overdrying of the dressings can lead to bone fractures and ligament snaps.
5. Sharp debridement is the removal of necrotic tissue with a scalpel or similar instrument.
6. Surgical debridement is the most popular method, as it allows a surgeon to quickly remove dead tissue with little pain to the patient.
7. Ultrasound-assisted wound therapy is the use of ultrasound waves to separate necrotic and healthy tissue.

Infection control

Infection has one of the greatest effects on the healing of a wound. Purulent discharge provides a breeding ground for excess bacteria, a problem especially in the immunocompromised patient. Symptoms of systemic infection include fever, pain, erythema, oedema, and warmth of the area, not to mention purulent discharge. Additionally, infected wounds may have a gangrenous smell, be discoloured, and may eventually exude even more pus.

In order to eliminate this bioburden, it is imperative to apply antiseptics and antimicrobials at once. It is not recommended to use hydrogen peroxide for this task as it is difficult to balance the toxicity of the wound with this. New dressings have been developed that have cadexomer iodine and silver in them, and they are used to treat bad infections.

It is not recommended to use systemic antibiotics to treat infection of a bedsore, as it can lead to bacterial resistance.

Nutritional support

Upon admission, the patient should have a consultation with a dietitian to determine the best diet to support healing, as a malnourished person does not have the ability to synthesize enough protein to repair tissue. The dietition should conduct a nutritional assessment that includes a battery of questions and a physical examination. If malnourishment is suspected, lab tests should be run to check serum albumin and lymphocyte counts. Additionally, a bioelectric impedance analysis should be considered.

If the patient is found to be at risk for malnutrition, it is imperative to begin nutritional intervention with dietary supplements and nutrients including, but not limited to, arginine, glutamine, vitamin A, vitamin B complex, vitamin E, vitamin C, magnesium, manganese, selenium and zinc. It is very important that intake of these vitamins and minerals be overseen by a physician, as many of them can be detrimental in incorrect dosages.

How to properly care for a bedsore

The most important care for a patient with bedsores is the relief of pressure. Once a bedsore is found, pressure should immediately be lifted from the area and the patient turned at least every two hours to avoid aggravating the wound. Nursing homes and hospitals usually set programs to avoid the development of bedsores in bedridden patients such as using a standing frame to reduce pressure and ensuring dry sheets by using catheters or impermeable dressings. For individuals with paralysis, pressure shifting on a regular basis and using a cushion featuring pressure relief components can help prevent pressure wounds.

Pressure-distributive mattresses are used to reduce high values of pressure on prominent or bony areas of the body. However, methods to evaluate the efficacy of these products have only been developed in recent years.[7]

Educating the caregiver

In the case that the patient will be returning to home care, it is very important to educate the family about how to treat their loved one's pressure ulcers. The cross-specialisation wound team should train the caregiver in the proper way to turn the patient, how to properly dress the wound, how to properly nourish the patient, and how to deal with crisis, among other things.

As this is a very difficult undertaking, the caregiver may feel overburdened and depressed, so it may be best to bring in a psychological consult.

Wound intervention

Once the patient has reached the point that intervention is possible, there are many different options. For patients with Stages I and II ulcers, the wound care team should use guidelines established by the American Medical Directors Association (AMDA) for the treatment of these low-grade sores.

For those with Stage III or IV ulcers, most interventions will likely include surgery such as a tissue flap, skin graft or other closure methods. A more recent intervention is negative pressure wound therapy, which is the application of topical negative pressure to the wound. This technique, developed by scientists at Wake Forest University, uses foam placed into the wound cavity which is then covered in a film which creates an airtight seal. Once this seal is established, the technician is able to remove exudate and other infectious materials in addition to aiding the body produce granulation tissue, the best bed for the creation of new skin.

There are, unfortunately, contraindications to the use of negative pressure therapy. Most deal with the unprepared patient, one who has not gone through the previous steps toward recovery, but there are also wound characteristics that bar a patient from participating: a wound with inadequate circulation, a raw debridled wound, a wound with necrotised tissue and eschar, and a fibrotic wound.

After negative pressure wound therapy, the patient should be reevaluated every two weeks to determine future therapy.

Complications

Pressure sores can trigger other ailments, and cause patients considerable suffering and financial cost.[8] Some complications include autonomic dysreflexia, bladder distension, osteomyelitis, pyarthroses, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation. Sores often recur because patients do not follow recommended treatment or develop seromas, hematomas, infections, or dehiscence. Paralytic patients are the most likely people to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from renal failure and amyloidosis.

See also

* Wound healing
* Gangrene
* Liquefactive necrosis

References

1. ^ Thomas DR, Marilyn R. Diebold and Linda M. Eggemeyer. A controlled, randomized, comparative study of a radiant heat bandage on the healing of stage 3–4 pressure ulcers: A pilot study. Journal of the American Medical Directors Association, Volume 6, Issue 1, January-February 2005, Pages 46-49.
2. ^ Niezgoda, Jeffrey A. and Susan Mendez-Eastman. The Effective Management of Pressure Ulcers. Advances in Skin & Wound Care: The Journal for Prevention and Healing, Volume 19, Number 1 - Supplement (2006): 3-15.
3. ^ National Pressure Ulcer Advisory Panel Board of Directors, "Pressure ulcers in America: Prevalence, incidence, and implications for the future," in An Executive Summary of the National Pressure Ulcer Advisory Panel Monograph, Jul/August 2001, ed. Janet Cuddigan et al.
4. ^ Jiricka, MK, P Ryan, MA Carvalho, and J Bukvich. Pressure ulcer risk factors in an ICU population. American Journal of Critical Care. Vol 4, Issue 5 (1995): 361-367.
5. ^ Niezgoda, Jeffrey A. and Susan Mendez-Eastman. The Effective Management of Pressure Ulcers. Advances in Skin & Wound Care: The Journal for Prevention and Healing, Volume 19, Number 1 - Supplement (2006): 3-15.
6. ^ 510(k)s Final Decisions Rendered for January 2004, http://www.fda.gov/cdrh/510k/sumjan04.html
7. ^ Bain DS, Ferguson-Pell MW. Remote monitoring of sitting behaviour of people with spinal injury. Journal of Rehabilitation Research and Development, Vol 39, 4, July 2002, Pages 513-520.
8. ^ Brem H, Kirsner RS, and Falanga V. Protocol for the successful treatment of venous ulcers. The American Journal of Surgery, Volume 188, Issue 1, Supplement 1, July 2004, Pages 1-8.

All About Basal cell carcinoma

2007-04-02T18:26:00.015-07:00

Basal cell carcinoma (BCC) is the most common skin cancer. It can be destructive and disfiguring. Risk is increased for individuals with a family history of the disease and a high cumulative exposure to UV light via sunlight or, in the past, carcinogenic chemicals especially arsenic. Treatment is with surgery, topical chemotherapy, x-ray, cryosurgery, photodynamic therapy. It is rarely life-threatening but if left untreated can be disfiguring, cause bleeding and produce local destruction (eg., eye, ear, nose, lip).

Forms

Various forms are recognised:

* Nodular: flesh-colored papule with telangiectasis. If it ulcerates, it becomes a "rodent ulcer" (ulcus rodens), an ulcerating nodule with (often) a pearly border.
* Cystic: rarer and hard to distinguish from the nodular form. It has a central cavity with fluid.
* Pigmented: a variant of the nodular form that may be confused with melanoma.
* Sclerosing/cicratising: a scar-like lesion.
* Superficial: a red scaling patch

About two thirds of the carcinomas occur in sun-exposed areas and one third occur in non-sun-exposed areas, emphasizing the genetic susceptibility of the basal cell cancer patients.

Diagnosis

To diagnose, a biopsy (where tissue is taken for pathological study) is done using local anesthesia. In small lesions, the tumor is generally removed in its entiriety, while larger ones are biopsied first and surgically removed later if it is confirmed that it is malignant.

Histopathology: Basal cell carcinoma is a malignant epithelial tumor arising only in skin, from the basal layer of the epidermis or of the pilosebaceous adnexa. Tumor is represented by compact areas, well delineated and invading the dermis, apparent with no connection with the epidermis. Tumor cells resemble normal basal cells (small, monomorphous) are disposed in palisade at the periphery of the tumor nests, but are spindle-shaped and irregular in the middle. Tumor clusters are separated by a reduced stroma with inflammatory infiltrate. 1

Pathophysiology

Basal cell carcinomas develop in the basal cell layer of the skin. Sunlight exposure leads to DNA crosslinking between thymidine residues. While DNA repair removes most UV-induced damage, not all crosslinks are excised. There is, therefore, cumulative DNA damage leading to mutations. Apart from the mutagenesis, sunlight depresses the local immune system, possibly decreasing immune surveillance for new tumor cells.

Histology of a nodular basal cell carcinoma

Prevention and early diagnosis

Basal cell carcinoma is the most common skin cancer. It occurs mainly in fair-skinned patients with a family history of this cancer. Sunlight is a factor in about two thirds of these cancers, but one third occur in non sun-exposed areas. Therefore, dermatologists recommend sun screens and annual skin cancer exams to prevent or provide early detection of this common tumor.

Treatment

Most basal cell carcinomas are removed surgically. A common method is "electrodessication and curettage" (ED&C). This is done by scraping the tumor out with a curette and cauterizing the base and margins. The wound is left to heal by itself (secondary intention healing). The cure rate and cosmetic result are excellent, especially in concave areas. It is also the most cost effective treatment. Surgical excision by the dermasurgeon is another option with the margins of excised tissue examined under the microscope. Certain types, like the sclerosing basal cell cancers may need a wider margin, as they develop subtle processes that project outside the visible part of the tumor. Although BCCs are termed carcinomas, they are not invasive cancers - and are therefore not included in national cancer statsitics.

Some superficial cancers respond to local therapy with 5-fluorouracil, a chemotherapy agent. Topical treatment with 5% IMIQUIMOD cream, with 5 applications per week for six weeks has a reported 70 - 90% success rate at reducing, even removing the BCC [basal cell carcinoma]. Imiquimod may be used prior to surgery to reduce the size of the carcinoma. See Chemotherapy.

Mohs micrographic surgery[1] has the highest cure rate and is especially indicated for recurrent tumors or tumors in areas (eg. eyelid or nose) where minimal amounts of tissue removal are important. Mohs surgery involves checking the base and edges under a microscope before the surgical repair of the site. Specially trained dermasurgeons do this procedure, usually in-office.

A new immune enhancement agent (topical imiquimod, "Aldara") is effective for the treatment of superficial skin cancers (basal cell and squamous cell cancer, and even malignant melanoma in-situ). It is also used pre-operatively to shrink nodular basal cell cancers, thus allowing a smaller surgical excision.

X-ray is still appropriate in older patients who are not candidates for surgery. Cryosurgery is another option, particularly for basal cell cancer invading cartilage, as the healthy cartilage is cryo-resistant.

Treating surgeons (dermasurgeons, plastic surgeons, or other specialists) will recommend one of these modalities as appropriate treatment depending on the tumor size, location, patient age and other variables.

There is also a new treatment using Euphorbia peplus a common garden weed. [2]

Prognosis

Although basal cell carcinoma rarely metastasizes, it grows locally without stopping. The cancer can impinge on vital structures and result in loss extension or loss of function or rarely death. The vast majority of cases can be successfully treated before serious complications occur.

Epidemiology

Basal cell cancer is the most common skin cancer. It is much more common in fair skinned individuals with a family history of basal cell cancer and increases in incidence closer to the equator or at higher altitude. According to Skin Cancer Foundation[3], there are approximately 800,000[4] new cases yearly in the United States alone.

Most sporadic BCC arise in small numbers on sun-exposed skin of people over age 50, although younger people may also be affected. The development of multiple basal cell cancer at an early age could be indicative of Nevoid basal cell carcinoma syndrome.

All About Urushiol-induced contact dermatitis

2007-04-02T18:26:00.014-07:00

Exposure

Urushiol-induced contact dermatitis is contracted by contact with a plant or any other object containing urushiol oil. Clothing or other materials that contact the plant and then, before being washed, contact the skin are common causes of exposure. Normally, it takes about twelve to twenty-four hours for the rash to first appear.

Urushiol is primarily found in the spaces between plant cells beneath the outer skin of the plant, so the effects of urushiol rash are less severe if the plant tissue remains undamaged on contact. Once the oil and resin has been thoroughly washed from the skin, the rash is usually not contagious. Urushiol does not spread once it has bound with the skin, and it is not found in weeping blisters. Although the rash may worsen during the first few days and may appear to spread to new areas, this is usually simply latent reaction.

Although simple skin exposure is most common, ingestion can also lead to serious, more systemic reactions. Burning plant material is commonly said to create urushiol laden smoke that causes systemic reaction as well as rash inside the throat and on the eyes. However, some sources dispute the danger of burning urushiol-containing plant material.[1]

Mechanism
Poison ivy rash after 2 days.

Chemically, urushiol is harmless to humans, but when it bonds to skin cells it initiates a T-cell mediated immune response. This immune response is directed towards the complex of urushiol derivatives which are bound up in the skin proteins. The result is an allergic eczematous contact dermatitis characterized by redness, swelling, papules, vesicles, blisters, and streaking. People vary greatly in their sensitivity to urushiol. Around 15%[1] to 30%[2] of people are immune to the effects, although at least 25% of people have strong reactions to poison ivy. Since the skin reaction is an allergic one, people may develop an increasingly strong reaction after repeated exposures, or show no immune response on their first exposure, but show definite sensitivity on following exposures.

The rash takes one to two weeks to run its course, but normally does not leave scars. Severe cases will have small (1-2 mm) clear fluid-filled blisters on the skin. Pus-filled vesicles, containing a whitish fluid, may indicate a secondary infection. Most poison ivy rashes, without infections, will self-resolve within 14 days without treatment. Excessive scratching may result in secondary infection, commonly by staphylococcal and streptococcal species. These may require the use of antibiotics.

Treatments

Primary treatment involves washing exposed skin thoroughly with soap and water. Soap is necessary as urushiol is a hydrophobic oil and is not washed off by plain water. Once an outbreak has occurred, cold compresses, Burow's solution, calamine lotion, antihistamines, and hydrocortisone ointment are commonly used to abate the symptoms.

No vaccine has been developed to counter urushiol symptoms, so "cures" are generally held to be those products that physically remove the urushiol. After about 15 minutes of exposure, the urushiol is chemically bonded to the skin and can only be removed with pharmaceutical products, which vary by person in effectiveness. Two of these products are:

* Tecnu - Originally developed as a treatment for radiation exposure, it was discovered later that Tecnu provided some relief for poison ivy exposure. It is a milky liquid and the main active ingredient is octylphenoxy-polyethoxyethanol. The four octyl groups of this chemical are too large to surround the non-polar molecules in the urushiol, which remains partially active and requires multiple applications. Also, the chemical makeup of the product requires that it be applied no later than eight hours after exposure to urushiol.
* Zanfel - Developed in 1999, this paste uses an ethoxylate molecule with the large octyl groups removed. This allows the molecule to "wrap" around the non-polar molecules of the urushiol and inactivate it. The other ingredient, sodium lauryl sarcosinate, allows the ethoxylate to form a micelle around the urushiol molecule. This creates a large molecule that contains flexible non-polar groups and soluble polar groups, allowing it to be rinsed away with water.

There are many myths that deal with treating toxicodendrons such as poison ivy. Most have been discredited, but some persist despite their falsehood:

* The fluid from the resulting blisters spreads poison ivy to others.
* Poison ivy is harmless when the leaves have fallen off.
* Ice, water, soap, lotions, dry cold air, can help cure poison ivy rash faster. In reality, skin cells react to the urushiol even after the urushiol has been washed off, and the methods listed are for soothing the rash.

See also

* Poison ivy
* Urushiol
* Toxicodendron
* Toxin

All About Autoeczematization

2007-04-02T18:26:00.013-07:00

Autoeczematization is also called -id reaction. It refers to eczema that is brought about by an infection with parasites, bacteria, fungi, or viruses. This rash occurs at a site distant from the infection causing it. It will clear up when the infection is cured.

All ABout Neurodermatitis

2007-04-02T18:26:00.012-07:00

Neurodermatitis can mean:

* Lichen simplex chronicus and its cousin, prurigo nodularis; these are types of eczema that are thought to be self-caused, or have unexplained origin, and are mostly localized; the older term was “localized or circumscribed neurodermatitis."
* Other types of "lichens" such as lichen striatus (aka linear neurodermatitis), which are part of the pruritic dermatoses spectrum.
* Atopic dermatitis – also known as childhood eczema; this usage is still common in parts of Europe; the older term was “disseminated neurodermatitis.”

There are still references in the older literature to the psychosomatic nature of these disorders, and their accompanying "psychogenic" itch. This is why the older terms had "neuro" in them: as a reference to the link with mental illness. There continues to be a suspicion of obsessive-compulsive behaviors leading to some forms of dermatitis.

All ABout Stasis dermatitis

2007-04-02T18:26:00.011-07:00

Stasis dermatitis refers to the skin changes that occur in the leg as a result of "stasis" or blood pooling from insufficient venous return, the common cause of this being from varicose veins leads to the alternative name of varicose eczema.

Insufficient venous return results in increased pressure in the capillaries with the result that both fluid and cells may "leak" out of the capillaries. This results in red cells breaking down with iron containing hemosiderin possibly contributing to the pathology of this entity.

In appearance the skin appears brown and may be weakened and ulcerate in areas.

The cracks and poor skin condition of this disorder predisposes for the entry of bacterial infection causing spreading cellulitis infection in the leg. If the skin condition deteriorates further and breaks down, a venous ulcer may form.

Treatment may consist of topical applications of steroid based creams and the use of compression stockings to help force the underlying buildup of fluids back out of the lower leg.

All ABout Nummular dermatitis

2007-04-02T18:26:00.010-07:00

Nummular dermatitis is one of the many forms of dermatitis. Also known as discoid dermatitis, it is characterized by round or oval-shaped itchy lesions. (The name comes from the Latin word "nummus," which means "coin.") The disorder is recurrent and chronic, and may appear at any age, although it is most common in people in their 60's. Nummular dermatitis does not appear to be a genetic condition, is not related to food allergies, and is not contagious.

The coin-shaped patches can affect any part of the body, but the legs and buttocks are the most common areas. Flare-ups are associated with dry skin, so the winter season is a particularly bad time for those with this condition.

One of the keys to treatment and prevention involves keeping the skin moisturized. Lotions, creams, and bath oils may help prevent an outbreak. If the condition flares up, a common treatment involves the application of topical corticosteroids. Oral antihistamines may help lessen itching. More severe cases sometimes respond to ultraviolet light treatment.

All About Dyshidrosis

2007-04-02T18:26:00.009-07:00

Dyshidrosis, also termed Dyshidrotic Eczema and Dyshidrotic Dermatitis, is a skin condition that is characterized by small blisters on the hands or feet. It is an acute, chronic, or recurrent dermatosis of the fingers, palms, and soles, characterized by a sudden onset of many deep-seated pruritic, clear vesicles; later, scaling, fissures and lichenification occur. The name comes from the word "dyshidrotic," meaning "bad sweating," which was once believed to be the cause. Sometimes called pompholyx (Greek for "bubble") which is generally reserved for the cases with blisters; in some countries, pompholyx refers to hand dyshidrosis.

While this condition is not contagious to others, recurrence is common and for many can be chronic.

Incidence/Prevalence in the USA is 20/100,000.

Symptoms

Small blisters with the following characteristics:

* Blisters are very small (1 mm or less in diameter). They appear on the tips and sides of the fingers, toes, palms, and soles.
* Blisters are opaque and deep-seated; they are either flush with the skin or slightly elevated and do not break easily. Eventually, small blisters come together and form large blisters.
* Blisters may itch, cause pain, or produce no symptoms at all. They worsen after contact with soap, water, or irritating substances.
* Scratching blisters breaks them, releasing the fluid inside, causing the skin to crust and eventually crack. This cracking is painful as well as unsightly and often takes weeks, or even months to heal.
* Fluid from the blisters is serum that accumulates between the irritated skin cells. It is not sweat as was previously thought.

Causes

* Unknown, but commonly linked to excessive sweating during periods of anxiety, stress, and frustration. Some patients reject this link to stress. Vesicular eruption of the hands may be caused by a local infection, with fungal infections being the most common. Sunlight is thought to bring on attacks, some patients link outbreaks to prolonged exposure to strong sunlight from late spring through to early autumn.[citation needed]. Others have also noted outbreaks occurring in conjunction with exposure to chlorinated pool water or highly treated city tap waters.
* Is caused by sweat retention. .keeping skin damp will trigger or worsen an outbreak. For this reason, people with dyshidrosis should wear gloves, socks, and shoes made of materials which "breathe well".
* Inherited, not contagious.
* Can be the secondary effect of problems in the gut.[citation needed] Some sufferers claim diet can ease symptoms (relieving internal condition of IBS or intestinal yeast infection).[citation needed] Also Inflammatory bowel diseases of Ulcerative colitis and Crohn's disease.[citation needed]

Treatment

* Hydrogen Peroxide
* Potassium permanganate dilute solution soaks
* Salt soaks
* Topical non-prescription steroid creams
* Zinc oxide ointment
* Stress management counseling
* Light treatment: UVA-1, PUVA, Grenz Rays
* Ciclosporin a strong immunosuppressant drug used to combat dishydrosis caused by ulcerative colitis
* Efalizumab (Raptiva) a medication used to treat psoriasis

All About Seborrhoeic dermatitis

2007-04-02T18:26:00.008-07:00

Seborrhoeic dermatitis is a skin disorder affecting the scalp, face and trunk causing scaly, flaky, itchy, red skin. It particularly affects the sebum-gland rich areas of skin.

Etiology

The cause of seborrheic dermatitis remains unknown, although many factors have been implicated. The ubiquitous yeast, Malassezia furfur (formerly known as Pityrosporum ovale), is involved,[1][2] as well as genetic, environmental, hormonal, and immune-system factors. [3][4] A suggestion that seborrheic dermatitis is an inflammatory response to this yeast has yet to be proven.[5] Those afflicted with seborrhoeic dermatitis have an unfavorable epidermic response to the infection, with the skin becoming inflamed and flaking.

Treatments

Soaps and detergents such as Sodium Laureth Sulfate may precipitate a flare-up, as they strip moisture from the top layers of the skin, and the drying property of these can cause flare-ups and may worsen the condition. Accordingly a suitable alternative should be used instead.

Among dermatologist recommended treatments are shampoos containing coal tar, ketoconazole, selenium sulfide, or zinc pyrithione.[6] For severe disease, keratolytics such as salicylic acid or coal tar preparations may be used to remove dense scale. Topical terbinafine solution (1%) has also been shown to be effective in the treatment of scalp seborrhea,[7] as may lotions containing alpha hydroxy acids or corticosteroids.

Chronic treatment with topical corticosteroids may lead to permanent skin changes, such as atrophy and telangiectasia.[8]

UV-A and UV-B light inhibit the growth of M. furfur[9], although caution should be taken to avoid sun damage.

See also

* Dermatitis
* Dandruff
* Cradle Cap
* Acne vulgaris, atopic dermatitis, mycoses, psoriasis, and rosacea, which may be confused with seborrhoeic dermatitis.

Footnotes

1. ^ Hay R, Graham-Brown R (1997). "Dandruff and seborrhoeic dermatitis: causes and management". Clin Exp Dermatol 22 (1): 3-6. PMID 9330043.
2. ^ Nowicki R (2006). "[Modern management of dandruff]". Pol Merkur Lekarski 20 (115): 121-4. PMID 16617752.
3. ^ Am Fam Physician 2000;61:2703-10,2713-4
4. ^ Janniger C, Schwartz R (1995). "Seborrheic dermatitis". Am Fam Physician 52 (1): 149-55, 159-60. PMID 7604759.
5. ^ Parry M, Sharpe G (1998). "Seborrhoeic dermatitis is not caused by an altered immune response to Malassezia yeast". Br J Dermatol 139 (2): 254-63. PMID 9767239.
6. ^ Schwartz R, Janusz C, Janniger C (2006). "Seborrheic dermatitis: an overview". Am Fam Physician 74 (1): 125-30. PMID 16848386.
7. ^ Faergemann J, Jones J, Hettler O, Loria Y (Jun 1996). "Pityrosporum ovale (Malassezia furfur) as the causative agent of seborrhoeic dermatitis: new treatment options". Br J Dermatol 134 Suppl 46: 12-5: discussion 38. PMID 8763461.
8. ^ Smith J, Wehr R, Chalker D (1976). "Corticosteroid-induced cutaneous atrophy and telangiectasia. Experimental production associated with weight loss in rats". Arch Dermatol 112 (8): 1115-7. PMID 952530.
9. ^ Wikler J, Janssen N, Bruynzeel D, Nieboer C (1990). "The effect of UV-light on pityrosporum yeasts: ultrastructural changes and inhibition of growth". Acta Derm Venereol 70 (1): 69-71. PMID 1967880.

All About Xerotic eczema

2007-04-02T18:26:00.007-07:00

Xerotic eczema refers to the skin changes that occur when skin becomes abnormally dry, itchy, and cracked (what does this mean?). Lower legs tend to be especially affected. It is common in older people. It is not uncommon in younger people in their 20's. It can appear in red, bumpy, pimple-like irritations. It is also apparent under the arms. Shaving can cause it to become inflammed, however, not shaving doesn't make it any less irritated. The only thing that helps it to "go away" is to NOT scratch it (even though it feels amazing when you do) and to apply anti-itch lotion as well as a moisturizing lotion frequently.

All About Contact dermatitis

2007-04-02T18:26:00.006-07:00

Contact dermatitis is a term for a skin reaction resulting from exposure to allergens or irritants. Phototoxic dermatitis occurs when the allergen or irritant is activated by sunlight.

Description

Only the superficial regions of the skin are affected in contact dermatitis. Inflammation of the affected tissue is present in the epidermis (the outermost layer of skin) and the outer dermis (the layer beneath the epidermis) (ESCD 2006)[1]. Unlike contact urticaria in which a rash appears within minutes of exposure and fades away within minutes to hours, contact dermatitis takes days to fade away and then only if the skin no longer comes in contact with the allergen or irritant.[2] Chronic contact dermatitis can develop where the removal of the offending agent no longer provides expected relief. In North America, the most common allergic contact dermatitis is caused by poison ivy. Common causes of irritant contact dermatitis are harsh (highly alkaline) soaps, detergents, and cleaning products.[3]

Types of contact dermatitis

There are three types of contact dermatitis: irritant contact, allergic contact, and photocontact dermatitis. Photocontact dermatitis is divided into two catergories: phototoxic and photoallergic.

Irritant Contact Dermatitis (ICD)

This is the most common form of contact dermatitis, affecting around 1-2% of healthy Europeans (ESCD 2006), and can be caused by either an acute or chronic exposure to a toxic insult. It is also referred to as non-allergic contact dermatitis (along with traumiterative or housewives' eczema) referring to its non-immunological mechanism of toxicity. It is caused by either chemical or physical irritants. People who do a lot of wetwork (mothers of small children, hairdressers, nurses, chefs) are very prone to developing ICD.

Chemical Irritant Contact Dermatitis (CICD) can be subdivided into acute and chronic ICD which is usually associated with strong and weak irritants respectively (HSE MS24)[4]. The following definition is provided by Mathias and Maibach (1978):[5] a nonimmunologic local inflammatory reaction characterized by erythema, edema, or corrosion following single or repeated application of a chemical substance to an identical cutaneous site. The mechanism of action varies between toxins. Detergents, surfactants, extremes of pH and organic solvents all have the common effect of directly affecting the barrier properties of the epidermis. These include removing fat emulsion, inflicting cellular damage on the epithelium, or increasing the transepidermal water loss by damaging the horny layer water-binding mechanisms and damaging the DNA which causes the layer to thin. As suggested previously, strong concentrations of irritants cause an acute effect, but this is not as common as the accumulative, chronic effect of weaker irritants whose deleterious effects build up with subsequent doses (ESCD 2006).

Common chemical irritants implicated: solvents (alcohol, xylene, turpentine, esters, acetone, ketones and others); metalworking fluids (neat oils, water-based matalworking fluids with surfactants); rubber (gloves); kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl sulfate); alkalis (drain cleaners, strong soap with lye residues).

Physical irritant contact dermatitis (PICD) is a less well researched form of ICD (Maurice-Jones et al)[6]. This is due to its highly varied and numerous mechanisms of action as well as a lack of a test for its diagnosis. A complete patient history combinated with negative allergic patch testing is usually necessary to reach a correct diagnosis. The simplest form of PICD results from prolonged rubbing, although the diversity of implicated irritants is far wider.[citation needed] Examples include paper friction, fiberglass, and scratchy clothing.

Many plants cause ICD by directly irritating the skin. Some plants act through their spines or irritant hairs. Some plant such as the buttercup, spurge and daisy, act by chemical means. The sap of these plants contains a number of alkaloids, glycosides, saponins, anthroquinones, and in the case of plant bulbs, irritant calcium oxalate crystals, all of which can cause CICD (Mantle and Lennard, 2001)[7].

Allergic Contact Dermatitis (ACD)

This condition is the manifestation of an allergic response caused by contact with a substance. A list of common allergens is shown in Table 1 (Kucenic and Belsito, 2002)[8]. Although less common than ICD, it is accepted to be the most prevalent form of immunotoxicity found in humans (Kimble et al 2002)[9]. By its allergic nature, this form is a hypersensitive reaction which is atypical within the population. The mechanisms by which these reactions occur are complex, with many levels of fine control. Their immunology centres around the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.

ACD arises as a result of two essential stages - an induction phase which primes and sensitises the immune system for an allergic response, and an elicitation phase in which this response is triggered (Kimble et al 2002). As such, ACD is termed a Type IV delayed hypersensitivity reaction involving a cell-mediated allergic response. Contact allergens are essentially soluble haptens (low in molecular weight) and, as such, have the physico-chemical properties that allow them to cross the stratum corneum of the skin. They can only cause their response as part of a complete antigen, involving their association with epidermal proteins forming hapten-protein conjugates. This in turn requires them to be protein-reactive.

The conjugate formed is then recognised as a foreign body by the Langerhans Cells (LC) (and in some cases Dentritic Cells (DC)), which then internalise the protein, transport it via the lymphatic system to the regional lymph nodes and present the antigen to T-lymphocytes. As mentioned earlier, this process is controlled by cytokines and chemokines, with tumour necrosis factor alpha (TNF-α) and certain members of the interleukin family (1, 13 and 18) and their action serves either to promote or to inhibit the mobilisation and migration of these LCs. (Kimble et al 2002) As the Langerhans cells are transported to the lymph nodes, they become differentiated and transform into Dentric Cells which are immunostimulatory in nature.

Once within the lymph glands, the differentiated DCs act to present the allergenic epitope associated with the allergen to T lymphocytes. As a result, these T cells divide and differentiate, clonally multiplying so that if the allergen is experienced again by the individual, these T cells will respond more quickly and more aggressively.

As mentioned briefly, the immunological reaction involved in ACD is highly complex with many levels of fine control. Kimbe et al (2002) explore these complexities in short. It appears that there are two major phenotypes of cytokine production (although there exists a gradient of subsets in between), and these are termed T-helper 1 and 2 (Th1 and Th2). Although these cells initially differentiate from a common stem cell, they develop with time as the immune system matures. Th1 phenotypes are characterised by their focus on Interleukin and Interferon, while Th2 cells action is centred more around the regulation of IgE by cytokines. The CD4 and CD8 T lymphocyte subsets also have been found to contribute to differential cytokine regulation, with CD4 having been shown to produce high levels of IL-4 and IL10 while solely CD8 cells are associated with low levels of IFN?. These two cell subtypes are also closely associated with the cell matrix interactions essential for the pathogenesis of ACD.

It has been suggested (White et al 1986) [10] that there appears to be a threshold to the mechanisms of allergic sensitisation by ACD-associated allergens. This is thought to be linked to the level at which the toxin induces the up-regulation of the required mandatory cytokines and chemokines. It has also been proposed that the vehicle in which the allergen reaches the skin could take some responsibility in the sensitisation of the epidermis by both assisting the percutaneous penetration and causing some form of trauma and mobilisation of cytokines itself.

Common allergens implicated:

* Nickel (nickel sulfate hexahydrate) - metal frequently encountered in jewelry and clasps or buttons on clothing
* Gold (gold sodium thiosulfate) - precious metal often found in jewelry
* Balsam of Peru (myroxylon pereirae) - a fragrance used in perfumes and skin lotions, derived from tree resin
* Thimerosal - a mercury compound used in local antiseptics and in vaccines
* Neomycin - a topical antibiotic common in first aid creams and ointments, cosmetics, deodorant, soap and pet food
* Fragrance mix - a group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes and dental products [11]
* Formaldehyde - a preservative with multiple uses, e.g., in paper products, paints, medications, household cleaners, cosmetic products and fabric finishes
* Cobalt chloride - metal found in medical products; hair dye; antiperspirant; metal-plated objects such as snaps, buttons or tools; and in cobalt blue pigment
* Bacitracin - a topical antibiotic
* Quaternium 15 - preservative in cosmetic products (self-tanners, shampoo, nail polish, sunscreen) and in industrial products (polishes, paints and waxes).[12]

Photocontact Dermatitis (PCD)

Sometimes termed "photoaggravated"(Bourke et al 2001)[13], and divided into two categories, phototoxic and photoallergic, PCD is the eczematous condition which is triggered by an interaction between an otherwise unharmful or less harmful substance on the skin and ultraviolet light (320-400nm UVA) (ESCD 2006), therefore manifesting itself only in regions where the sufferer has been exposed to such rays. Without the presence of these rays, the photosensitiser is not harmful. For this reason, this form of contact dermatitis is usually associated only with areas of skin which are left uncovered by clothing. The mechanism of action varies from toxin to toxin, but is usually due to the production of a photoproduct. Toxins which are associated with PCD include the psoralens. Psoralens are in fact used therapeutically for the treatment of psoriasis, eczema and vitiligo.

Photocontact dermatitis is another condition where the distinction between forms of contact dermatitis is not clear cut. Immunological mechanisms can also play a part, causing a response similar to ACD.

Prevention

Since contact dermatitis relies on an irritant or an allergen to initiate the reaction, it is important for the patient to identify the responsible agent and avoid it. This can be accomplished by having patch tests, a method commonly known as allergy testing. The patient must know where the irritant or allergen is found to be able to avoid it. It is important to also note that chemicals sometimes have several different names. This doesn't always have a great success rate. [14]

Summary

The distinction between the various types of contact dermatitis is based on a number of factors. The morphology of the tissues, the histology, and immunologic findings are all used in diagnosis of the form of the condition. However, as suggested previously, there is some confusion in the distinction of the different forms of contact dermatitis (Reitschel 1997)[15]. Using histology on its own is insufficient, as these findings have been acknowledged not to distinguish (Rietschel, 1997), and even positive patch testing does not rule out the existence of an irritant form of dermatitis as well as an immunological one. It is important to remember, therefore, that the distinction between the types of contact dermatitis is often blurred, with, for example, certain immunological mechanisms also being involved in a case of irritant contact dermatitis.

References

1. ^ ESDC. What is contact dermatitis. European Society of Contact Dermatitis, http://orgs.dermis.net
2. ^ DermNet NZ: Contact Dermatitis. Retrieved on 2006-08-14.
3. ^ Irritant Contact Dermatitis, at DermNetNZ, http://www.dermnetnz.org/dermatitis/contact-irritant.html
4. ^ HSE Guidance Notes. Guidance Note MS 24 - Health Surveillance of occupational skin disease. http://www.hse.gov.uk/pubns/ms24.pdf
5. ^ Mathias CG, Maibach HI. Dermatotoxicology monographs I. Cutaneous irritation: factors influencing the response to irritants. Clin Toxicol. 1978;13(3):333-46. Review. No abstract available.
6. ^ Morris-Jones R, Robertson SJ, Ross JS, White IR, McFadden JP, Rycroft RJ. Dermatitis caused by physical irritants. Br J Dermatol. 2002 Aug;147(2):270- 5. Review.
7. ^ Mantle D, Lennard TWJ. Plants and the skin. Brit J Derm Nurs. 2001 (Summer).
8. ^ Kucenic MJ, Belsito DV.Occupational allergic contact dermatitis is more prevalent than irritant contact dermatitis: a 5-year study. J Am Acad Dermatol. 2002 May;46(5):695-9.
9. ^ Kimble I, Basketter DA, Gerberick GF, Dearman RJ. Allergic contact dermatitis. Int Immunopharmacol. 2002 Feb;2(2-3):201-11. Review.
10. ^ White SI, Friedmann PS, Moss C, Simpson JM.The effect of altering area of application and dose per unit area on sensitization by DNCB. Br J Dermatol. 1986 Dec;115(6):663-8.
11. ^ Allergy to fragrance mix at DermNetNZ, http://dermnetnz.org/dermatitis/fragrance-allergy.html
12. ^ Mayo Clinic study, http://http://www.mayoclinic.org/news2006-rst/3268.html
13. ^ Bourke J, Coulson I, English J; British Association of Dermatologists. Guidelines for care of contact dermatitis. Br J Dermatol. 2001 Dec;145(6):877-85.
14. ^ DermNet NZ: Contact Dermatitis. Retrieved on 2006-08-18.
15. ^ Rietschel RL. Mechanisms in irritant contact dermatitis. Clin Dermatol. 1997 Jul-Aug;15(4):557-9.

All About Eczema

2007-04-02T18:26:00.005-07:00

Eczema is a form of dermatitis, or inflammation of the upper layers of the skin. The term eczema is broadly applied to a range of persistent or recurring skin rashes characterized by redness, skin edema, itching and dryness, with possible crusting, flaking, blistering, cracking, oozing or bleeding. Areas of temporary skin discoloration sometimes characterize healed lesions, though scarring is rare.

Types

ICD-10 codes are provided where available. The term eczema refers to a set of clinical characteristics. Classification of the underlying diseases has been haphazard and unsystematic, with many synonyms used to describe the same condition. A type of eczema may be described by location (e.g. hand eczema), by specific appearance (eczema craquele or discoid), or by possible cause (varicose eczema). Further adding to the confusion, many sources use the term eczema and the term for the most common type of eczema (atopic eczema) interchangeably.
More severe eczema
More severe eczema

The European Academy of Allergology and Clinical Immunology (EAACI) has published a position paper which simplifies the nomenclature of allergy-related diseases including atopic and allergic contact eczemas (Johansson et al., 2001, Allergy 56:813). Non-allergic eczemas are not affected by this proposal.

The classification below is clustered by incidence frequency.

More common eczemas

* Atopic eczema (aka infantile e., flexural e., atopic dermatitis) is believed to have a hereditary component, and often runs in families whose members also have hay fever and asthma. Itchy rash is particularly noticeable on face and scalp, neck, inside of elbows, behind knees, and buttocks. Experts are urging doctors to be more vigilant in weeding out cases that are in actuality irritant contact dermatitis. It is very common in developed countries, and rising. (L20)

* Contact dermatitis is of two types: allergic (resulting from a delayed reaction to some allergen, such as poison ivy or nickel), and irritant (resulting from direct reaction to, say, a solvent). Some substances act both as allergen and irritant (e.g. wet cement). Other substances cause a problem after sunlight exposure, bringing on phototoxic dermatitis. About three quarters of cases of contact eczema are of the irritant type, which is the most common occupational skin disease. Contact eczema is curable provided the offending substance can be avoided, and its traces removed from one’s environment. (L23; L24; L56.1; L56.0)

A patch of eczema that has been scratched

* Xerotic eczema (aka asteatotic e., e. craquele or craquelatum, winter itch, pruritus hiemalis) is dry skin that becomes so serious it turns into eczema. It worsens in dry winter weather, and limbs and trunk are most often affected. The itchy, tender skin resembles a dry, cracked, river bed. This disorder is very common among the older population. Ichthyosis is a related disorder. (L85.3; L85.0)

* Seborrhoeic dermatitis (aka cradle cap in infants, dandruff) causes dry or greasy scaling of the scalp and eyebrows. Scaly pimples and red patches sometimes appear in various adjacent places. In newborns it causes a thick, yellow crusty scalp rash called cradle cap which seems related to lack of biotin, and is often curable. (L21; L21.0)

Less common eczemas

* Dyshidrosis (aka dyshidrotic e., pompholyx, vesicular palmoplantar dermatitis, housewife’s eczema) only occurs on palms, soles, and sides of fingers and toes. Tiny opaque bumps called vesicles, thickening, and cracks are accompanied by itching which gets worse at night. A common type of hand eczema, it worsens in warm weather. (L30.1)

* Discoid eczema (aka nummular e., exudative e., microbial e.) is characterized by round spots of oozing or dry rash, with clear boundaries, often on lower legs. It is usually worse in winter. Cause is unknown, and the condition tends to come and go. (L30.0)

* Venous eczema (aka gravitational e., stasis dermatitis, varicose e.) occurs in people with impaired circulation, varicose veins and edema, and is particularly common in the ankle area of people over 50. There is redness, scaling, darkening of the skin and itching. The disorder predisposes to leg ulcers. (I83.1)

* Dermatitis herpetiformis (aka Duhring’s Disease) causes intensely itchy and typically symmetrical rash on arms, thighs, knees, and back. It is directly related to celiac disease, and can often be put into remission with appropriate diet. (L13.0)

* Neurodermatitis (aka lichen simplex chronicus, localized scratch dermatitis) is an itchy area of thickened, pigmented eczema patch that results from habitual rubbing and scratching. Usually there is only one spot. Often curable through behavior modification and anti-inflammatory medication. Prurigo nodularis is a related disorder showing multiple lumps. (L28.0; L28.1)

* Autoeczematization (aka id reaction, autosensitization) is an eczematous reaction to an infection with parasites, fungi, bacteria or viruses. It is completely curable with the clearance of the original infection that caused it. The appearance varies depending on the cause. It always occurs some distance away from the original infection. (L30.2)

* There are also eczemas overlaid by viral infections (e. herpeticum, e. vaccinatum), and eczemas resulting from underlying disease (e.g. lymphoma). Eczemas originating from ingestion of medications, foods, and chemicals, have not yet been clearly systematized. Other rare eczematous disorders exist in addition to those listed here.

Diagnosis

Eczema diagnosis is generally based on the appearance of inflamed, itchy skin in eczema sensitive areas such as face, chest and other skin crease areas. For evaluation of the eczema, a scoring system can be used (for example, SCORAD, a scoring system for atopic dermatitis).

Given the many possible reasons for eczema flare ups, a doctor is likely to ascertain a number of other things before making a judgment:

* An insight to family history
* Dietary habits
* Lifestyle habits
* Allergic tendencies
* Any prescribed drug intake
* Any chemical or material exposure at home or workplace

To determine whether an eczema flare is the result of an allergen, a doctor may test the blood for the levels of antibodies and the numbers of certain types of cells. In eczema, the blood may show a raised IgE or an eosinophilia.

The blood can also be sent for a specific test called Radioallergosorbent Test (RAST) or a Paper Radioimmunosorbent Test (PRIST). In the test, blood is mixed separately with many different allergens and the antibody levels measured. High levels of antibodies in the blood signify an allergy to that substance.

Another test for eczema is skin patch testing. The suspected irritant is applied to the skin and held in place with an adhesive patch. Another patch with nothing is also applied as a control. After 24 to 48 hours, the patch is removed. If the skin under the suspect patch is red and swollen, the result is positive and the person is probably allergic to that substance.

Occasionally, the diagnosis may also involve a skin biopsy: removal of a small piece of affected skin for microscopic examination in a pathology laboratory.

Blood tests and biopsies are not always necessary for eczema diagnosis. However, doctors will at times require them if the symptoms are unusual, severe or in order to identify particular triggers.

Treatment

Moisturizing

Dermatitis severely dries out the skin, and keeping the affected area moistened can promote healing and retain natural moisture. This is the most important self-care treatment that one can use in atopic eczema.

The use of anything that may dry out the skin should be discontinued and this includes both normal soaps and bubble baths that remove the natural oils from the skin.

The moistening agents are called 'emollients'. The rule to use is: match the thicker ointments to the driest, flakiest skin. Light emollients like Aqueous cream may dry the skin if it is very flaky.

Emollient bath oils should be added to bath water and then suitable agents applied after patting the skin dry. Generally twice daily applications of emollients work best and while creams are easy to apply, they are quickly absorbed into the skin, therefore needing frequent re-application. Ointments, with less water content, stay on the skin for longer and need fewer applications.

Typical emollients are: Oilatum or Balneum bath oils, Medi Oil, Aqueous cream for washing with, Diprobase or Doublebase pump-action creams also used for washing and may be later applied directly to the skin.Sebexol, Epaderm ointment and Eucerin lotion or cream may be helpful with itching. Moisturizing gloves can be worn while sleeping.

As an alternative to wet-wrap therapy for rehydrating unbroken skin direct application of water-proof tape for an extended period, with or without other medicinal balms, can stop dryness and prevent mechanical abrasions of the itch-cycle and reduce lichenification.

One alternative treatment, fashionable in the Victorian and Edwardian eras, was Sulphur. Recently Sulphur has re-gained some credibility as a safe alternative to steroids and coal tar.

[edit] Eczema and detergents

The first and primary recommendation is that people suffering from eczema shouldn't use detergents of any kind unless absolutely necessary. Current medical thought is that people wash too much and that eczema sufferers should use cleansers only when water is not sufficient to remove dirt from skin.

Another point of view is that detergents are so ubiquitous in modern environments and so persistent in tissues and surfaces, safe soaps are necessary to remove them in order to eliminate the eczema in a percentage of cases. Although most recommendations use the terms "detergents" and "soaps" interchangeably, and tell eczema sufferers to avoid both, detergents and soaps are not the same and are not equally problematic to eczema sufferers. Detergents increase the permeability of skin membranes in a way that soaps and water alone do not. Sodium lauryl sulfate, the most common household detergent, has been shown to amplify the allergenicity of other substances ("increase antigen penetration")[1].

The use of detergents in recent decades has increased dramatically, while the use of soaps began to decline when detergents were invented, and leveled off to a constant around the '60s. Complicating this picture is the recent development of mild plant-based detergents for the natural products sector.

Unfortunately there is no one agreed upon best kind of cleanser for eczema sufferers. Different clinical tests, sponsored by different personal product companies, unsurprisingly tout various brands as the most skin friendly based on specific properties of various products and different underlying assumptions as to what really determines skin friendliness. The terms "hypoallergenic" and "doctor tested" are not regulated (according to Consumer Reports[citation needed]), and no research has been done showing that products labeled "hypoallergenic" are in fact less problematic than any others.

Dermatological recommendations in choosing a soap generally include:

* Avoid harsh detergents or drying soaps.
* Choose a soap that has an oil or fat base; a "superfatted" soap is best.
* Use an unscented soap.
* Patch test your soap choice, by using it only on a chosen area until you are sure of its results.
* Use a non-soap based cleanser.

How to use soap when one must

* Use soap sparingly
* Avoid using washcloths, sponges, or loofahs
* Use soap only on areas where it is necessary
* Soap up only at the very end of your bath
* Use a fragrance free barrier type moisturizer such as vaseline or aquaphor before drying off
* Use care when selecting lotion, soap, or fragrance, avoiding suspected allergens. Ask your doctor for recommendations.
* Never rub your skin dry, or else your skin's oil/moisture will be on the towel and not your body

Itch relief

Antihistamine medication may reduce the itch during a flare up of eczema, and the reduced scratching in turn reduces damage & irritation to the skin (the Itch cycle).

Capsaicin applied to the skin acts as a counter irritant (see Gate control theory of nerve signal transmission). Other agents that act on nerve transmissions, like menthol, also have been found to mitigate the body's itch signals, providing some relief. Recent research suggests Naloxone hydrochloride and dibucaine suppress the itch cycle in atopic-dermatitis model mice as well.

Corticosteroids

Dermatitis is often treated by doctors with prescribed Glucocorticoid (a corticosteroid steroid) ointments, creams or lotions. For mild-moderate eczema a weak steroid may be used (e.g. Hydrocortisone or Desonide), whilst more severe cases require a higher-potency steroid (e.g. Clobetasol propionate). They cannot cure eczema, but are highly effective in controlling, or suppressing, symptoms in most cases. It is believed by alternative health practitioners that the suppression of eczema can often cause more serious health complaints, such as asthma.

Corticosteroids must be used sparingly to avoid possible side effects, the most significant of which is that their prolonged use can cause the skin to thin and become fragile (atrophy). High strength steroids used over large areas may be significantly absorbed into the body causing bone demineralization (osteoporosis). Finally by their immunosuppression action they can, if used alone, exacerbate some skin infections (fungal or viral). If using on the face, only a low strength steroid should be used and care must be taken to avoid the eyes.

Hence, a steroid of an appropriate strength to promptly settle an episode of eczema should be sparingly applied. Once the desired response has been achieved it should be discontinued and replaced with emollients as maintenance therapy.

Immunomodulators

Topical immunomodulators like pimecrolimus (Elidel® and Douglan®) and tacrolimus (Protopic®) were developed after corticosteroid treatments, effectively suppressing the immune system in the affected area, and appear to yield better results in some populations. However, such suppression is believed by alternative health practitioners to have possible adverse health effects. The US Food and Drug Administration has issued a public health advisory [1] about the possible risk of lymph node or skin cancer from use of these products, but many professional medical organizations disagree with the FDA's findings;

* The postulation is that the immune system may help remove some pre-cancerous abnormal cells which is prevented by these drugs. However, any chronic inflammatory condition such as eczema, by the very nature of increased metabolism and cell replication, has a tiny associated risk of cancer (see Bowen's disease).
* Current practice by UK dermatologists [2] is not to consider this a significant real concern and they are increasingly recommending the use of these new drugs. The dramatic improvement on the condition can significantly improve the quality of life of sufferers (and families kept awake by the distress of affected children). The major debate, in the UK, has been about the cost of such newer treatments and, given only finite NHS resources, when they are most appropriate to use.[3]
* In addition to cancer risk, there are other potential side effects with this class of drugs. Adverse reactions including severe flushing, photosensitive reactivity and possible drug interaction in patients who consume even small amounts of alcohol.[citation needed]

Antibiotics

The disruption to the skin's normal barrier protection through dry and cracked skin allows easy entry for bacteria. Scratching by the patient both introduces infection and spreads it from one area to another. Any skin infection further irritates the skin and a rapid deterioration in the condition may ensue; the appropriate antibiotic should be given.

[edit] Light therapy

Light therapy using ultraviolet light can help[citation needed]. UVA is mostly used but UVB and Narrow Band UVB are also used. Ultraviolet light exposure carries its own risks, particularly later skin cancers. When light therapy alone is found to be ineffective, it is combined with a substance called psoralen. This PUVA (Psoralen + UVA) combination therapy is termed photo-chemotherapy. Psoralens make the skin more sensitive to UV light, allowing lower doses of UVA to be used.

Diet and Nutrition

Recent studies provide hints that food allergy may trigger atopic dermatitis. For these people, identifying the allergens could allow an avoidance diet, although this approach is still in an experimental stage[2].

Dietary elements reported to trigger Eczema by sufferers include dairy products and coffee (both caffeinated and decaffeinated), soya, eggs, nuts and wheat.

Alternative therapies

Non-conventional medical approaches include traditional herbal medicine and others. Patients should inform their doctor/allergist/dermatologist if they are pursuing one of these treatment routes. Patients can also wear clothing designed specifically to manage the itching, scratching and peeling associated with eczema. Sulphur has been used for many years as a treatment in the alleviation of eczema, although this could be suppressive. Many patients find that swimming in the ocean will relieve symptoms and clear up the red patchy scales. Oatmeal is a common kitchen remedy to relieve itching, and can be applied topically as a cream or, as a colloid, in the bath.

Herbal Medicine

Historical sources - notably traditional Chinese medicine and Western herbalism - suggest a wide variety of treatments, each of which may vary from individual to individual as to efficacy or harm. Toxicity may be present in some. Some of these remedies are for topical use.

* Potentilla chinensis
* Aebia clematidis
* Clematis armandii
* Rehmannia glutinosa
* Paeonia lactiflora (Chinese Peony)
* Lophatherum gracile
* Dictamnus dasycarpus
* Tribulus terrestris
* Glycyrrhiza uralensis
* Glycyrrhiza glabra (Licorice)
* Schizonepeta tenuifolia (Neem)
* Schizonepeta tennuifolia
* Azadirachta indica
* evening primrose oil
* tea tree oil
* burdock
* rooibos
* calamine
* oatmeal
* crocodile oil
* cod liver oil
* neem oil
* Aloe Propolis cream
* Raw Goat's Milk
* Hemp Cream

Research

Other than direct treatments of the symptoms, no cure is presently known for most types of dermatitis; even cortisone treatments and immunomodulation may often have only minor effects on what may be a complex problem. As the condition is often related to family history of allergies (and thus heredity), it is probable that gene therapy or genetic engineering might help.

Damage from the enzymatic activity of allergens is usually prevented by the body's own protease inhibitors, such as, LEKTI, produced from the gene SPINK5. Mutations in this gene are known to cause Netherton’s syndrome, which is a congenital erythroderma. These patients nearly always develop atopic disease, including hay fever, food allergy, urticaria and asthma. Such evidence supports the hypothesis that skin damage from allergens may be the cause of eczema, and may provide a venue for further treatment[3].

Another study identified a gene that the researchers believe to be the cause of inherited eczema and some related disorders. The gene produces the protein filaggrin, the lack of which causes dry skin[4]

Psychological effects

Eczema often comes and goes in cycles, meaning that at some times of the year sufferers are able to feel normal, while at other times they will distance themselves from social contact. Sufferers with visible marks generally feel fine (physically) and can act normal, but when it is mentioned they may become withdrawn and self-conscious. Since it is a condition made worse by scratching, a sufferer with highly visible sores aggravated by scratching often feels as if everyone is looking at the marks and that they are self induced. Although scratching does give a sense of release, it is usually a temporary solution and can lead to problems with constant scratching. Sufferers often shy away from scratching in public, but the solution is to scratch in privacy. In cases of children with eczema, visible scars or scratch marks can lead to suspicion of home abuse or self-mutilation, which causes possible peer rejection and may add to a general level of stress.

References

1. ^ Corazza M, Virgili A. Allergic contact dermatitis from ophthalmic products: can pretreatment with sodium lauryl sulfate increase patch test sensitivity? Contact Dermatitis 2005; 52(5): 239-41. PMID 15898995
2. ^ Kanny G. Atopic dermatitis in children and food allergy: combination or causality? Should avoidance diets be initiated? Ann Dermatol Venereol 2005; 132 Spec No 1: 1S90-103. PMID 15984300
3. ^ Walley AJ, Chavanas S, Moffatt MF, Esnouf RM, Ubhi B, Lawrence R, Wong K, Abecasis GR, Jones EY, Harper JI, Hovnanian A, Cookson WO. Gene polymorphism in Netherton and common atopic disease. Nat Genet 2001; 29(2): 175-8. PMID 11544479
4. ^ Palmer CN et al.. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat Genet 2006; 38(4): 441-6. PMID 16550169

All About Atopic dermatitis - eczema

2007-04-02T18:26:00.004-07:00

Atopic dermatitis, sometimes called eczema, is a kind of dermatitis, an atopic skin disease. Atopic dermatitis afflicts humans, particularly young children; it is also a well-characterized disease in domestic dogs.

Presentation
Atopic dermatitis by a child

The skin of a patient with atopic dermatitis reacts abnormally and easily to irritants, food and environmental allergens and becomes red, flaky and very itchy. It also becomes vulnerable to surface infections caused by bacteria. The skin on the flexural surfaces of the joints (for example inner sides of elbows and knees) are most commonly affected regions in people. In dogs with atopic dermatitis, the skin of the face, front feet and the ears are most commonly affected.

Atopic dermatitis in people often occurs together with other atopic diseases like hay fever, asthma and conjunctivitis. It is a familial and chronic disease and its symptoms can increase or disappear over time. There is no cure for it, but its symptoms can be managed with various treatments. Dogs with atopic dermatitis seldom have respiratory disease, but may be afflicted with inflammatory bowel disease.

Originally controversial, the association of food allergy with atopic dermatitis has now been clearly demonstrated, especially in severe disease of infancy. The same is true of the disease in domestic dogs.

Atopic dermatitis in older children and adults is often confused with psoriasis.

Treatment

The disease severity can be reduced by minimizing drying of the skin and avoiding or minimizing contact with known allergens. The issue of allergies often complicates a case of atopic dermatitis.

Topical treatments focus on reducing the dryness of the skin. Moisturizers (Emollients) are available, some only by prescription.

Most soaps wash away the oils produced by the skin that normally serve to prevent drying. Using a soap substitute such as aqueous cream helps keep the skin moisturized.

If moisturizers on their own don't help, topical steroid ointments or creams may be used. These are safe provided they are prescribed by a doctor.

Although many people are intimidated by the term 'steroids,' their proper use can result in atopic dermatitis being brought under control.

Alternative medicines may (illegally) contain very strong steroids [1].

The immunosuppressant Tacrolimus can be used as a topical preparation in the treatment of severe atopic dermatitis.

Many of the same types of treatment are used in domestic dogs with atopic dermatitis. In addition, domestic dogs may be successfully managed with allergen-specific immunotherapy; many are treated with low-dose cyclosporine lipid emulsion.

All About Dermatitis herpetiformis

2007-04-02T18:26:00.003-07:00

Dermatitis herpetiformis (DH) or Duhring's Disease, is a skin disorder often associated with celiac disease. It is a chronic, extremely itchy rash consisting of papules and vesicles. Dermatitis herpetiformis is associated with sensitivity of the intestine to gluten in the diet (celiac sprue).

Dermatitis herpetiformis usually begins in the twenties, though children may sometimes be affected. It is seen in both men and women. Though the cause of the rash is unknown, dermatitis herpetiformis is frequently associated with gluten (a protein found in cereals) sensitivity in the small bowel.

Symptoms

Dermatitis herpetiformis breakouts are usually extremely itchy. In many people the vesicles or papules appear on the elbows, knees, back, and buttocks (pressure points). It may also present as a patch of red skin with little water blisters scattered about. It is a systemic condition; the unpredictable skin rash may appear or be exacerbated by any irritation such as dry skin, scratching or clothing that is rough or scratchy. The fact that the rash is most prevalent at pressure points (where clothing rubs the most) may be why the symptoms sometimes appear to be symmetrical.

Signs and tests

A skin biopsy and direct immunofluorescence test of the skin are performed in most cases; doctors may additionally recommend a biopsy of the intestines.

Treatment

Dapsone, an antibiotic, may help the majority of patients.

A strict gluten-free diet will also be recommended to help control the disease. Adherence to this diet may eliminate the need for medications and prevent later complications.

Social impact

Lifelong diet The lifelong diet can be difficult and socially troublesome, especially in young patients, but it is crucial in order to avoid serious health consequences. Teenagers in particular occasionally rebel against the dietary strictures and suffer relapses or complications as a result. The widespread use of wheat byproducts in prepared food, soups and sauces can make dining out problematic. This is especially true in the United States, where dermatitis herpetiformis disease is less widely-known among the wider population than it is in Europe. However, certain types of restaurant (e.g., Japanese, Thai, Indian, and Latin American) already offer a wide range of gluten-free menu options, and many major restaurant chains have responded to growing awareness of celiac disease (and by default dermatitis herpetiformis) by posting information about the gluten content of their menu items on their websites.

It is important for people to understand that one does not "get over" dermatitis herpetiformis ; it is present for life. As coeliac disease has become better understood, the availability of gluten-free replacements for everyday treats such as muffins, bagels, pasta and the like has continually improved, as has their quality. This has also benefited those with dermatitis herpetiformis.

It is easy for people to think they have removed all gluten from their diet, but to continue to consume one or two products that they do not associate with gluten. For example, to eat only gluten-free foods but to continue to drink beer may easily make all that hard work useless. However, even this problem may now be overcome and there are many specialist brews around the world that may be described as gluten free beer.

However, the case of beer raises the main problem of dermatitis herpetiformis and coeliac disease: while the diet is strict and the effects of the disease are serious, the main symptom of the disease can be social isolation with those with Dermatitis herpetiformis afraid to become involved in normal social life. Parties can be difficult, weddings and funerals hard, holidays awkward, a meal out a nightmare, travel is made more stressful, and even the trip to a bar or pub one that requires the individual to be constantly aware of the disease. It is too easy for the coeliacs and those with dermatitis herpetiformis to withdraw from these normal activities, and many people with these complaints are working to create normal activities where they can forget the problem. It is important for newly diagnosed with either dermatitis herpetiformis or coeliacs to ensure that they do get involved in social activities and are not afraid to "make a fuss".

Religious Issues

The Eucharist: The Christian sacrament of the Eucharist presents a unique challenge for Christian sufferers of dermatitis herpetiformis or coeliac disease.

In its classical form, the bread and/or communion wafers have traditionally contained wheat flour, and therefore gluten. Coeliacs and those with dermatitis herpetiformis are therefore presented with a choice between denying themselves a central part of their religious practice or placing themselves at risk of serious illness. In response to this, some makers of communion wafers have begun making gluten-free versions (usually made of rice), which are now widely available. Many churches permit (or have no official policy on) use of these wafers, while other churches do not allow them.

In particular, Roman Catholic doctrine requires that the Eucharistic host (the communion wafer) must contain at least some unleavened wheat, as did the bread served at the Last Supper. The Catholic Church has approved the use of low-gluten wafers, but even these are not gluten-free. Some Catholic sufferers have requested permission to use rice wafers; these petitions have so far been denied.

However, official Roman Catholic doctrine is that a Catholic may validly receive communion by consuming a communion wafer and/or the consecrated wine. The Council of Trent decreed that taking either wine or wafer qualifies as a valid Communion:

"For we do not receive in the Sacred Host one part of Christ and in the Chalice the other, as though our reception of the totality depended upon our partaking of both forms; on the contrary, under the appearance of bread alone, as well as under the appearance of wine alone, we receive Christ whole and entire (cf. Council of Trent, Sess. XIII, can. iii). Therefore, any Catholic can receive the Eucharist in the 'fullness of the sacrament' (Catechism, Section 1390) simply in a sip of consecrated wine (even an approved low-alcohol wine); even those who cannot safely consume wheat (or indeed, any other grain) can safely partake of the Eucharist."

The matter has been controversial, however, and on August 22, 1994, the Congregation for the Doctrine of the Faith apparently banned those with coeliacs and dermatitis herpetiformis from the priesthood stating, "Given the centrality of the celebration of the Eucharist in the life of the priest, candidates for the priesthood who are affected by celiac disease or suffer from alcoholism or similar conditions may not be admitted to holy orders." After considerable upset and debate, the congregation softened the ruling on July 24, 2003 to "Given the centrality of the celebration of the Eucharist in the life of a priest, one must proceed with great caution before admitting to Holy Orders those candidates unable to ingest gluten or alcohol without serious harm,".

Eastern Orthodox Position: The Eastern Orthodox Church also requires that the bread used at the Eucharist be made with wheat flour; here the bread is leavened with yeast. In the Orthodox practice, the consecrated bread and wine are given together from a chalice with a spoon. Some Orthodox sufferers have been able to receive communion simply by having the priest take only wine in the spoon; others, more sensitive to wheat, have had to have some of the wine set aside before the bread is added to the chalice. This latter case is extremely unusual, and is strictly speaking only permissible with the blessing of the diocesan bishop. While the Orthodox do not have such an explicit rationale as the Roman Catholic Church, their general understanding is that, in the case of exceptions made for the sake of Economy, the Holy Spirit makes up whatever is lacking.

Coeliacs, dermatitis herpetiformis, and Passover The Jewish festival of Pesach (Passover) may present problems with its obligation to eat matzo. Matzo is normally made from wheat or other gluten-containing grains. Oat matzo is now available, however. Many products prepared for Passover are also non-gebrokts, which means they are free of wheat, barley, spelt, oats, and rye. Potato starch is the primary starch used to replace the grains. These products make it easier to participate in Passover.

Specialist breads, pastas, and beer

Although these diseases may tend to isolate individuals with the complaint, the situation is becoming less difficult year by year. Manufacturers are now making a wide range of very acceptable breads, and some pastas (notoriously horrible in the past) are virtually indistinguishable from "normal" pasta. Restaurants are beginning to offer gluten free menus and are recognising the size of the market that is largely not catered for. Coeliacs and those with dermatitis herpetiformis should not be afraid to ask establishments how they can cater for them. Where the question has been asked repeatedly, the proprietors tend to recognise the need, and become aware of the revenue that is lost where they do not provide a full range of products.

In many ways beer seems to be the hardest gluten free product to "get right". However, gluten free beer is now available and there is now a range of ales, beers, and lagers to choose from. Around the world standards of "gluten free" vary. For example, while in the United Kingdom a beer with less than 20 parts per million gluten (20ppm) is "gluten free", in Australia it is not possible to describe any product as such if any gluten can be detected at all. Similarly, some "gluten free" breads can contain low levels of gluten in one country, in another they would contravene labelling or food standards legislation.
Gluten free beers
Gluten free beers

However, while large scale commercial beers are out of the question for those who cannot consume gluten[1] [2] [3] (regardless of the sometimes misleading advice on some brewery websites), it is likely that most people with dermatitis herpetiformis coeliacs will be able to drink beer at under 20ppm (in moderation) without causing themselves any harm. It is important, however, for consumers of all "low gluten" foods and beverages to tell their consultant, and to ensure that even if the obvious symptoms are absent, there are no other negative effects continuing that they are unaware of.

However, the development of a range of gluten free beers is an example of those who cannot consume gluten "working together to socialize normally and avoid isolation caused by their special dietary needs. It also represents part of the return to a ‘normal’ life"[4].

References

1. ^ Ask the Beer Fox - Is Straub's Beer Gluten Free ?. Carolyn Smagalski, Bella Online (2006).
2. ^ Is Nigerian Guinness Gluten Free ?. Carolyn Smagalski, Bella Online (2006).
3. ^ Ask the Beer Fox – Is Standard Lager Beer Safe for Coeliacs?. Carolyn Smagalski, www.glutenfreebeerfestival.com (2006).
4. ^ First-Ever Gluten-Free Beer Festival Quenches Celiacs’ Thirst. Robert La France, Glutenfreeda.com (2006).

All About Swimmer's itch

2007-04-02T18:26:00.002-07:00

Swimmer’s itch, duck itch, or cercarial dermatitis, is a short-term, immune reaction occurring in the skin of humans that have been infected by water-borne trematode parasites. Symptoms, which include itchy, raised papules, commonly occur within hours of infection and do not generally last more than a week.

The trematodes that cause swimmer’s itch are parasitic schistosomes that use both snails and vertebrates as hosts in their life cycles. Most cases are caused by parasites that use waterfowl as the vertebrate host. These avian schistosomes cannot complete their life cycles in mammals, but can accidentally infect humans, giving rise to mildly itchy spots on the skin. Within hours, these spots become raised papules that are more intensely itchy. The papules are caused by localized inflammatory immune reactions, each corresponding to the penetration site of a single parasite, which dies in the skin within hours.

Two schistosome genera that infect waterfowl and are associated with swimmer’s itch are Trichobilharzia and Gigantobilharzia. However, swimmer’s itch can also be caused by schistosome parasites of non-avian vertebrates, such as Schistosomatium douthitti, which infects snails and rodents.

The schistosomes that give rise to swimmer’s itch should not to be confused with those of the genus Schistosoma, which infect humans and cause the serious human disease schistosomiasis, or with larval stages of thimble jellyfish (Linuche unguiculata), which give rise to seabather's eruption.

Life cycles of non-human schistosomes

The non-human schistosomes use two hosts in their life cycles. One is a snail, the other, is a bird or mammal. It was once thought these parasites occured in Australian crocodiles, however, it was later found that they belonged to a family of blood trematodes that occur mainly in turtles, the spirorchiids(8). Schistosomes are gonochoristic and sexual reproduction takes place in the vertebrate host. In genera that infect birds, adult worms occur in tissues and veins of the host’s gastrointestinal tract, where they produce eggs that are shed into water with host feces. One European species, Trichobilharzia regenti, instead infects the bird host’s nasal tissues, where its eggs are shed with lachrymal secretions.

Once a schistosome egg is immersed in water, a short-lived, non-feeding, free-living stage known as the miracidium emerges. The miracidium uses cilia to follow chemical and physical cues thought to increase its chances of finding the first intermediate host in its life cycle, a snail. After infecting a snail, it develops into a mother sporocyst, which in turn undergoes asexual reproduction, yielding large numbers of daughter sporocysts, which asexually produce another short-lived, free-living stage, the cercaria. Cercariae use a tail-like appendage (often forked in genera causing swimmer’s itch) to swim to the surface of the water, as well as other physical and chemical cues, in order to locate the next and final (definitive) host in the life cycle, a bird. After infecting a bird, the parasite develops into a schistosomulum and migrates through the host’s circulatory system (or nervous system in case of T. regenti) to the final location within the host body where it matures and, if it encounters a mate, sheds eggs to begin the cycle anew.

Risk factors

Humans usually become infected with avian schistosomes after swimming in lakes or other bodies of slow-moving fresh water. Some laboratory evidence indicates snails shed cercariae most intensely in the morning and on sunny days, and exposure to water in these conditions may therefore increase risk. Duration of swimming is positively correlated with increased risk of infection in Europe[1] and North America[2], and shallow inshore waters -- snail habitat -- undoubtedly harbour higher densities of cercariae than open waters offshore. Onshore winds are thought to cause cercariae to accumulate along shorelines.[3] Studies of infested lakes and outbreaks in Europe and North America have found cases where infection risk appears to be evenly distributed around the margins of water bodies[4] as well as instances where risk increases in endemic swimmer's itch "hotspots"[5]. Children may become infected more frequently and more intensely than adults but this probably reflects their tendency to swim for longer periods inshore, where cercariae also concentrate.[6] Stimuli for cercarial penetration into host skin include unsaturated fatty acids, such as linoleic and linolenic acids. These substances occur naturally in human skin and are found in sun lotions and creams based on plant oils.

Control measures

Various strategies, targeting either the mollusc or avian hosts of schistosomes, have been used by lakeside residents in recreational areas of North America to deal with outbreaks of swimmer's itch. In Michigan, for decades authorities used copper sulphate as a molluscicide to reduce snail host populations and thereby the incidence of swimmer's itch. The results with this agent have been inconclusive, possibly because

* snails become tolerant
* local water chemistry reduces the molluscicide's efficacy
* local currents diffuse it
* adjacent snail populations repopulate a treated area. [7]

More importantly, perhaps, copper sulphate is toxic to more than just molluscs, and the effects of its use on aquatic ecosystems are not well understood. Another method targeting the snail host, mechanical disturbance of snail habitat, has been also tried in some areas of North America[8] and Lake Anecy in France, with promising results. Some work in Michigan suggests that administering praziquantel to hatchling waterfowl can reduce local swimmer's itch rates in humans.[9] Work on schistosomiasis showed that water-resistant topical applications of the common insect repellent DEET prevented schistosomes from penetrating the skin of mice.[10]

Public education of risk factors, a good alternative to the above mentioned interventionist strategies, can also reduce human exposure to cercariae.

Note: If infected, a good and very effective relief is an over-the-counter prescription of Novo-Hydroxyzin. [11]

Other names

Swimmer's itch is has various other names. In eastern nations, it is often named in reference to the rice paddies where it is contracted, producing names which translate to "rice paddy itch". For example, in Japan it is called "kubure" or "kobanyo", in Malaysia, "sawah", and in Thailand, "hoi con".

In the United States it is known to some as "duckworms" (in coastal New Jersey) or "clam digger's itch".[12]

See also

Dermatitis
Schistosomiasis
Schistosoma

[edit] References

1. ↑ Blankespoor, HD and RL Reimink (1991) The control of swimmer’s itch in Michigan: Past, present, and future. Michigan Academician 24: 7 – 23
2. ↑ Blankespoor, CL, RL Reimink and HD Blankespoor (2001) Efficacy of Praziquantel in treating natural schistosome infections in common mergansers. Journal of Parasitology 87: 424 – 426
3. ↑ Chamot, E, L Toscani and A Rougement (1998) Public health importance and risk factors for cercarial dermatitis associated with swimming in Lake Leman at Geneva, Switzerland. Epidemiology and Infection 120: 305 – 314
4. ↑ Lindblade, KA (1998) The epidemiology of cercarial dermatitis and its association with limnological characteristics of a northern Michigan lake. Journal of Parasitology 84: 19 – 23
5. ↑ Leighton, BJ, S Zervos and JM Webster (2000) Ecological factors in schistosome transmission, and an environmentally benign method for controlling snails in a recreational lake with a record of schistosome dermatitis. Parasitology International 49: 9 – 17
6. ↑ Salafsky, B, K Ramaswamy, Y He, J Li and T Shibuya (1999) Development and evaluation of lipodeet, a new long-acting formulation of N,N-diethyl-m-toluamide (DEET) for the prevention of schistosomiasis. American Journal of Tropical Medicine and Hygiene 61: 743 – 750
7. ↑ Verbrugge, LM, JJ Rainey, RL Reimink and HD Blankespoor (2004) Prospective study of swimmer’s itch incidence and severity. Journal of Parasitology 90: 697 – 704

8. Brant, SV, ES Loker (2005) "Can specialized pathogens colonize distantly related hosts? Schistosome evolution as a case study." PLoS Pathogens 1: e38

All About Dermatitis

2007-04-02T18:26:00.001-07:00

Dermatitis is a blanket term literally meaning "inflammation of the skin". It is usually used to refer to eczema, which is also known as Dermatitis eczema. There are several different types. Usually all of them have in common an allergic reaction to specific allergens.

Specific types of dermatitis

(ICD-10 codes are provided where available.)

* (B65.3) cercarial dermatitis
* (L13.0) dermatitis herpetiformis
* (L20) atopic dermatitis
* (L21) seborrhoeic dermatitis
* (L23-L25) contact dermatitis
o (L23.7) urushiol-induced contact dermatitis
* (L30.0) nummular dermatitis
* (L30.1) dyshidrotic dermatitis

All About Aquagenic pruritus

2007-04-02T18:26:00.000-07:00

Aquagenic pruritus is a skin disease characterized by the development of severe, prickling-like epidermal discomfort that is without observable skin lesions and that is evoked by contact with water at any temperature.

Symptoms are commonly felt 15 minutes after contact with water, and persist for roughly 40 minutes.

The disease appears more commonly in middle aged males. Aquagenic pruritis may also be associated with a condition known as Polycythemia Vera.

Etymology

The name is derived from Latin: Aquagenic, meaning water-induced, and Pruritus, meaning itch.

Treatment

Treatments can include applying copious amounts of capsaicin cream on the affected areas, or even Ultraviolet-B Phototherapy.

Since pruritus is a result of histamine, H1 and H2 blockers such as Claritin or Cimetidine can be prescribed.

The symptoms may recur after each water exposure for years. Many sufferers now control the itch by turning the shower water to hot for the last 5 minutes, and/or using heatpads or hairdryers on their skin immediately after showering. The use of cotton clothes and bedding can prevent itch or provide relief to some sufferers.

All About Athlete's foot

2007-04-02T17:56:00.006-07:00

Athlete's foot or tinea pedis is a fungal infection of the skin of the foot, usually between the toes, caused by the pathogen fungi.

Causes

The body normally hosts a variety of saprotrophic microorganisms, including bacteria and fungi. Some of these are useful to the body. Pathogenic or disease causing organisms or the overgrowth of saprotrophic ones can multiply rapidly and cause infection. Athlete's foot is a layman's description of a skin fungal infection. Fungal infections of the skin are called dermatophytosis. Dermatophytes may be spread from other humans (anthropophilic), animals (zoophilic) or may come from the soil (geophilic). Anthropophillic dermatophytes are restricted to human hosts and produce a mild, chronic inflammation. Zoophilic organisms are found primarily in animals and cause marked inflammatory reactions in humans who have contact with infected cats, dogs, cattle, horses, birds, or other animals. Geophilic species are usually recovered from the soil but occasionally infect humans and animals. They cause a marked inflammatory reaction, which limits the spread of the infection and may lead to a spontaneous cure but may also leave scars. Infections or infestations occur when dermatophytes grow and multiply in the skin.

Symptoms
Intertrigo between toes

Athlete's foot causes scaling, flaking and itching of the affected skin. Blisters and cracked skin may also occur, leading to exposed raw tissue, pain, swelling and inflammation. The infection can be spread to other areas of the body, such as the armpits, knees, elbows, and the groin, and usually is called by a different name once it spreads (such as tinea cruris or jock itch for an infection of the skin and groin respectively).

Treatments

Since the fungus thrives in a moist warm environment keeping the feet dry and cool can cure the infection. It is recommended to wear open sandals, or even better barefoot as much as possible. [1]

However avoid walking barefoot in warm moist environments since you may infect other people, and allowing your feet to stay wet can help the fungus grow.

Keep the feet clean- but make sure they are fully dry after washing them. This may require showering in the evening instead of the morning, and staying barefoot afterwards.

Change socks daily, and try to alternate shoes on different days, to allow the shoes to fully dry out.

Placebo controlled studies report that good foot hygiene alone can cure athlete's foot even without medication in 30-40% of the cases. [2]

Conventional treatments

The infection is often treated with topical antifungal agents such as miconazole, itraconazole, terbinafine and a keratolytic such as salicylic acid. Topical agents only clear the infection about 30% of the time and provide mycologic cures (absence of organisms) less than 15% of the time. The time line for cure may be long, often 45 days or longer. However, because the itching associated with the infection subsides quickly, patients may not complete the courses of therapy prescribed. Washing socks, underwear and bed clothes at 60C or 140F will also help prevent any reinfection.

Some topical applications such as Castellani's Paint, often used for intertrigo, work well but in small selected areas. Carbol Fuscin Red dye used in this treatment like many other vital stains is both fungicidal and bacteriocidal; however, because of the staining are cosmetically undesirable. For many years gentian violet was also used for interdigital and other bacterial and fungal infections.

Oral treatment with griseofulvin was begun early in the 1950s. Because of the tendency to cause liver problems and to provoke aplastic anemia the drugs were used cautiously and sparingly. Over time it was found that those problems were due to the size of the crystal in the manufacturing process and microsize and now ultramicrosize crystals are available with few of the original side effects. Oral treatment provides long lasting mycologic cure.

If the fungal invader is not a dermatophyte but a yeast, other medications such as fluconazole may be used. Typically diflucan is used for candidal vaginal infections moniliasis but has been shown to be of benefit for those with cutaneous yeast infections as well. The most common of these infections occur in the web spaces (intertriginous) and at the base of the fingernail or toenail. The hall mark of these infections is a cherry red color surrounding the lesion and a yellow thick pus.

Undecylenic acid (Castor oil derivative) is an effective fungicide for fungal skin infections such as athlete's foot.

Alternative treatments

Topical oils

Users report instant relief from itching after topical application of tea tree oil or crocodile oil, allowing lesions to heal due to the cessation of scratching the itch.[citation needed]

Urine therapy

Proponents of urine therapy claim that urine is very effective at killing athlete's foot. Urea, the "active ingredient" in urine, is already used in many drugs and treatments made by pharmaceutical companies to treat athlete's foot. This controversial treatment method recommends urinating on the infected area once a day in the shower. According to supporters, urine therapy not only kills existing fungi, it prevents new fungi from growing in the infected area.[citation needed]

One biochemist states that urea is only used to soften the outer layers of skin so that antifungal drugs can reach fungi below the surface, and that the urea must be concentrated and applied for a long period of time in order to be effective.[1] According to another article about high-concentration urea cream, the compound is used to "dissolve proteins and [as a] denaturant. The ability of urea to macerate [tissue] has been attributed to a 'proteolytic effect', but others attribute the maceration to the hydrating properties of urea."[2] This use requires a high concentration of urea, up to 40%, and extended exposure. Urea itself without the presence of an additional antifungal drug is not referred to in scholarly literature as having antifungal properties. Thus, it is unlikely that urinating on one's feet in the shower will significantly improve a case of athlete's foot.[3]

This theory was recently covered on The Straight Dope for March 30th, 2007 [3]

Footnotes

1. ^ Onken M (29 March 2003). Re: Peeing in the shower reduces foot fungus. True or false. Why?. MadSci Network. Retrieved on 2006-10-22.
2. ^ Shah M (2003). "Urea ointment (40%)". Indian Journal of Dermatology, Venereology and Leprologu 69 (6): 421-2.
3. ^ Burgess J (15 July 2006). "Water cure". New Scientist 2560: 89.

All About Spider angioma

2007-04-02T17:56:00.005-07:00

Spider angiomas, also known as "nevus araneus," are a type of angioma found slightly below the skin's surface. They often contain a central red spot, and reddish extensions that radiate outward like a spider's web.

Seen in

* Pregnancy.

They are often associated with high estrogen levels, so they are commonly found on pregnant women.

* Liver disease.

People with impaired liver function may also exhibit spider angiomas, because they are not making sufficient levels of coagulation factors. As such, they are at an increased risk of bleeding out, and thus microhemorrhages are seen as spider angiomas.

[edit] Location

* Trunk
* face

Treatment

As with cherry angiomas, no treatment is medically necessary. Electrosurgery, electrolysis and laser treatments are effective on this type of angioma.

All About Cherry angioma

2007-04-02T17:56:00.004-07:00

Cherry angioma is the most common kind of angioma. It is also called a Senile angioma or Campbell de Morgan spot.

Structure

These are made up of clusters of tiny capillaries at the surface of the skin, and range in color from bright red to purple. When they first develop, they may only be a few millimeters across, but sometimes grow to a centimeter or more in diameter. As they grow larger, they tend to expand in thickness, and may take on the raised and rounded shape of a dome. Because the blood vessels comprising the angioma are so close to the skin's surface, cherry angiomas may bleed profusely if they are injured.

Treatment

Physicians may use cryosurgery, electrosurgery, or laser treatment to remove cherry angiomas. Aestheticiennes use electrolysis.

All About Angioma

2007-04-02T17:56:00.003-07:00

Angiomas are benign tumors that are made up of small blood vessels. They usually appear at or near the surface of the skin. Angiomas may appear anywhere on the body, and aren't considered dangerous. However, they may be present as symptoms of another more serious disorder, such as cirrhosis. When they are removed, it is generally for cosmetic reasons.

Types

* cherry angioma
* Spider angioma

All About Actinic keratosis

2007-04-02T17:56:00.002-07:00

Actinic keratosis (also called solar keratosis, senile keratosis, or AK) is a premalignant condition of thick, scaly, or crusty patches of skin. It is most common in fair-skinned people who are frequently exposed to the sun, because their pigment isn't very protective. It usually is accompanied by solar damage. Since some of these pre-cancers progress to squamous cell carcinoma, they should be treated.

When skin is exposed to the sun constantly, thick, scaly, or crusty bumps appear. The scaly or crusty part of the bump is dry and rough. The growths start out as flat scaly areas, and later grow into a tough, wart-like area.

An actinic keratosis site commonly ranges in between 2 to 6 millimeters, and can be dark or light, tan, pink, red, a combination of all these, or the same pigment of one's skin. It may appear on any sun-exposed area, such as the face, ears, neck, scalp, chest, back of hands, forearms, lips etc.

Epidemiology

Actinic keratosis may appear as early as 30 years of age in susceptible people who spend a lot of time outdoors. People with skin phototypes I and II are more likely to be affected, as are albinos and Immunosuppressed patients (Marshall, 1974; Fitzpatrick, 1988; Abel 1989; Lookingbill et al, 1995). As much as 100% of elderly whites get AK (Gordon and Silverstone, 1969; Scotto et al, 1983), but is rare in darker-skinned people. About 10% of people with AK eventually develop squamous cell carcinoma of the skin (Glogau, 2000).

Prevention

Preventative measures recommended for AK are similar to those for skin cancer:

* Not staying in the sun for long periods of time without sunscreen.
* Frequently applying powerful sunscreens with SPF ratings greater than 15 and that also block both UVA and UVB light.
* Using sunscreen even in winter sun exposure.
* Wearing sun protective clothing such as hats, long-sleeved shirts, long skirts, or pants.
* Avoiding sun exposure during noon hours is very helpful because ultraviolet light is the most powerful at that time.

Diagnosis

Doctors can usually identify AK by doing a thorough examination. A biopsy may be necessary when the keratosis is large and/or thick, to make sure that the bump is a keratosis and not a skin cancer. Seborrheic keratoses are other bumps that appear in groups like the actinic keratosis but are not caused by sun exposure, and are not related to skin cancers. Seborrheic keratoses may be mistaken for an actinic keratosis.

Treatment

Various modalities are employed in the treatment of actinic keratosis:

* Cryosurgery, e.g. with liquid nitrogen, by "freezing off" the AKs.
* 5-fluorouracil (a chemotherapy agent): a cream that contains this medication causes AKs to become red and inflamed before they fall off.
* Photodynamic therapy: this new therapy involves injecting a chemical into the bloodstream, which makes AKs more sensitive to any form of light.
* Electrocautery: burning off AKs.
* Immunotherapy: topical treatment with imiquimod (Aldara™), an immune enhancing agent
* Different forms of surgery.

Regular follow-up after treatment is advised by many doctors. The regular checks are to make sure new bumps have not developed and that old ones haven't become thicker and/or have skin disease.

References

* Abel EA (1989). "Cutaneous manifestations of immunosuppression in organ transplant recipients". J Am Acad Dermatol 21 (2 Pt 1): 167-79. PMID 2671063.
* Fitzpatrick TB (1988). "The validity and practicality of sun-reactive skin types I through VI". Arch Dermatol 124 (6): 869-71. PMID 3377516.
* Glogau RG (2000). "The risk of progression to invasive disease". J Am Acad Dermatol 42 (1 Pt 2): 23-4. PMID 10607353.
* Gordon D, Silverstone H. (1969). "The biologic effects of ultraviolet radiation", in Ubach F, editor: The Biologic Effects of Ultraviolet Radiation. Oxford (UK): Pergamon Press, p. 625.
* Lookingbill DP, Lookingbill GL, Leppard B (1995). "Actinic damage and skin cancer in albinos in northern Tanzania: findings in 164 patients enrolled in an outreach skin care program". J Am Acad Dermatol 32 (4): 653-8. PMID 7896957.
* Marshall V (1974). "Premalignant and malignant skin tumours in immunosuppressed patients". Transplantation 17 (3): 272-5. PMID 4592184.
* Scotto J, Fears TR, Fraumeni JF. Incidence of nonmelanoma skin cancer in the United States. Publication No (NIH) 82-2433. Washington, DC: US Dept Health and Human Services; 1983.

All About Acne (Acne Vulgaris)

2007-04-02T17:56:00.001-07:00

Acne vulgaris is an inflammatory disease of the skin, caused by changes in the pilosebaceous units (skin structures consisting of a hair follicle and its associated sebaceous gland). Acne lesions are commonly referred to as pimples, spots or zits.

The condition is most common in puberty. It is considered an abnormal response to normal levels of the male hormone testosterone. The response for most people diminishes over time and acne thus tends to disappear, or at least decrease, after one reaches his or her early twenties. There is, however, no way to predict how long it will take for it to disappear entirely, and some individuals will continue to suffer from acne decades later, into their thirties and forties and even beyond.[citation needed] Acne affects a large percentage of humans at some stage in life.

The term acne comes from a corruption of the Greek άκμή (acme in the sense of a skin eruption) in the writings of Aëtius Amidenus. The vernacular term bacne or backne is often used to indicate acne found specifically on one's back.

The most common form of acne is known as "acne vulgaris", meaning "common acne." Excessive secretion of oils from the sebaceous glands accompanies the plugging of the pores with naturally occurring dead skin cells (corneocytes) blocking hair follicles. The accumulation of these corneocytes in the duct appears to be due to a failure of the normal keratinization process in the skin which usually leads to shedding of skin cells lining the pores. Oil secretions are said to build up beneath the blocked pore, providing a perfect environment for the skin bacteria Propionibacterium acnes and the lipophilic (oil/lipid-loving) yeast Malassezia[citation needed] to multiply uncontrollably. Under the microscope, however, there is no evidence of pooled trapped sebum. Indeed the oil percolates through the plugged duct onto the surface. In response to the bacterial and yeast populations, the skin inflames, producing the visible lesion. The face, chest, back, shoulders and upper arms are especially affected. The typical acne lesions are: comedones, papules, pustules, nodules and inflammatory cysts. These are the more inflamed form of pus-filled or reddish bumps, even boil-like tender swellings. Non-inflamed 'sebaceous cysts', more properly called epidermoid cysts, occur either in association with acne or alone but are not a constant feature. After resolution of acne lesions, prominent unsightly scars may remain.

Aside from scarring, its main effects are psychological, such as reduced self-esteem[1] and depression or suicide.[2] Acne usually appears during adolescence, when people already tend to be most socially insecure. Early and aggressive treatment is therefore advocated to lessen the overall impact to individuals.[1]

[edit] Causes of acne

Exactly why some people get acne and some do not is not fully known. It is known to be partly hereditary. Several factors are known to be linked to acne:

* Hormonal activity, such as menstrual cycles and puberty
* Diet
* Stress, through increased output of hormones from the adrenal (stress) glands.
* Hyperactive sebaceous glands, secondary to the three hormone sources above.
* Accumulation of dead skin cells.
* Bacteria in the pores, to which the body becomes 'allergic'.
* Skin irritation or scratching of any sort will activate inflammation.
* Use of anabolic steroids.
* Any medication containing halogens (iodides, chlorides, bromides), lithium, barbiturates, or androgens.
* Exposure to high levels of chlorine compounds, particularly chlorinated dioxins, can cause severe, long-lasting acne, known as Chloracne.

Traditionally, attention has focused mostly on hormone-driven over-production of sebum as the main contributing factor of acne. More recently, more attention has been given to narrowing of the follicle channel as a second main contributing factor. Abnormal shedding of the cells lining the follicle, abnormal cell binding ("hyperkeratinization") within the follicle, and water retention in the skin (swelling the skin and so pressing the follicles shut) have all been put forward as important mechanisms. Several hormones have been linked to acne: the male hormones testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulfate (DHEAS), as well as insulin-like growth factor 1 (IGF-I). In addition, acne-prone skin has been shown to be insulin resistant[citation needed].

Development of acne vulgaris in later years is uncommon, although this is the age group for Rosacea which may have similar appearances. True acne vulgaris in adults may be a feature of an underlying condition such as pregnancy and disorders such as polycystic ovary syndrome or the rare Cushing's syndrome. Dermatologists are seeing more cases of menopause-associated acne as fewer women replace the natural anti-acne ovarian hormone estradiol whose production fails as women arrive at menopause. The lack of estradiol also causes thinning hair, hot flashes, thin skin, wrinkles, vaginal dryness, and predisposes to osteopenia and osteoporosis as well as triggering acne (known as acne climacterica in this situation).

[edit] Misconceptions about causes

There are many misconceptions and rumors about what does and does not cause the condition:

[edit] Diet

Diet. One study suggested that chocolate, french fries, potato chips and sugar, among others, affect acne. A high GI (glycemic index) diet that causes sharp rises in blood sugar worsens acne. This, however, has been refuted by dermatologists and has been accepted as myth.[3] If this study's conclusions are verified then a low GI diet may help acne, but a recent review of somewhat dated scientific literature cannot affirm either way.[4] A recent study, based on a survey of 47,335 women, did find a positive epidemiological association between acne and consumption of partially skimmed milk, instant breakfast drink, sherbet, cottage cheese and cream cheese.[5] The researchers hypothesize that the association may be caused by hormones (such as several sex hormones and bovine IGF-I) present in cow milk. Although the association between milk and acne has been definitively shown, the ingredient in the milk responsible for the acne is still unclear. Most dermatologists are awaiting confirmatory research linking diet and acne but some support the idea that acne sufferers should experiment with their diets, and refrain from consuming such fare if they find such food affects the severity of their acne.[6]

Seafood, on the other hand, may contain relatively high levels of iodine. Iodine is known to make existing acne worse but there is probably not enough to cause an acne outbreak.[7]< Still, people who are prone to acne may want to avoid excessive consumption of foods high in iodine.

It has also been suggested that there is a link between a diet high in refined sugars and other processed foods and acne. According to this hypothesis, the startling absence of acne in non-westernized societies could be explained by the low glycemic index of these cultures' diets. Others have cited possible genetic reasons for there being no acne in these populations, but similar populations shifting to Western diets do develop acne. Note also that the populations studied consumed no milk or other dairy products.[8] Further research is necessary to establish whether a reduced consumption of high-glycemic foods (such as soft drinks, sweets, white bread) can significantly alleviate acne, though consumption of high-glycemic foods should in any case be kept to a minimum, for general health reasons.[9] Avoidance of 'junk food' with its high fat and sugar content is also recommended.[10] On the other hand there is no evidence that fat alone makes skin more oily or acne worse.

[edit] Hygiene

Deficient personal hygiene. Acne is not caused by dirt. This misconception probably comes from the fact that comedones look like dirt stuck in the openings of pores. The black color is simply not dirt but compact keratin. In fact, the blockages of keratin that cause acne occur deep within the narrow follicle channel, where it is impossible to wash them away. These plugs are formed by the failure of the cells lining the duct to separate and flow to the surface in the sebum created there by the body.

[edit] Sex

Sex. Common myths state that masturbation causes acne and, conversely, that celibacy or sexual intercourse can cure it. Though it has been widely accepted that these are not true due to lack of scientific study on the subject, it is also important to note sexual activity has been observed to result in hormonal spikes, which has been linked to acne.[11]

[edit] Treatments

[edit] Timeline of acne treatment

The history of acne reaches back to the dawn of recorded history. In Ancient Egypt, it is recorded that several pharaohs were acne sufferers. From Ancient Greece comes the English word 'acne' (meaning 'point' or 'peak'). Acne treatments are also of considerable antiquity:

* Ancient Rome : bathing in hot, and often sulfurous, mineral water was one of the few available acne treatments. One of the earliest texts to mention skin problems is De Medicina by the Roman writer Celsus.
* 1800s: Nineteenth century dermatologists used sulphur in the treatment of acne. It was believed to dry the skin.
* 1920s: Benzoyl Peroxide is used
* 1930s: Laxatives were used as a cure for what were known as 'chastity pimples'
* 1950s: When antibiotics became available, it was discovered that they had beneficial effects on acne. They were taken orally to begin with. Much of the benefit was not from killing bacteria but from the anti-inflammatory effects of tetracycline and its relatives. Topical antibiotics became available later.
* 1960s: Tretinoin (original Trade Name Retin A) was found effective for acne. This preceeded the development of oral isotretinoin (sold as Accutane and Roaccutane) since the early 1980s.
* 1980s: Accutane is introduced in America
* 1990s: Laser treatment introduced
* 2000s: Blue/red light therapy

Some old treatments, like laxatives, have fallen into disuse but others, like spas, are recovering their popularity.

[edit] Available treatments

There are many products sold for the treatment of acne, many of them without any scientifically-proven effects. Generally speaking successful treatments give little improvement within the first week or two; and then the acne decreases over approximately 3 months, after which the improvement starts to flatten out. Treatments that promise improvements within 2 weeks are likely to be largely disappointing. Short bursts of cortisone, quick bursts of antibiotics and many of the laser therapies offer a quick reduction in the redness, swelling and inflammation when used correctly, but none of these empty the pore of all the materials that trigger the inflammation. Emptying the pores takes months.

Modes of improvement are not necessarily fully understood but in general treatments are believed to work in at least 4 different ways (with many of the best treatments providing multiple simultaneous effects):

* normalising shedding into the pore to prevent blockage
* killing P. acnes
* antinflammatory effects
* hormonal manipulation

A combination of treatments can greatly reduce the amount and severity of acne in many cases. Those treatments that are most effective tend to have greater potential for side effects and need a greater degree of monitoring, so a step-wise approach is often taken. Many people consult with doctors when deciding which treatments to use, especially when considering using any treatments in combination. There are a number of treatments that have been proven effective:
Cotton pads soaked in salicylic acid solution can be used to exfoliate the skin.
Cotton pads soaked in salicylic acid solution can be used to exfoliate the skin.

[edit] Exfoliating the skin

This can be done either mechanically, using an abrasive cloth or a liquid scrub, or chemically. Common chemical exfoliating agents include salicylic acid and glycolic acid, which encourage the peeling of the top layer of skin to prevent a build-up of dead skin cells which combine with skin oil to block pores. It also helps to unblock already clogged pores.[citation needed] Note that the word "peeling" is not meant in the visible sense of shedding, but rather as the destruction of the top layer of skin cells at the microscopic level. Depending on the type of exfoliation used, some visible flaking is possible. Moisturizers and anti-acne topicals containing chemical exfoliating agents are commonly available over-the-counter. Mechanical exfoliation is less commonly used as many benefits derived from the exfoliation are negated by the act of mechanically rubbing and irritating the skin.
Benzoyl peroxide cream.
Benzoyl peroxide cream.

[edit] Topical Bactericidals

Widely available OTC bactericidal products containing benzoyl peroxide may be used in mild to moderate acne. The gel or cream containing benzoyl peroxide is rubbed, twice daily, into the pores over the affected region. Bar soaps or washes may also be used and vary from 2 to 10% in strength. In addition to its therapeutic effect as a keratolytic (a chemical that dissolves the keratin plugging the pores) benzoyl peroxide also prevents new lesions by killing P.acnes. Unlike antibiotics, benzoyl peroxide has the advantage of being a strong oxidizer (essentially a mild bleach) and thus does not appear to generate bacterial resistance. However, it routinely causes dryness, local irritation and redness. A sensible regimen may include the daily use of low-concentration (2.5%) benzoyl peroxide preparations, combined with suitable non-comedogenic moisturisers to help avoid overdrying the skin.[12] This has occasioned widespread editorial comment.[13]

[edit] Phototherapy

[edit] Blue and red light

It has long been known that short term improvement can be achieved with sunlight. However, studies have shown that sunlight worsens acne long-term, presumably due to UV damage.[citation needed] More recently, visible light has been successfully employed to treat acne (Phototherapy) - in particular intense blue light generated by purpose-built fluorescent lighting, dichroic bulbs, LEDs or lasers. Used twice weekly, this has been shown to reduce the number of acne lesions by about 64%;[14] and is even more effective when applied daily. The mechanism appears to be that a porphyrin (Coproporphyrin III) produced within P. acnes generates free radicals when irradiated by blue light.[15] Particularly when applied over several days, these free radicals ultimately kill the bacteria.[16] Since porphyrins are not otherwise present in skin, and no UV light is employed, it appears to be safe, and has been licensed by the U.S. FDA.[17] The treatment apparently works even better if used with red visible light (660 nanometer) resulting in a 76% reduction of lesions after 3 months of daily treatment for 80% of the patients;[18] and overall clearance was similar or better than benzoyl peroxide. Unlike most of the other treatments few if any negative side effects are typically experienced, and the development of bacterial resistance to the treatment seems very unlikely. After treatment, clearance can be longer lived than is typical with topical or oral antibiotic treatments; several months is not uncommon. The equipment or treatment, however, is relatively new and reasonably expensive.

[edit] Photodynamic therapy

In addition, basic science and clinical work by dermatologists Yoram Harth and Alan Shalita and others has produced evidence that intense blue/violet light (405-425 nanometer) can decrease the number of inflammatory acne lesion by 60-70% in 4 weeks of therapy, particularly when the P.acnes is pretreated with delta-aminolevulinic acid (ALA), which increases the production of porphyrins. However this photodynamic therapy is controversial and apparently not published in a peer reviewed

[edit] Less widely used treatments

* Azelaic acid (brand names Azelex, Finevin, Skinoren) is suitable for mild, comedonal acne.[19]
* Zinc. Orally administered zinc gluconate has been shown to be effective in the treatment of inflammatory acne, although less so than tetracyclines.[20][21]
* Tea Tree Oil (Melaleuca Oil) has been used with some success, and has been shown to be an effective anti-inflammatory in skin infections [22]
* Heat therapy - Zeno product uses heat at a specific temperature to kill bacteria and to treat mild to moderate acne.[citation needed]
* Nicotinamide, (Vitamin B3) used topically in the form of a gel, has been shown in a 1995 study to be more effective than a topical antibiotic used for comparison, as well as having less side effects.[23] Topical nicotinamide is available both on prescription and over-the-counter. Some users choose to make their own at home, mixing together crushed nicotinamide pills with aloe vera gel.[citation needed] The property of topical nicotinamide's benefit in treating acne seems to be its anti-inflammatory nature. It is also purported to result in increased synthesis of collagen, keratin, involucrin and flaggrin.[citation needed]
* In some cases, people found that bathing in salt water (pure from the ocean) noticed lessened redness and decreased size in their acne.

[edit] Future treatments

Laser surgery has been in use for some time to reduce the scars left behind by acne, but research is now being done on lasers for prevention of acne formation itself. The laser is used to produce one of the following effects:

* to burn away the follicle sac from which the hair grows
* to burn away the sebaceous gland which produces the oil
* to induce formation of oxygen in the bacteria, killing them

Since lasers and intense pulsed light sources cause thermal damage to the skin there are concerns that laser or intense pulsed light treatments for acne will induce hyperpigmented macules (spots) or cause long term dryness of the skin. As of 2005, this is still mostly at the stage of medical research rather than established treatment.

Because acne appears to have a significant hereditary link, there is some expectation that cheap whole-genome DNA sequencing may help isolate the body mechanisms involved in acne more precisely, possibly leading to a more satisfactory treatment. (Crudely put, take the DNA of large samples of people with significant acne and of people without, and let a computer search for statistically strong differences in genes between the two groups). However, as of 2005, DNA sequencing is not yet cheap, and all this may still be decades off. It is also possible that gene therapy could be used to alter the skin's DNA.

Phage therapy has been proposed to kill P. acnes, and has seen some use, particularly in Georgia.[24]

[edit] Preferred treatments by types of acne vulgaris

* Comedonal (non-inflammatory) acne: local treatment with azelaic acid, salicylic acid, topical retinoids, benzoyl peroxide.
* Mild papulo-pustular (inflammatory) acne: benzoyl peroxide or topical retinoids, topical antibiotics (such as erythromycin).
* Moderate inflammatory acne: benzoyl peroxide or topical retinoids combined with oral antibiotics (tetracyclines). Isotretinoin is an option.
* Severe inflammatory acne, nodular acne, acne resistant to the above treatments: isotretinoin, or contraceptive pills with cyproterone for females with virilization or drospirenone.
* Most physicians state that topical retinoids are the preferred treatment for all forms of acne vulgaris.
* There are also certain treatments for acne mentioned in Ayurveda using herbs such as Aloevera, Aruna, Haldi, and Papaya.[25]

[edit] Acne scars

Severe acne often leaves small scars where the skin gets a "volcanic" shape. Acne scars are difficult and expensive to treat, and it is unusual for the scars to be successfully removed completely.[citation needed]

The psychological and emotional effects caused by acne scars can be as devastating to one's confidence as the acne once was.

Acne scars generally fall into two categories: physical scars and pigmented scars. Physical acne scars are often referred to as "Icepick" scars. This is because the scars tend to cause an indentation in the skins surface. Pigmented scars is a slightly misleading term, suggesting a change in the skin's pigmentation. This is not true. Pigmented scars are usually the result of nodular or cystic acne (the painful 'bumps' lying under the skin). They often leave behind an inflamed red mark. Often, the pigmentation scars can be avoided simply by avoiding aggravation of the nodule or cyst. When sufferers try to 'pop' cysts or nodules, pigmentation scarring becomes significantly worse, and may even bruise the affected area. Pigmentation scars often fade with time, and those who suffered from acne before, and have developed scars are generally relieved that the acne has gone, and emotional effects of acne scars tend to be less distressing.

Acne scars are unsightly, and it is for this reason they can be psychologically and emotionally distressing. However, there are a range of treatments available. If acne scars are causing severe psychological distress, social withdrawal and/or emotional ill-health, a physician should be contacted.

[edit] Grading scale

There are multiple grading scales for grading the severity of acne vulgaris,[26] three of these being: Leeds acne grading technique: Counts and categorises lesions into inflammatory and non-inflammatory (ranges from 0-10.0). 'Cook's acne grading scale: Uses photographs to grade severity from 0 to 8 (0 being the least severe and 8 being the most severe). Pillsbury scale: Simple classifies the severity of the acne from 1 (least severe) to 4 (most severe).

[edit] See also

* Blackhead
* Keratosis pilaris
* Pimple
* Rosacea

[edit] References

* James W (April 7 2005). "Clinical practice. Acne.". N Engl J Med 352 (14): 1463-72. PMID 15814882.
* Webster G (31 August 2002). "Acne vulgaris.". BMJ 325 (7362): 475-9. PMID 12202330.

[edit] Footnotes

1. ^ a b Goodman G (2006). "Acne and acne scarring - the case for active and early intervention" (PDF). Aust Fam Physician 35 (7): 503-4. PMID 16820822.
2. ^ Purvis D, Robinson E, Merry S, Watson P (2006). "Acne, anxiety, depression and suicide in teenagers: a cross-sectional survey of New Zealand secondary school students". J Paediatr Child Health 42 (12): 793-6. PMID 17096715.
One study has estimated the incidence of suicidal ideation in patients with acne as 7.1% :
* Picardi A, Mazzotti E, Pasquini P (2006). "Prevalence and correlates of suicidal ideation among patients with skin disease". J Am Acad Dermatol 54 (3): 420-6. PMID 16488292.
3. ^ CHOICE - Citizens for Healthy Options In Children's Education (Nov 2003). Acne Has Nothing to Do with Diet - Wrong!.
4. ^ Magin P, Pond D, Smith W, Watson A (2005). "A systematic review of the evidence for 'myths and misconceptions' in acne management: diet, face-washing and sunlight". Fam Pract 22 (1): 62-70. PMID 15644386.
5. ^ Adebamowo CA, Spiegelman D, Danby FW, Frazier AL, Willett WC, Holmes MD (2005). "High school dietary dairy intake and teenage acne". J Am Acad Dermatol 52 (2): 207-14. PMID 15692464.
6. ^ Fries JH (1978). "Chocolate: a review of published reports of allergic and other deleterious effects, real or presumed". Ann Allergy 41 (4): 195-207. PMID 152075.
7. ^ Danby FW (2007). "Acne and iodine: Reply". J Am Acad Dermatol 56 (1): 164-5. PMID 17190637.
8. ^ Loren Cordain, et al. "Acne Vulgaris - A Disease of Western Civilization" Arch Dermatol. 2002;138:1584-1590. Observation
9. ^ Smith R, Mann N, Makelainen H, Braue A, Varigos G (2004). "The effect of short-term altered macronutrient status on acne vulgaris and biochemical markers of insulin sensitivity". Asia Pac J Clin Nutr 13 (Suppl): S67. PMID 15294556.
10. ^ Anderson, Laurence. 2006. Looking Good, the Australian guide to skin care, cosmetic medicine and cosmetic surgery. AMPCo. Sydney. ISBN 0-85557-044-X.
11. ^ Endocrine effects of masturbation in men.
12. ^ The iPLEDGE Program - Guide to Best Practices for Isotretinoin - "The resource to help the prescriber prepare, plan treatments, and prevent pregnancies during the course of isotretinoin therapy" (PDF) (2005).
13. ^ Bernadine Healy. "Pledging for Accutane", US News Best Health, 2005-05-09.
14. ^ Kawada A, Aragane Y, Kameyama H, Sangen Y, Tezuka T (2002). "Acne phototherapy with a high-intensity, enhanced, narrow-band, blue light source: an open study and in vitro investigation". J Dermatol Sci 30 (2): 129-35. PMID 12413768.
15. ^ Kjeldstad B (1984). "Photoinactivation of Propionibacterium acnes by near-ultraviolet light". Z Naturforsch [C] 39 (3-4): 300-2. PMID 6730638.
16. ^ Ashkenazi H, Malik Z, Harth Y, Nitzan Y (2003). "Eradication of Propionibacterium acnes by its endogenic porphyrins after illumination with high intensity blue light". FEMS Immunol Med Microbiol 35 (1): 17-24. PMID 12589953.
17. ^ "New Light Therapy for Acne" U.S. Food and Drug Administration, FDA Consumer magazine, November-December 2002 Notice
18. ^ Papageorgiou P, Katsambas A, Chu A (2000). "Phototherapy with blue (415 nm) and red (660 nm) light in the treatment of acne vulgaris." (PDF). Br J Dermatol 142 (5): 973-8. PMID 10809858.
19. ^ MedlinePlus (2001-07-24). Azelaic Acid (Topical).
20. ^ Dreno B, Amblard P, Agache P, Sirot S, Litoux P (1989). "Low doses of zinc gluconate for inflammatory acne". Acta Derm Venereol 69 (6): 541-3. PMID 2575335.
21. ^ Dreno B, Moyse D, Alirezai M, Amblard P, Auffret N, Beylot C, Bodokh I, Chivot M, Daniel F, Humbert P, Meynadier J, Poli F (2001). "Multicenter randomized comparative double-blind controlled clinical trial of the safety and efficacy of zinc gluconate versus minocycline hydrochloride in the treatment of inflammatory acne vulgaris". Dermatology 203 (2): 135-40. PMID 11586012.
22. ^ Koh KJ; Pearce AL; Marshman G; Finlay-Jones JJ; Hart PH Department of Dermatology, Flinders Medical Centre, Bedford Park, South Australia, Australia (2002). "Tea tree oil reduces histamine-induced skin inflammation". Dermatology: 147. ISSN 0007-0963.
23. ^ Shalita A, Smith J, Parish L, Sofman M, Chalker D (1995). "Topical nicotinamide compared with clindamycin gel in the treatment of inflammatory acne vulgaris.". Int J Dermatol 34 (6): 434-7. PMID 7657446.
24. ^ The star ledger- Germs that fight germs
25. ^ Ayurveda Encyclopedia, "Acne Treatment"
26. ^ Leeds, Cook's and Pillsbury scales obtained from here

All About Dermatology

2007-04-02T17:56:00.000-07:00

Dermatology (from Greek derma, "skin") is a branch of medicine dealing with the skin and its appendages (hair, nails, sweat glands etc). A medical doctor who specializes in dermatology is a dermatologist.

Scope of the field

Dermatologists are physicians (medical doctors) specializing in the diagnosis and treatment of diseases and tumors of the skin and its appendages. There are medical and surgical sides to the specialty. Dermatologic surgeons practice skin cancer surgery (including Mohs' micrographic surgery), laser surgery, photodynamic therapy (PDT) and cosmetic procedures using botulinum toxin ('Botox'), soft tissue fillers, sclerotherapy and liposuction. Dermatopathologists interpret tissue under the microscope (histopathology). Pediatric dermatologists specialize in the diagnoses and treatment of skin disease in children. Immunodermatologists specialize in the diagnosis and management of skin diseases driven by an altered immune system including blistering (bullous) diseases like pemphigus. In addition, there are a wide range of congenital syndromes managed by dermatologists.

Training programs

Residency training program in North America

A minimum of 11 years of college and post graduate training is required to become a dermatologist in the United States and Canada. This includes graduation from a 4-year college in the college they will take Pre-Medicine, a 4-year medical school followed by a year of post graduate training in medicine, surgery or pediatrics (called an internship) after which a physician may apply for admission to graduate dermatology residency training. Dermatology residencies are among the most competitive in terms of admission. Following the successful completion of formal residency training in dermatology (3 years) the physician is qualified to take certifying board examinations (written) by the American Board of Dermatology or the American Osteopathic College of Dermatology. Once board certified, dermatologists become Diplomates of the American Board of Dermatology or the American Osteopathic College of Dermatology AOCD. They are then eligible to apply for fellowship status in the American Academy of Dermatology. Some dermatologists undertake advanced subspecialty training in programs known as fellowships after completion of their residency training. These fellowships are either one or two years in duration. Fellowships in dermatology include pediatric dermatology, surgical dermatology including Mohs micrographic surgery, dermatopathology (pathology of skin diseases) and dermatological immunology.

Training program in Australia

An Australian specialist dermatologist will have completed 6 years of medical school, one internship year and at least one year of general medical or surgical service in the public hospital system, prior to becoming eligible for specialist training in dermatology. The selection process is rigorous and transparent; candidates must pass science and pharmacology exams and engage in monitored and assessed practical training in medical and surgical dermatology. At the completion of the 5 year training programme, trainees sit a national written examination held over two days. Successful candidates may then proceed to the practical viva examination (held over 2 days) after which they may apply for fellowship status with the Australasian College of Dermatologists.

Training program in India

To be a dermatologist in India, a minimum of 2 years (for diploma )or 3 years (for MD) of training is required after graduation from medical school and internship. The period involves rigorous training in all aspects of general dermatology, cosmetic dermatology,dermatopathology, dermatosurgery, venereal diseases (including HIV) and leprosy. At the end of the training period the resident has to go through written tests and clinical exams. The postgraduate qualification awarded is DVD(Diploma in Venereology and Dermatology) and MD (dermatology, venereology and leprosy). Many specialists also go for certification by the national board (for the award of 'diplomate of national board'). Indian Association of Dermatologists, Venereologists and Leprologists(IADVL)is one of the largest Dermatolological associations in the world. Log on to www.iadvl.org

Subspecialties

The skin is the largest organ of the body and obviously the most visible. Although many skin diseases are isolated, some are manifestations of internal disease. Hence, a dermatologist is schooled in aspects of surgery, rheumatology (many rheumatic diseases can feature skin symptoms and signs), immunology, neurology (the "neurocuteaneous syndromes", such as neurofibromatosis and tuberous sclerosis), infectious diseases and endocrinology. The study of genetics is also becoming increasingly important.

Venereology and phlebology

Venereology, the subspecialty that diagnoses and treats sexually transmitted diseases, and phlebology, the specialty that deals with problems of the superficial venous system, are both part of a dermatologist's expertise.

Cosmetic dermatology

Cosmetic dermatology has long been an important part of the field, and dermatologists have been the primary innovators in this area. In the 1900's dermatologists employed dermabrasion to improve acne scarring and fat microtransfer was used to fill in cutaneous defects. More recently, dermatologists have been the driving force behind the development and safe and effective employment of lasers, new dermal filling agents (collagen and hyaluronic acid), botulinum toxin ("Botox"), nonabrative laser rejuvenation procedures, intense pulsed light systems, photodynamic therapy, and chemical peeling.

Dermatologic surgery

Dermatologic surgery is performed by all dermatologists. Surgery is an integral part of dermatology residency training; thus all dermatologists are well trained in cutaneous surgery. Specialized training through a 1 year dermatologc surgery fellowship is available upon completion of the dermatology residency, and usually focuses on training in Mohs micrographic surgery. Most dermatologic surgeons who have a special interest in this field apply for fellowship status in the American Society for Dermatologic Surgery, a professional organization dedicated to supporting and educating these physicians.

Techniques available to a dermatologic surgeon include lasers, traditional scalpel surgery, electrosurgery, cryosurgery, photodynamic therapy, liposuction, blepharoplasty (cosmetic eyelid surgery), minimally-invasive facelift surgery (e.g., the S-lift), and a variety of topical and injectable agents such as dermal fillers including fat transfer and hyaluronic acid. Some specially trained dermatologic surgeons perform Mohs cancer surgery, which can be an effective method for the treatment of recurrent, indistinct, or difficult skin cancers.

Diagnosis

Any mole that is irregular in color or shape should be examined by a dermatologist to determine if it is a malignant melanoma, the most serious and life-threatening form of skin cancer. Following a visual examination and a dermatoscopic exam (an invaluable new instrument that illuminates a mole without reflected light), a dermatologist may biopsy a suspicious mole. If it is malignant, it will be excised in the dermatologist's office.

Medical history

The first step of any contact with a physician is the medical history. In order to classify a cutaneous eruption, the dermatologist will ask detailed questions on the duration and temporal pattern of skin problems, itching or pain, relation to food intake, sunlight, over-the-counter creams and clothing. When an underlying disease is suspected, an additional detailed history of related symptoms will be elicited (such as arthritis in a suspected case of lupus erythematosus).

Physical examination

Dermatology has the obvious benefit of having easy access to tissue for diagnosis. Physical examination is generally done under bright light and preferably involves the whole body. At this stage, the doctor may apply Wood's light, which may aid in diagnosing types of mycosis or demonstrate the extent of pigmented lesions, or use a dermatoscope which enlarges a suspected lesion and visualizes it without reflected light. The dermatoscope is helpful in differentiating a benign naevus from melanoma or a seborrheic keratosis from a mole. A morphological classification of dermatological lesions is important in the diagnosis of dermatological disorders. Dermatologic diagnosis is often dependent upon pattern recognition of lesions and symptoms.

Microbiology

Culture or Gram staining of suspected infectious lesions may identify a pathogen and help direct therapy.

[edit] Biopsy

If the diagnosis is uncertain or a cutaneous malignancy is suspected, the dermatologic surgeon may perform a small punch biopsy (using a local anesthetic) for examination under the microscope by the dermatologist who is a trained dermatopathologist.

Therapy

The skin is obviously accessible to topical local therapy. Antibiotic creams can help eliminate infections, while inflammatory skin diseases (such as eczema and psoriasis) often respond to steroid creams or topical anthralin. Dermatologists are innovators of new immune enhancing treatments, like topical imiquimod for superficial cancers and injection immunotherapy for warts as discussed below.

Topical medications

Topical medications treat many dermatological diseases, but dermatologists also use oral medications. Antibiotics and immune suppressants or immune enhancing agents (injection immunotherapy or topical imiquimod) for dermatological diseases or tumors. Isotretinoin ("Accutane") is used for severe cystic acne vulgaris and often produces a life-time remission of this disfiguring disease. Isotretinoin prescribing in the U.S. is now controlled by a cumbersome FDA governmental website called iPLEDGE. Various new modalities of treatment are in the foray, with the advent of laser technology things are quite promising.

Photomedicine

Photomedicine involves the use of ultraviolet light, often in combination with oral or topical agents, to treat skin disease (eg. psoriasis or mycosis fungoides).

Surgical therapies

Surgical intervention by a dermatologic surgeon may be necessary, for example, to treat varicose veins or skin cancer. Varicose veins can be treated with sclerotherapy (injecting an agent that obliterates the vein) or the long-pulsed Nd:YAG laser. Skin cancers can be managed with excision (including Mohs cancer surgery), cryosurgery, x-ray, or with the recent topical immune enhancing agent imiquimod. (See above section on "Dermatologic Surgery" for more details.)

Psychodermatology and hypnodermatology

Main article: Psychodermatology
Main article: Hypnodermatology

Psychodermatology and hypnodermatology involve using hypnosis in combination with other pseudo-psychological therapies to treat skin disorders.

Research

From the basic science of cutaneous genetics and immunology, to the practical application of new knowledge and technology in the diagnosis and management of skin disease (like psoriasis) and surgical treatment of skin cancer, dermatologists have been among the leaders in the field. The annual meeting of the American Academy of Dermatology is one of the keys for rapid dissemination of new knowledge to the practicing dermatologist and dermatologic surgeon.

Dermatological diseases

* List of dermatological diseases

See also

* dermatopathology
* skin
* hair

History

The work De morbis cutaneis ("On the diseases of the skin" - 1572) by Geronimo Mercuriali from Forlì (Italy) is known as the first scientific tractation about Dermatology.