eMedicine Specialties > Dermatology > Reactive & Inflammatory Dermatoses

Dyshidrotic Eczema

Sadegh Amini, MD, Senior Clinical Research Fellow, Skin Research Group, Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami
Anne E Burdick, MD, MPH, Professor of Dermatology, Director of Leprosy Program, Associate Dean for TeleHealth and Clinical Outreach, University of Miami Miller School of Medicine

Updated: Aug 17, 2009

Introduction

Background

Dyshidrotic eczema is a recurrent or chronic relapsing form of vesicular palmoplantar dermatitis of unknown etiology. Dyshidrotic eczema also is termed pompholyx, which derives from cheiropompholyx, which means "hand and bubble" in Greek.

The etiology of dyshidrotic eczema is unresolved and is believed to be multifactorial. Dyshidrotic eczema is considered a reaction pattern caused by various endogenous conditions and exogenous factors.

Pathophysiology

Several hypotheses have been proposed for the pathophysiology of dyshidrotic eczema. The original hypothesis of sweat gland dysfunction has been disputed because vesicular lesions are not associated with sweat ducts. However, hyperhidrosis is an aggravating factor in 40% of patients with dyshidrotic eczema. Improvement in pruritus, erythema, vesicles, and hand dermatitis with fewer or no signs of relapse has been obtained after botulinum toxin A injection.[1 ]

Dyshidrotic eczema may be associated with atopy and familial atopy. Of patients with dyshidrosis, 50% have atopic dermatitis.

Exogenous factors (eg, contact dermatitis to nickel, balsam, cobalt; sensitivity to ingested metals; dermatophyte infection; bacterial infection) may trigger episodes. These antigens may act as haptens with a specific affinity for palmoplantar proteins of the stratum lucidum of the epidermis. The binding of these haptens to tissue receptor sites may initiate pompholyx.

Evidence shows that the ingestion of metal ions such as cobalt can induce both type I and type IV hypersensitivity reactions, and, in addition, they can also act as atypical haptens activating T lymphocytes through human leucocyte antigen–independent pathways, causing systemic allergic dermatitis in the form of dyshidrotic eczema.[2,3 ]

Emotional stress and environmental factors (eg, seasonal changes, hot or cold temperatures, humidity) reportedly exacerbate dyshidrosis.

Dyshidroticlike eczematous eruptions with the use of intravenous immunoglobulin infusions have been reported.

In some patients, a distant fungal infection can cause palmar pompholyx as an id reaction. In one study, one third of pompholyx occurrences on the palms resolved after treatment for tinea pedis.

Frequency

United States

Dyshidrotic eczema occurs in 5-20% of patients with hand eczema and more commonly occurs in warmer climates and during spring and summer months (seasonal or summer pompholyx).

International

Dyshidrotic eczema comprised 1% of initial consultations in a 1-year Swedish study. In a study of 107,206 Swedish individuals, 51 (0.05%) were diagnosed with dyshidrosis. Of all hand dermatitis cases in that population, 3% had dyshidrosis.[4 ]
 
In a retrospective study reviewing records of 714 Portuguese patients during a 6-year period, Magina et al found dyshidrotic eczema to be the third most common type of hand dermatitis (20.3%).[5 ]

Mortality/Morbidity

Dyshidrotic eczema can be severe, resulting in occupational disability and time away from work; however, disability compensation usually is not provided for this condition.

Sex

The male-to-female ratio for dyshidrotic eczema is 1:1.

Age

Dyshidrotic eczema affects individuals aged 4-76 years; the mean age is 38 years. After middle age, the frequency of dyshidrotic eczema episodes tends to decrease.

Clinical

History

Patients report pruritus of hands and feet with a sudden onset of vesicles. Burning pain or pruritus occasionally may be experienced before vesicles appear. Dyshidrotic eczema episodes vary in frequency from once per month to once per year. Patients with dyshidrotic eczema may report a variety of factors that possibly are related to eruptions, as follows:

  • Emotional stress
  • Personal or familial atopic diathesis (eg, asthma, hay fever, sinusitis)
  • Certain work exposures (eg, cobalt) and/or recreational exposures
  • Recent exposure to contact allergens (eg, nickel, balsams, paraphenylenediamine, chromate, sesquiterpene lactones) before condition flares
  • Exposure to contact irritants before condition flares
  • Recent exposure to costume jewelry (patients with palmar pompholyx and allergic to nickel)
  • Recent treatment with intravenous immunoglobulin therapy[6,7 ]
  • HIV related: Two cases were reported of HIV-positive patients who developed dyshidrotic eczema as an immune reconstitution inflammatory syndrome shortly after highly active antiretroviral therapy.[8 ]Pompholyx has also been described as a manifestation of symptomatic HIV infection, including individuals who do not respond to topical and systemic therapies and whose condition resolves only after initiation of combination antiretroviral therapy.[9 ]

Physical

Symmetric crops of clear vesicles and/or bullae on the palms and lateral aspects of fingers characterize dyshidrotic eczema (Media Files 1-2, Media Files 5-7, and Media File 9). Feet, soles, and the lateral aspects of toes also may be affected.

Tense vesicles and bullae on the palm. Courtesy o...

Tense vesicles and bullae on the palm. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.




Close-up view of tense vesicles and bullae of the...

Close-up view of tense vesicles and bullae of the palm. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.




Small tense vesicles on the fingers.

Small tense vesicles on the fingers.




Small, discrete, coalesced vesicles on the dorsal...

Small, discrete, coalesced vesicles on the dorsal hand.




Small, discrete, coalesced vesicles on the finger...

Small, discrete, coalesced vesicles on the fingers.




Small discrete vesicles of the lateral fingers.

Small discrete vesicles of the lateral fingers.




  • In mildly affected patients, vesicles are present only on the lateral aspects of the fingers and, occasionally, involve feet and toes (Media File 9).
  • Vesicles are deep seated with a tapiocalike appearance, without surrounding erythema (Media File 2). They may become large, form bullae, and become confluent (Media File 8). Vesicles typically resolve without rupturing, followed by desquamation.
  • Hands are involved solely in 80% of patients, feet solely in 10% (Media File 3), and both hands and feet are involved in 10% of patients (Media File 8).


Discrete yellow pustules on the sole of the foot....

Discrete yellow pustules on the sole of the foot. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.




Palms and soles of a patient with a dyshidrosis f...

Palms and soles of a patient with a dyshidrosis flare. The patient unroofed a large bulla on the right sole.


  • With long-standing disease, patients' fingernails may reveal dystrophic changes (eg, irregular transverse ridging, pitting, thickening, discoloration).
  • Interdigital maceration and desquamation of the interdigital spaces often are present, despite the possible absence of a dermatophyte infection.
  • Vesicles and/or bullae may become infected secondarily, and pustular lesions may be present. Cellulitis and lymphangitis may develop.
  • The Dyshidrotic Eczema Area and Severity Index was developed based on severity grades for the number of vesicles per square centimeter, erythema, desquamation, itch, and the extent of affected areas. The index was found to be a simple standardized method for assessing the condition and was used to assess disease severity and treatment effectiveness in 2 clinical studies. Further evaluation with larger patient groups is needed.

Causes

The cause of dyshidrotic eczema is unknown. The condition often appears related to other skin diseases (eg, atopic dermatitis, contact dermatitis, allergy to ingested metals, dermatophyte infection, bacterial infection, environmental or emotional stress). Several factors may participate in causing dyshidrotic eczema.

  • Genetic factors: Monozygotic twins have been affected simultaneously by dyshidrotic eczema. The pompholyx gene has been mapped to band 18q22.1-18q22.3, in the autosomal dominant form of familial pompholyx.
  • Atopy: As many as 50% of patients with dyshidrotic eczema have reportedly had personal or familial atopic diathesis (eczema, asthma, hayfever, allergic sinusitis).
    • The serum immunoglobulin E (IgE) level frequently is increased, even in patients who do not report a personal or familial history of atopy.
    • Occasionally, dyshidrotic eczema is the first manifestation of an atopic diathesis.
  • Nickel sensitivity: This may be a significant factor in dyshidrotic eczema.
    • Nickel sensitivity was reportedly low in some studies of dyshidrosis patients but significantly elevated in other studies.
    • Increased nickel excretion in the urine has been reported during exacerbations of pompholyx.
    • Ingested metals have been found to provoke exacerbations of pompholyx in some patients.
  • Low-nickel diets: These have reportedly decreased the frequency and severity of pompholyx flares.
    • A high palmoplantar perspiration rate has been suggested to result in a local concentration of metal salts that may provoke the vesicular reaction.
    • Contact allergy has been documented in 30% of patients with dyshidrotic eczema.
  • Cobalt sensitivity: The oral ingestion of cobalt manifests systemic allergic dermatitis as dyshidrotic eczema less frequently than the oral ingestion of nickel. Much more common is the simultaneous occurrence nickel and cobalt allergy seen in 25% of nickel-sensitive patients developing pompholyx. In these cases, the eczema is usually more severe. When suspected as the cause of the dyshidrotic eczema, high oral ingestion of cobalt should be taken in consideration, regardless of the patch test results.[2 ]
  • Low-cobalt diet: A point-based diet has been proposed to help patients limit cobalt ingestion and to keep the serum level below the threshold for developing flares, which is approximately less than 12 mcg/d. This diet has demonstrated higher compliance than an avoidance diet list. In addition, this diet also reduces the amount of nickel consumed.[2 ]
  • Exposure to sensitizing chemicals or metals: Dyshidrotic eczema outbreaks are sometimes associated with exposure to sensitizing chemicals or metals (eg, chromium, cobalt, carba mix, fragrance mix, diaminodiphenylmethane, dichromates, benzoisothiazolones, paraphenylenediamine, perfumes, fragrances, balsam of Peru, Primula plant).
  • Id reaction: Controversy surrounds the possible existence of an id reaction, which is considered to be a distant dermatophyte infection (tinea pedis, kerion of scalp) triggering a palmar pompholyx reaction (also termed pompholyx dermatophytid).
  • Fungal infection: Pompholyx occasionally resolves when a tinea pedis infection is treated, then relapses when the fungal infection recurs, supporting the existence of this reaction pattern. Of patients who have a vesicular reaction to intradermal trichophytin testing, less than one third have experienced a resolution of pompholyx after treatment with antifungal agents.
  • Emotional stress: This is a possible factor in dyshidrotic eczema. Many patients report recurrences of pompholyx during stressful periods. Improvement of dyshidrotic eczema using biofeedback techniques for stress reduction supports this hypothesis.
  • UV-A light: A group of 5 patients with pompholyx developed typical lesions morphologically and histologically consistent with a vesicular dermatitis after a provocation with long-wavelength UV-A light. Of interest, UV-B phototherapy and photochemotherapy are well-known efficient therapies for pompholyx. Further studies ruled out contact dermatitis, polymorphic light eruption, and heat as the culprit of the lesions in these patients, confirming that the reaction was a true photosensitivity rather than a photoaggravation.[10 ]Pompholyx caused by exposure to UV-A may be considered a variation of seasonal (summer) pompholyx.
  • Other factors: Isolated reports describe other possible causative factors, such as aspirin ingestion, oral contraceptives, cigarette smoking, and implanted metals, among others. A 3-year prospective study of the causes of dyshidrotic eczema (pompholyx) in 120 patients found causes of pompholyx related to contact exposure (67.5%), including cosmetic products (31.7%) and metals (16.7%); interdigital-plantar intertrigo (10%); and internal causes (6.7%), with an additional 15% with undiagnosed (idiopathic) causes, probably related to atopic factors.[11 ]Specifically, note the following:
    • Contact allergy was found in 89 (74.2%) of 120 of the patients. The most frequent allergens were nickel, shower gel, chromium, fragrance, shampoo, and balsam of Peru. Less frequent allergens were lanolin, cobalt, thiuram, lauryl sulfate, fresh tobacco, p -phenylenediamine (PPD), formaldehyde, parabens, and octyl gallate. In 97 of 193 positive patch test results, correlation existed between the application of the agent and pompholyx recurrence. The relevance of the analysis was confirmed in 81 (67.5%) of 120 patients. In summary, the most frequent causes of pompholyx related to contact with substances were hygiene product intolerance (46.7%), metal allergy (25%), and others (28.3%).
    • Intertrigo occurred in 19 (15.8%) of 120 patients. Of those, 80% presented with dermatophytosis and 20% presented with candidiasis. After 3 weeks of antifungal therapy, 6 of 19 patients remained symptomatic for pompholyx.
    • With regard to internal causes, 30 patients presented with a positive patch test result for metals, but only 2 presented with exacerbations of the lesions after a challenge test.
    • Of 58 patients with a history of smoking tobacco, 5 presented with a positive reaction, and 2 of those reactions were considered relevant.
    • Drug allergy was determined to be the causative agent in 3 patients (amoxicillin in 2 and intravenous immunoglobulin in 1).
    • Food-related pompholyx was detected in 4 patients, and after a challenge test, reactivation occurred in 3 patients (2 for paprika and 1 for orange juice).

Differential Diagnoses

Acropustulosis of Infancy
Juvenile plantar dermatosis
Bullous Pemphigoid
Linear IgA-disease with (hemorrhagic) pompholyx
Contact Dermatitis, Allergic
Pemphigoid Gestationis
Contact Dermatitis, Irritant
Pemphigus Vulgaris
Epidermolysis Bullosa
Pityriasis Rubra Pilaris
Erythema Multiforme
Subcorneal Pustular Dermatosis
Fixed Drug Eruptions
Urticaria, Contact Syndrome
Friction Blisters
Vesicular mycosis fungoides
Herpes Simplex
Impetigo, bullous

Other Problems to Be Considered

Dyshidrosiform pemphigoid
Inflammatory tinea pedis or tinea manus
Palmoplantar pustular psoriasis
Pustular bacterid

Workup

Laboratory Studies

  • Diagnosis is usually made clinically.
  • Bacterial culture and sensitivity exclude secondary infection.
  • Blood tests are not usually ordered; however, IgE levels are commonly elevated.

Other Tests

  • Use patch testing to exclude allergic contact dermatitis.
  • Measuring thiopurine methyltransferase levels allows accurate dosing of azathioprine.

Procedures

  • Perform potassium hydroxide wet mount preparation to exclude dermatophyte infection.
  • Punch biopsy for hematoxylin and eosin staining usually is not necessary.
  • Punch biopsy for periodic acid-Schiff staining may help exclude dermatophytosis in patients with unresponsive disease.
  • Use punch biopsy for direct immunofluorescence to exclude bullous pemphigoid.

Histologic Findings

  • Spongiosis with an epidermal lymphocytic infiltrate and intraepidermal vesicles or bullae are present. The vesicles are not associated with sweat glands.

Treatment

Medical Care

Some mildly affected patients experience spontaneous resolution within 2-3 weeks. Biofeedback therapy for stress reduction has succeeded in some patients. Outpatient care is multifaceted.

  • The following treatment is appropriate if bullae are present.
    • Use compresses with Burow solution (10% aluminum acetate) in a 1:40 dilution until bullae resolve (usually, within a few days).
    • Compresses with a 1:10.000 solution of potassium permanganate are also effective.
    • Drain large bullae with a sterile syringe, and leave the roof intact.
    • Prescribe systemic antibiotics that cover Staphylococcus aureus and group A streptococci.
  • Topical corticosteroids are the mainstay of treatment.
    • Typically, use class I steroids initially, then class II or III steroids.
    • Ointments penetrate skin better than creams; patients may prefer creams during the day.
    • Topical antipruritics with pramoxine are useful.
  • Systemic corticosteroids can also be used.
    • Either oral prednisone or intramuscular triamcinolone suspension may be used for severe episodes.
    • Tapering of prednisone can follow intramuscular treatment.
  • Topical calcineurin inhibitors may be helpful.
    • Some patients may benefit from topical tacrolimus or pimecrolimus. Several studies have demonstrated their efficacy and tolerability in the treatment of chronic hand dermatitis,[12 ]and long-term occlusive therapy has also been determined to be efficacious, particularly in persons with severe dyshidrotic eczema.[12 ]
    • Advantages of topical calcineurin inhibitors over topical corticosteroids include the lack of development of tachyphylaxis, telangiectasias, and thinning and atrophy of the skin.[13 ]
    • Personal experience of the coauthor shows effective control in several patients followed in her practice with topical calcineurin inhibitor therapy alone. Note that topical calcineurin inhibitors can exacerbate irritant hand dermatitis.
  • UV-A or UV-A1 alone or with oral or topical psoralen: Hand and/or foot UV-A therapy (UV-A or UV-A1 alone or with oral or topical psoralen) improves the eruption and pruritus when administered 2-3 times per week. The dose typically starts at 0.5 J per treatment and is increased by 0.5 J at every other or every third treatment.
  • 8-Methoxypsoralen (MOP) plus UV-A (bath-PUVA): Topical application of MOP and UV-A (bath-PUVA) has been demonstrated to be the preferred method for the treatment of dyshidrotic eczema compared with oral PUVA.[14 ]Local narrow-band UV-B has been shown to be as effective as bath-PUVA in patients with chronic hand eczema of dry and dyshidrotic types.[15 ]
  • Botulinum toxin A: Injections may be helpful in some patients. Botulinum toxin A intradermal injections as an adjuvant to topical corticosteroids has been tested in a study in which 6 patients who completed an 8-week trial achieved significant reductions in the Dyshidrotic Eczema Area and Severity Index (DASI) scores and faster reductions of pruritus and vesiculation.[13 ]In another study, 7 of 10 vesicular pompholyx patients achieved good-to-very good responses after the injection of botulinum toxin A alone, with a reduction of pruritus.[16 ]
  • Other therapies
    • For severe refractory pompholyx, azathioprine, methotrexate mycophenolate mofetil, cyclosporine, or etanercept may be helpful.
      • Etanercept has been administered subcutaneously to one patient with recalcitrant hand pompholyx at a dose of 25 mg twice a week. The patient achieved complete remission for 4 months, after which the patient had a relapse. The etanercept dose was increased to 50 mg twice a week without improvement.[17 ]
      • Consider measuring thiopurine methyltransferase levels, which may help guide azathioprine therapy. Accurate dosing avoids both toxicity and underdosing.
    • Nickel chelators, such as disulfiram (Antabuse), occasionally are used in nickel-sensitive patients who demonstrate a positive oral provocation test.
    • Tap water iontophoresis with pulsed direct current may be helpful as adjuvant treatment.
    • Khellin, a furanochromone similar to methoxypsoralen, may be used in combination with photochemotherapy (sun exposure) for recalcitrant palmoplantar cases. Khellin, unlike other psoralens, does not induce skin phototoxicity (erythema) and hyperpigmentation of healthy skin after UV-A radiation therapy.
    • Alitretinoin activates the retinoid X receptor and all retinoic receptors.
      • It has been studied in 319 patients with chronic hand dermatitis (70 with pompholyx) refractory to standard therapy in a randomized, double-blind, placebo-controlled, multicenter trial in which oral alitretinoin was administered at doses of 10 mg, 20 mg, or 40 mg once daily of for 12 weeks. Although alitretinoin induced a significant clinical improvement in a dose-dependent fashion (53% improvement in disease status and 70% reduction in clinical features), no difference was noted in the group of patients with pompholyx compared with placebo.[13,18 ]
      • In another randomized, double-blind, placebo-controlled, multicenter trial, oral alitretinoin showed a response rate of 33% at a dose of 30 mg/d, compared with 23% at a dose of 10 mg/d and 16% with placebo in 377 patients with pompholyx.[19 ]
      • Headache and mucocutaneous adverse events, including dry skin, rash, alopecia, exfoliative dermatitis, and hyperlipidemia, were the most common adverse events in these trials.
      • Alitretinoin 1% gel has been evaluated for the treatment of classic Kaposi sarcoma,[20 ]photoaging,[21 ] pyogenic granuloma,[22 ]and cutaneous T-cell lymphoma.[23 ]Currently, alitretinoin 1% gel has not been used for the topical treatment of pompholyx.
      • Currently, a phase 3, randomized, double-blind (subject, investigator), placebo-controlled, parallel-assignment, safety/efficacy study is being conducted on the treatment of chronic hand dermatitis (including pompholyx) using oral alitretinoin at 30 mg/d (1 capsule) for up to 24 weeks; the estimated completion date is 2010.[24 ]Also see Efficacy and Safety of a Retinoid in the Treatment of Severe Chronic Hand Eczema (HANDEL).
    • Newer and potential agents for pompholyx, such as topical bexarotene, systemic alitretinoin, leukotriene receptor antagonists, leukotriene synthesis inhibitors, phosphodiesterase-4 inhibitors, and monoclonal antibodies, have shown to be effective for the treatment of chronic hand dermatitis and other inflammatory conditions, including atopic dermatitis. Controlled studies need to be conducted to establish their efficacy and safety for the treatment of dyshidrotic eczema (pompholyx).

Consultations

  • Psychologist - For stress reduction using biofeedback therapy and other techniques
  • Allergist - For oral provocation test for nickel, cobalt, or chromium salts
    • Oral challenges occasionally are positive in patients who demonstrate negative patch tests to these metals.
    • The test is considered positive if a patient's dyshidrotic eczema flares after metal is ingested.

Diet

For nickel-sensitive patients, consider a low-nickel diet for 3-4 weeks. The diet regimen is only rarely successful and is difficult for patients to follow. The diet requires avoiding foods rich in nickel, such as canned foods, foods cooked using nickel-plated utensils, herring, oysters, asparagus, beans, mushrooms, onions, corn, spinach, tomatoes, peas, whole grain flour, pears, rhubarb, tea, cocoa, chocolate, and baking powder. A list of additional nickel-containing foods has been reported by Lofgren and Warshaw.[4 ]

For cobalt-sensitive patients, consider a low-cobalt diet that avoids apricots, beans, beer, beets, cabbage, cloves, cocoa, chocolate, coffee, liver, nuts, scallops, tea, and whole grain flour. A point-based low-cobalt diet has been described by Stuckert and Nedorost.[2 ]

Activity

Bedrest may be necessary if bullae develop on the feet. Additionally, if palmar bullae develop, patients may not be able to work or perform the activities of daily living.

Medication

The goals of pharmacotherapy for dyshidrotic eczema are to reduce morbidity and prevent complications.

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli. Topical ointments are more potent but greasier than creams.


Clobetasol (Temovate)

For severe episodes. Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.

Dosing

Adult

Apply cream or ointment bid to severely affected areas for up to 2 wk; not to exceed 50 g/wk

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; viral or fungal skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function and result in thinning of skin in prolonged therapy


Fluocinolone (Fluonid, Synalar)

Ointment is a class II, cream is a class III steroid. High-potency; like all topical steroids, has anti-inflammatory, antipruritic, and vasoconstrictive properties.

Dosing

Adult

Apply cream or ointment sparingly bid as severity warrants

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; herpes simplex infection, fungal, viral, or tubercular skin lesions

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause adverse systemic effects if used over large areas, denuded areas, on occlusive dressings, or during prolonged treatment periods; prolonged use may result in thinning of skin


Prednisone (Deltasone, Meticorten, Orasone)

Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation
by reversing increased capillary permeability and suppressing PMN activity.

Dosing

Adult

0.5-1 mg/kg/d PO qam; taper over 2 wk

Pediatric

Administer as in adults

Interactions

Ketoconazole, erythromycin, clarithromycin, estrogens, and birth control pills increase levels
Aminoglutethimide, phenytoin, phenobarbital, rifampin, cholestyramine, and ephedrine decrease levels
Levels of potassium-depleting diuretics (due to potentiation of potassium loss and digitalis toxicity) and cyclosporine may increase; levels of isoniazid, insulin (resistance is induced), and salicylates may decrease; monitor anticoagulant therapy and theophylline levels

Contraindications

Absolute: Systemic fungal infection, herpes simplex keratitis, hypersensitivity (usually with corticotropin, occasionally with IV preparations)
Relative: Hypertension, active TB, CHF, prior psychosis, positive intermediate purified protein derivative test result, glaucoma, severe depression, diabetes mellitus, active peptic ulcer disease, cataracts, osteoporosis, recent bowel anastomosis, and pregnancy

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur


Betamethasone (Celestone, Soluspan)

For severe acute episodes. Rapid onset (within 1 h) with 72-h duration. For inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability.

Dosing

Adult

5-9 mg IM as single dose

Pediatric

Not advised

Interactions

Aminoglutethimide, phenytoin, phenobarbital, rifampin, cholestyramine, and ephedrine decrease levels
Levels of potassium-depleting diuretics (due to potentiation of potassium loss and digitalis toxicity) and cyclosporine may increase; levels of isoniazid, insulin (resistance is induced), and salicylates may decrease; monitor anticoagulant therapy and theophylline levels

Contraindications

Absolute: Systemic fungal infection, herpes simplex keratitis, hypersensitivity (usually with corticotropin, occasionally with IV preparations)
Relative: Hypertension, active TB, CHF, prior psychosis, positive intermediate purified protein derivative test result, glaucoma, severe depression, diabetes mellitus, active peptic ulcer disease, cataracts, osteoporosis, recent bowel anastomosis, and pregnancy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Increases risk of multiple complications, including severe infections; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications
If given by injection, bruising, infection, cold abscess, temporary depression in skin, and temporary discoloration of skin (usually lightened) may occur at injection site


Triamcinolone (Aristocort)

For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. Long duration, 4-6 wk.

Dosing

Adult

40-60 mg IM as single dose

Pediatric

2.5-15 mg (10 mg/mL or 40 mg/mL solutions) IM single dose; repeat prn

Interactions

Aminoglutethimide, phenytoin, phenobarbital, rifampin, cholestyramine, and ephedrine decrease levels
Levels of potassium-depleting diuretics (due to potentiation of potassium loss and digitalis toxicity) and cyclosporine may increase; levels of isoniazid, insulin (resistance is induced), and salicylates may decrease; monitor anticoagulant therapy and theophylline levels

Contraindications

Absolute: Systemic fungal infection, herpes simplex keratitis, hypersensitivity (usually with corticotropin, occasionally with IV preparations)
Relative: Hypertension, active TB, CHF, prior psychosis, positive intermediate purified protein derivative test result, glaucoma, severe depression, diabetes mellitus, active peptic ulcer disease, cataracts, osteoporosis, recent bowel anastomosis, and pregnancy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Multiple complications may occur (eg, severe infections, hyperglycemia, myopathy, peptic ulcer disease, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression)
If given by injection, bruising, infection, cold abscess, temporary depression in skin, and temporary discoloration of skin (usually lightened) may occur at injection site

Immunosuppressives

For severe acute episodes.[25,26,27 ]


Tacrolimus, topical (Protopic)

For short-term treatment or intermittent long-term treatment in unresponsive or intolerant cases. Inhibits T-lymphocyte activation. Some patients may benefit from topical tacrolimus or pimecrolimus. Primary author follows several patients in her practice who are controlled with topical calcineurin inhibitors alone. Available at 0.03% and 0.1% ointment.

Dosing

Adult

Apply bid to affected areas; continue for 1 wk after clearing

Pediatric

<2 years: Not established
>2-15 years: Apply 0.03% ointment bid to affected areas; continue for 1 wk after clearing
>15 years: Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; local infection at treatment site; Netherton syndrome; children <2 y; immunodeficiency syndromes; caution in herpes simplex or varicella-zoster virus infections, eczema herpeticum, or erythroderma

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Serious adverse reactions include varicella-zoster virus infection and eczema herpeticum; common adverse reactions include skin burning, pruritus, flulike symptoms, headache, erythema, allergic reaction, skin tingling, hyperesthesia, acne, folliculitis, rash, and urticaria; do not use with occlusive dressings; limit use to affected skin.
Product insert revised and contains boxed warning stating long-term safety of calcineurin inhibitors has not been established; although causal relationship has not been established, rare cases of malignancy (eg, skin and lymphoma) have been reported; only 0.03% ointment indicated for use in children aged 2-15 y


Pimecrolimus, topical (Elidel)

For short-term treatment or intermittent long-term treatment in unresponsive or intolerant cases. Inhibits T-lymphocyte activation. Available at 1% cream

Dosing

Adult

Apply bid to affected areas; discontinue after clearing

Pediatric

<2 years: Not indicated
>2 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; local infection at treatment site; Netherton syndrome; children <2 y; immunodeficiency syndromes; caution in herpes simplex or varicella-zoster virus infection, eczema herpeticum, and erythroderma

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Serious adverse reactions include varicella-zoster or herpes simplex virus infection, eczema herpeticum, angioneurotic edema, and anaphylaxis; common adverse reactions include skin burning, flulike symptoms, headache, nasopharyngitis, cough, pyrexia, erythema, hypersensitivity reaction, skin infection, herpes simplex, skin papilloma, erythema, and pruritus
Do not use with occlusive dressings; limit use to affected skin; avoid continuous long-term use; reevaluate if symptoms persist >6 wk.
product insert revised and contains boxed warning stating long-term safety of calcineurin inhibitors has not been established; although causal relationship has not been established, rare cases of malignancy (eg, skin and lymphoma) have been reported; only 0.03% ointment indicated for use in children aged 2-15 y


Methotrexate (Rheumatrex, Folex)

Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Antimetabolite that inhibits DNA synthesis and cell reproduction in malignant cells; may suppress immune system. Satisfactory response seen within 3-6 wk following administration. Adjust dose gradually to attain satisfactory response.

Dosing

Adult

Administer 1. 5- to 10-mg test dose; check CBC count in 1 wk; if results are normal, continue weekly 1-time 7.5-mg doses (may split if GI upset, ie, 8 am, 8 pm, 8 am dosing); increase dose by 2.5 mg/wk each month (may taper by 2.5 mg/wk each month when decreasing dose to lowest possibility)

Pediatric

Not recommended

Interactions

Salicylates, NSAIDs, dipyridamole, probenecid, retinoids, ethanol, triamterene, pyrimethamine, sulfonamides, tetracycline, chloramphenicol, penicillin or other broad-spectrum antibiotics, trimethoprim, dapsone, theophylline, phenytoin, phenothiazines, barbiturates, and nitrofurantoin (impair folic acid absorption), ascorbic acid, phenylbutazone, cyclosporin, aminoglycosides

Contraindications

Absolute: Pregnancy or desire to get pregnant, active peptic ulcer, alcoholism, primary/secondary immunodeficiency, blood dyscrasias, active hepatitis, cirrhosis, chronic renal failure, and active infections
Relative: History of excessive ethanol intake or substance abuse, increased LFT results, recent hepatitis, diabetes mellitus, obesity, history of heritable liver disease, unreliable patient, CrCl <50 mL/min, males contemplating conception (must discontinue for 3 mo)

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Monitor CBC counts, differentials, renal panel, urinalysis, and LFT results monthly; CrCl baseline recommended for patients >50 y; monitor more frequently during initial dosing, dose adjustments, or if risk of elevated methotrexate levels (eg, dehydration); has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant drop in blood cell counts occurs; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly (possibility of increased toxicity with NSAIDs including salicylates not tested yet)


Azathioprine (Imuran)

Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.

Dosing

Adult

100-150 mg/d PO initially; then 50-100 mg/d PO maintenance after improvement occurs; more accurate dosing possible with measurement of thiopurine methyltransferase level

Pediatric

Not established

Interactions

Allopurinol increases risk of pancytopenia; captopril/ACE inhibitors may increase risk of anemia and leukopenia; increased dose of warfarin may be necessary; may need increased dose of pancuronium for adequate paralysis; live-virus vaccines, co-trimoxazole (increased risk of hematologic toxicity); rifampicin (transplants possibly rejected); clozapine (increased risk of agranulocytosis)

Contraindications

Absolute: Documented hypersensitivity, pregnancy or attempting pregnancy, and clinically significant active infection
Relative: Concurrent use of allopurinol; prior treatment with alkylating agents (cyclophosphamide, chlorambucil, melphalan, others) (high risk of neoplasia)
Pediatric: Safety and efficacy not established

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

TPMT testing is not entirely reliable; it involves testing the activity of TPMT activity in RBCs, which correlates with systemic TPMT activity; functional enzyme test has been shown to have variability between test sites, and kits may contain varying amounts of enzyme inhibitor; starting at low doses, monitoring for pancytopenia, and then increasing dose is alternative; if clinical response is not good, patient may be a homozygote for high activity and may need an increased dose
Possible increased risk of lymphoproliferative disorders with long-term therapy; increases risk of neoplasia; caution with liver disease and renal impairment; hematologic toxicities may occur


Cyclosporine (Neoral)

Cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft versus host disease for a variety of organs. For children and adults, base dosing on ideal body weight.

Dosing

Adult

3-5 mg/kg/d PO

Pediatric

Not established

Interactions

Increase levels: Erythromycin, clarithromycin, azithromycin, norfloxacin ciprofloxacin, cephalosporins, doxycycline, ketoconazole, itraconazole, fluconazole, ritonavir, indinavir, saquinavir, nelfinavir, diltiazem, verapamil, nicardipine, cimetidine, methylprednisolone, dexamethasone, thiazides, furosemide, allopurinol, bromocriptine, danazol, amphotericin B, metoclopramide, oral contraceptive pills, warfarin, and grapefruit juice.
Decrease levels: Rifampin, rifabutin, nafcillin, carbamazepine, phenobarbital, phenytoin, valproate, octreotide, and ticlopidine.
Potentiate renal toxicity: Tobramycin, gentamicin, ketoconazole, azapropazone, TMP-SMZ, vancomycin, sulindac, amphotericin B, indomethacin, naproxen, cimetidine, ranitidine, diclofenac, tacrolimus, and melphalan.
Decreased renal clearance may lead to digitalis toxicity; atorvastatin renal clearance may be decreased, leading to myositis; methylprednisolone or prednisolone renal clearance may be decreased, leading to convulsions; concurrent ACE inhibitors, potassium supplements, and potassium-sparing diuretics may increase risk of hyperkalemia

Contraindications

Absolute: Significantly decreased renal function, uncontrolled hypertension, documented hypersensitivity, and clinically cured or persistent malignancy (except nonmelanoma skin cancer)
Relative: Age <18 or >64 y (transplant recipients as young as 1 y have been treated with no unusual effects; however safety in patients <18 y has not been established); controlled hypertension; planning to receive a live attenuated vaccine; active infection or evidence of immunodeficiency; concurrent phototherapy, coal tar, methotrexate, or other immunosuppressive agents; pregnancy or lactation; unreliable patient; and severe hepatic dysfunction

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Evaluate renal and liver functions often by measuring BUN, serum creatinine, serum bilirubin, and liver enzyme levels; may increase risk of infection and lymphoma; reserve IV use only for those who cannot take PO

Antibiotics

For dyshidrosis with secondary impetiginization.


Dicloxacillin (Dynapen, Dycill)

Binds to one or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. For infections caused by penicillinase-producing staphylococci. May use to initiate therapy when staphylococcal infection is suspected

Dosing

Adult

250-500 mg PO qid for 7-10 d

Pediatric

25-50 mg/kg/d PO divided qid for 7-10 d

Interactions

May decrease effects of anticoagulants; probenecid and disulfiram may increase levels; with concurrent use, tetracyclines may decrease effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor PT in patients taking anticoagulant medications; toxicity may increase in patients with renal impairment


Cephalexin (Keflex)

First-generation cephalosporin arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora; used for skin infections or prophylaxis in minor procedures.

Dosing

Adult

250-500 mg PO qid for 7-10 d

Pediatric

25-50 mg/kg/d PO divided bid for 7-10 d (125 and 250 mg/5 mL)

Interactions

Coadministration with aminoglycosides increases nephrotoxic potential

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections, and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy


Erythromycin (E.E.S., E-Mycin, Ery-Tab)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
Age, weight, and severity of infection determine proper dosage in children. When bid dosing is desired, one half of total daily dose may be taken q12h. Double the dose for more severe infections.

Dosing

Adult

250-500 mg PO qid for 7-10 d

Pediatric

25-50 mg/kg/d PO divided qid

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (administer pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur

Antihistamines

To treat pruritus associated with dyshidrosis. Desloratadine (Clarinex) is a long-acting tricyclic histamine antagonist selective for H1 receptor. Is a major metabolite of loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine. The dose for adults and children >12 y is 5 mg PO daily. Decrease dose in hepatic impairment. Data limited regarding drug interactions; however, erythromycin and ketoconazole increase desloratadine and 3-hydroxydesloratadine plasma concentrations, but no increase in clinically relevant adverse effects, including QTc, was observed. Adverse effects were similar to placebo, and it rarely causes pharyngitis or dry mouth.


Loratadine (Claritin)

Nonsedating; selectively inhibits peripheral histamine H1 receptors.

Dosing

Adult

10 mg PO, usually in morning

Pediatric

<6 years: Not established
6-11 years: 10 mg Redi-Tab or 10 mL syr daily (1 mg/mL)

Interactions

Ketoconazole, erythromycin, procarbazine, and alcohol may increase levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Initiate therapy at lower dose in liver impairment


Hydroxyzine (Atarax)

Antagonizes H1 receptors in periphery. Sedating; may suppress histamine activity in subcortical region of CNS.

Dosing

Adult

10-50 mg PO q4-6h, often at bedtime

Pediatric

0.5 mg/kg PO q4-6h or 10 mg/5 mL

Interactions

CNS depression may increase with alcohol or other CNS depressants when coadministered

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated with clinical exacerbations of porphyria (may not be safe for porphyric patients); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness


Pramoxine (Pramosone)

Topical antihistamine and mild anti-inflammatory. Blocks nerve conduction and impulses by inhibiting depolarization of neurons. Available alone or as 1% or 2.5% cream or ointment. Available OTC as Prax.

Dosing

Adult

Topically apply cream or ointment bid/tid to affected area

Pediatric

Apply as in adults
<12 years: Not indicated

Interactions

None reported

Contraindications

Documented hypersensitivity; do not apply over large areas and avoid contact with eyes and nose

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Serious adverse reactions include anaphylactic reactions and skin sloughing (rare); common adverse reactions include contact dermatitis, edema, burning, stinging, and tenderness; caution in patients with trauma in area to be treated

Nickel chelators

Minimize effects of nickel in eczema.


Disulfiram (Antabuse)

Thiuram derivative that interferes with aldehyde dehydrogenase. For patients highly allergic to nickel with severe vesicular hand dermatitis. Chelating effect of disulfiram helps reduce the body's nickel burden in individuals allergic to nickel. Do not administer if patient has ingested alcohol within last 12 h. Supplied as a 250-mg tab.

Dosing

Adult

250-500 mg/d PO (range 125-500 mg); not to exceed 500 mg/d

Pediatric

Not established

Interactions

Increases effects of diazepam and chlordiazepoxide; metronidazole, isoniazid, and phenytoin may increase toxicity of disulfiram; coadministration with warfarin may increase PT; coadministration with alcohol may cause disulfiram reaction

Contraindications

Documented hypersensitivity; severe myocardial disease and coronary occlusion

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hypothyroidism, hepatic cirrhosis, hepatic disease or insufficiency, seizure disorders, diabetes mellitus, cerebral damage, and nephritis

Follow-up

Further Outpatient Care

  • Schedule follow-up and check blood pressure 1 week after initiating prednisone.

Deterrence/Prevention

  • Advise dyshidrotic eczema patients to avoid known contact irritants or allergens.
  • Advise dyshidrotic eczema patients to reduce stress (may help some patients).
  • Advise dyshidrotic eczema patients to follow a hand care regimen.
  • Advise regular prophylactic use of emollients.

Complications

  • Secondary bacterial infection of dyshidrotic eczema vesicles or bullae can result in cellulitis, lymphangitis, and septicemia (rare).
  • Dystrophic nail changes may develop with transverse ridging, thickening, discoloration, and pitting of nails.

Prognosis

  • Dyshidrotic eczema follows a chronic intermittent course. Fewer episodes occur after middle age.

Patient Education

  • Instruct dyshidrotic eczema patients to avoid contact with certain allergens or irritants (eg, nickel).
  • Instruct dyshidrotic eczema patients to follow a hand care routine that avoids irritants.
  • Instruct dyshidrotic eczema patients to use emollients regularly.
  • For excellent patient education resources, visit eMedicine's Skin, Hair and, Nails Center. Also, see eMedicine's patient education article Eczema.

Miscellaneous

Medicolegal Pitfalls

  • Failure to guard against or inform dyshidrotic eczema patients of the potential development of adverse systemic effect with prolonged use of systemic steroids (eg, hypertension, diabetes mellitus, weight gain, cataracts, osteoporosis)
  • Failure to acquire an adequate history of exposure to potential allergic and irritant contactants (contactants at patient's work may be a contributing factor or cause recurrent episodes)
  • Failure to consider other possible diagnoses

Special Concerns

  • Substances used to systemically challenge patients with possible ingested allergens may trigger exacerbations. Vasculitis or erythema multiforme may develop during this testing.

Multimedia

Tense vesicles and bullae on the palm. Courtesy o...

Media file 1: Tense vesicles and bullae on the palm. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.

Close-up view of tense vesicles and bullae of the...

Media file 2: Close-up view of tense vesicles and bullae of the palm. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.

Discrete yellow pustules on the sole of the foot....

Media file 3: Discrete yellow pustules on the sole of the foot. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.

Multiple tense vesicles on the palm.

Media file 4: Multiple tense vesicles on the palm.

Small tense vesicles on the fingers.

Media file 5: Small tense vesicles on the fingers.

Small, discrete, coalesced vesicles on the dorsal...

Media file 6: Small, discrete, coalesced vesicles on the dorsal hand.

Small, discrete, coalesced vesicles on the finger...

Media file 7: Small, discrete, coalesced vesicles on the fingers.

Palms and soles of a patient with a dyshidrosis f...

Media file 8: Palms and soles of a patient with a dyshidrosis flare. The patient unroofed a large bulla on the right sole.

Small discrete vesicles of the lateral fingers.

Media file 9: Small discrete vesicles of the lateral fingers.

References

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Keywords

dyshidrotic eczema, pompholyx, vesicular palmoplantar eczema, atopic dermatitis, contact dermatitis, hand eczema, atopic diathesis, asthma, hay fever, allergic sinusitis, contact allergens, intravenous immunoglobulin therapy, interdigital maceration, desquamation of interdigital spaces

cellulitis, lymphangitis, Dyshidrotic Eczema Area and Severity Index, allergy to ingested metals, dermatophyte infection, emotional stress, nickel sensitivity, id reaction, tinea pedis infection, pompholyx dermatophytid, palmar pompholyx reaction, implanted metals.

Contributor Information and Disclosures

Author

Sadegh Amini, MD, Senior Clinical Research Fellow, Skin Research Group, Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami
Sadegh Amini, MD is a member of the following medical societies: American Society for Dermatologic Surgery, International Society for Dermatologic Surgery, and International Society of Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Anne E Burdick, MD, MPH, Professor of Dermatology, Director of Leprosy Program, Associate Dean for TeleHealth and Clinical Outreach, University of Miami Miller School of Medicine
Anne E Burdick, MD, MPH is a member of the following medical societies: Washington State Medical Association
Disclosure: Nothing to disclose.

Medical Editor

John D Wilkinson, MD, MBBS, MRCS, FRCP, Chairman, Clinical Director, Department of Dermatology, Amersham Hospital and High Wycombe Hospital, UK
John D Wilkinson, MD, MBBS, MRCS, FRCP is a member of the following medical societies: American Academy of Dermatology and Royal College of Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Ivan D. Camacho, MD, in the development and writing of this article.

Further Reading

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