Dyshidrotic Eczema



Dyshidrotic eczema is a type of eczema (dermatitis) of unknown cause that is characterized by a pruritic vesicular eruption on the fingers, palms, and soles. The condition affects teenagers and adults and may be acute, recurrent, or chronic. A more appropriate term for this vesicular eruption is pompholyx, which means bubble. The clinical course of dyshidrotic eczema can range from self-limited to chronic, severe, or debilitating. The condition's unresponsiveness to treatment can be frustrating for the patient and physician (see the images below).

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

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Multiple tense vesicles on the palm.

Some believe the terms pompholyx and dyshidrosis are obsolete and favor a new term, such as "acute and recurrent vesicular hand dermatitis." The etiology of dyshidrotic eczema is unresolved and is believed to be multifactorial. Dyshidrotic eczema is considered to be a reaction pattern caused by various endogenous conditions and exogenous factors.

See All About Allergies: Be Ready for Spring, a Critical Images slideshow, to help identify a variety of allergens and symptoms.


The hypothesis of sweat gland dysfunction has been disputed because vesicles have not been shown to be associated with sweat ducts. A 2009 case report provided clear histopathologic evidence that sweat glands do not play a role in dyshidrosis.[1] 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 onabotulinumtoxinA injection.[2]

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 type I and type IV hypersensitivity reactions. In addition, they can also act as atypical haptens, activating T lymphocytes through human leukocyte antigen–independent pathways, causing systemic allergic dermatitis in the form of dyshidrotic eczema.[3, 4]

Emotional stress[5] and environmental factors (eg, seasonal changes, hot or cold temperatures, humidity) reportedly exacerbate dyshidrosis. In addition, dyshidrosislike eczematous eruptions with the use of intravenous immunoglobulin infusions have been reported.

Dyshidrosislike eczematous eruptions with the use of intravenous immunoglobulin (IVIG) infusions have been reported. A 2011 search of the literature identified pompholyx as one of the most important cutaneous adverse effects of IVIG, being present in 62.5% of the patients reported, with 75% of those patients developing the lesions after just one IVIG treatment.[6] The eruption tends to be mild and to wane over time. It usually responds very well to topical steroids,[7, 8, 9]  but it may become recurrent and more aggressive after repeated doses of IVIG.

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. The factors believed to be associated with dyshidrotic eczema are discussed in more detail below.

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.[10]

Mutations on the filaggrin gene leading to loss of filaggrin, a structural protein of the stratum corneum involved in the barrier function of the skin, causes dyskeratinization, increased transepidermal water loss, and an increase in the transepidermal antigen transfer. Combined, these features have been associated with the development of icthyosis and atopic dermatitis, and they may be involved in the development of irritant and allergic contact dermatitis, which are well-known conditions associated with dyshidrotic eczema. Chronic hand dermatitis, including dyshidrotis eczema, has also been associated with defects in the skin barrier, and, in a few cases, it has been also associated with mutations in the filaggrin gene; however, these have not reached statistical significance.[11]

Aquaporins have been shown to be expressed in patients with atopic dermatitis and may also be related to exacerbation and chronicity of pompholyx. Aquaporins are channel proteins located on cell membranes that increase their permeability, in particular aquaglyceroporins. Aquaglyceroporins can transport water and glycerol. Aquaporin-3 and aquaporin-10 are normally expressed in the basal layer of the epidermis, and immunohistochemical staining had demonstrated their presence in all epidermal layers in patients with pompholyx. These channels may participate in the increase of transepidermal water loss seen in atopic dermatitis and possibly in pompholyx. Owing to osmotic gradients, among other factors, the direction of water and glycerol through aquaporins is from the skin to the environment, possibly contributing with skin dehydration, even immediately after hand washing. Hypothetically, topical and/or systemic inhibition of the expression of aquaporins in the epidermis could contribute with the preservation of water and glycerol, decreasing the frequency and severity of pompholyx exacerbations.[12]


As many as 50% of patients with dyshidrotic eczema have reportedly had personal or familial atopic diathesis (eczema, asthma, hay fever, 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 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 does the oral ingestion of nickel. Much more common is the simultaneous occurrence of 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.[3]

A point-based, low-cobalt 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 reduces the amount of nickel consumed.[3]

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.

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 to cosmetic products (31.7%) and metals (16.7%); interdigital-plantar intertrigo (10%); and internal factors (6.7%), with an additional 15% of patients having undiagnosed (idiopathic) causes probably related to atopic factors.[13]

Contact allergy was found in 89 (74.2%) of the 120 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 the 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 the 120 patients. Of those individuals, 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 of these patients (2 for paprika and 1 for orange juice).

Ultraviolet A light

In a case series, 5 patients with prior diagnosis of pompholyx developed lesions morphologically and histologically consistent with a vesicular dermatitis after provocation with long-wavelength ultraviolet A (UVA) light. Further workup ruled out contact dermatitis, polymorphic light eruption, and heat as the culprit, confirming that the reaction was due to true photosensitivity rather than to photoaggravation.[14]

Pompholyx caused by UVA exposure may possibly be considered a variation of seasonal (summer) pompholyx. In the United States, dyshidrotic eczema is more commonly seen in warmer climates and during the spring and summer months. A study in Turkey also revealed a higher prevalence of dyshidrotic eczema in the summer months.[15]

In a case series, three patients with histories of frequent pompholyx exacerbations, mostly during summer (ie, photoaggavated pompholyx), were subjected to photoprovocation testing, with positive development of pompholyx lesions in two of them. Patients reported lesions after exposure to solar-simulated ultraviolet radiation and broadband UVA. They were treated with photoprotective measures in addition to the standard treatment for pompholyx, resulting in a decrease in the frequency and severity of the exacerbations. The authors suggested that the condition may be underdiagnosed and recommended recognition and early detection to institute sun protection as soon as possible and to avoid starting phototherapy or photochemotherapy in this particular subset of pompholyx patients.[16]

Of interest, UVB phototherapy and photochemotherapy are well-known, efficient treatments for pompholyx.


Occurrence in the United States

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

International occurrence

Dyshidrotic eczema accounted for 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.[17]

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%).[18]

Sex- and age-related demographics

The male-to-female ratio for dyshidrotic eczema has variably been reported as 1:1 and 1:2. Dyshidrotic eczema affects individuals aged 4-76 years; the mean age is 38 years. The peak incidence of the condition occurs in patients aged 20-40 years. After middle age, the frequency of dyshidrotic eczema episodes tends to decrease.


Dyshidrotic eczema follows a chronic, intermittent course, with fewer episodes occurring after middle age. Some mildly affected patients experience spontaneous resolution within 2-3 weeks. (See Treatment and Medication.)

Patient Education

Instruct dyshidrotic eczema patients to avoid contact with certain allergens or irritants (eg, nickel), to follow a hand care routine that avoids irritants, and to use emollients regularly. In addition, inform individuals with this disorder about the difficulty of achieving successful treatment. For patient education information, see the Skin Conditions and Beauty Center, as well as Eczema (Atopic Dermatitis). (See Treatment and Medication.)


Patients report pruritus of the hands and feet with a sudden onset of vesicles. Burning pain or pruritus occasionally may be experienced before vesicles appear. Tiny vesicles erupt first along lateral aspects of the fingers and then on the palms or soles. Palms and soles may be red and wet with perspiration. The vesicles usually persist for 3-4 weeks. Vesicle outbreaks may occur in waves. A photo-induced form of hand dermatitis resembling dyshidrotic eczema has been described.[14]

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:

Two cases were reported of HIV-positive patients who developed dyshidrotic eczema as an immune reconstitution inflammatory syndrome shortly after highly active antiretroviral therapy.[21] Pompholyx has also been described as a manifestation of symptomatic HIV infection, including in individuals who do not respond to topical and systemic therapies and whose condition resolves only after the initiation of combination antiretroviral therapy.[22]

One publication provides an algorithm for the diagnosis of chronic hand dermatitis, which offers an easy way of classifying these conditions, helping in the decision making when choosing treatment modalities.[23]

Physical Examination

Symmetrical crops of clear vesicles and/or bullae on the palms and lateral aspects of the fingers characterize dyshidrotic eczema. The feet, the soles, and the lateral aspects of toes also may be affected. (See the images below.)

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Small tense vesicles on the fingers.

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Small, discrete, coalesced vesicles on the dorsal hand.

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Small, discrete, coalesced vesicles on the fingers.

In mildly affected patients, vesicles are present only on the lateral aspects of the fingers and, occasionally, involve feet and toes. (See the image below.)

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Small discrete vesicles of the lateral fingers.

Vesicles are deep seated and have a tapiocalike appearance, without surrounding erythema. They may become large, form bullae, and become confluent. Vesicles typically resolve without rupturing, followed by desquamation. (See the image below.)

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

In 80% of patients, only the hands are involved, while in 10% of patients, the disease affects only the feet, and in another 10% of patients, the hands and feet are involved together. (See the images below.)

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

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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.

Severity index

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.[24] 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 two clinical studies. Further evaluation with larger patient groups is needed.


Secondary bacterial infection of dyshidrotic eczema vesicles or bullae can result in cellulitis, lymphangitis, and septicemia (rare). Dystrophic nail changes may develop, with the occurrence of transverse ridging, thickening, discoloration, and pitting. Dyshidrotic eczema has no associated mortality, although some severe cases can become debilitating. A 2015 study determined that dyshidrosis is a risk factor in the development of herpes zoster.[25]

Approach Considerations

The diagnosis of dyshidrotic eczema is usually made clinically, although bacterial culture and sensitivity tests exclude secondary infection. Blood tests are not usually ordered; however, immunoglobulin E levels are commonly elevated.

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

Use patch testing to exclude allergic contact dermatitis. Measuring thiopurine methyltransferase levels allows accurate dosing of azathioprine. Systemic evaluation is recommended in recalcitrant cases, including serology for human T-cell lymphotrophic virus type 1 (HTLV1), which can rule out dyshidrosis-like variant of adult T-cell leukemia/lymphoma.[30] 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 to 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.

Approach Considerations

In dyshidrotic eczema, typical first-line treatment includes high-strength topical steroids and cold compresses. Short courses of oral steroids are the second line of treatment for acute flares, and other immunosuppressants have also been tried. Corticosteroids are cornerstones of topical therapy. Guidelines have been established by the National Institute of Clinical Evidence.[31] Calcineurin inhibitors may also be effective.[32]

Variable effects have been reported using oral administration of psoralen and subsequent exposure to long-wavelength UV light (PUVA) therapy. Topical photochemotherapy with 8-methoxypsoralen is probably as effective as systemic photochemotherapy or high-dose UVA-1 irradiation. For recalcitrant cases, corticosteroids are combined with immunosuppressants.

An evolving treatment seems to be the intradermal injection of onabotulinumtoxinA. Probiotics have been suggested as a potential treatment for eczema.[33] Topical khellin and natural sunlight therapy have been suggested for patients with recalcitrant palmoplantar pompholyx.[34] Tap water iontophoresis with pulsed direct current may be helpful as adjuvant treatment.[35]

Excellent results have been reported with the use of oxybutynin in two patients with coexistent hyperhidrosis and dyshidrotic eczema.[36] Further studies are needed before recommending this treatment modality.

Identification of the causes of stress and the use of stress management techniques as adjuncts may be helpful in some patients. Biofeedback therapy for stress reduction has succeeded in some individuals.

Treatment for bullae

The following treatment is appropriate if bullae are present:


Bed rest 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.


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


Consultation with a psychologist may be helpful for stress reduction using biofeedback therapy and other techniques.[37] Consultation with an allergist may be helpful for oral provocation tests 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.

Ultraviolet A Light

Paradoxically, although sometimes linked as a possible cause, UVA or UVA-1 alone or with oral or topical psoralen has been used in treatment. Hand and/or foot UVA therapy (UVA or UVA-1 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.[38, 39]

Topical application of 8-methoxypsoralen plus UVA (bath-PUVA) has been demonstrated to be the preferred method for the treatment of dyshidrotic eczema, compared with oral PUVA.[40] Local, narrow-band UVB has been shown to be as effective as bath-PUVA in patients with chronic hand eczema of dry and dyshidrotic types.[41]


Topical corticosteroids are the mainstay of treatment. Typically, use class I steroids initially, then class II or III steroids. Ointments penetrate the skin better than creams do, although 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 administered for severe episodes. Tapering of prednisone can follow intramuscular treatment. Schedule follow-up and check blood pressure 1 week after initiating prednisone.

Calcineurin Inhibitors

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,[42] and long-term occlusive therapy has also been determined to be efficacious, particularly in persons with severe dyshidrotic eczema.[42]

Advantages of topical calcineurin inhibitors over topical corticosteroids include the lack of development of tachyphylaxis, telangiectasias, and thinning and atrophy of the skin.[43] Personal experience of the coauthor has shown effective control with topical calcineurin inhibitor therapy alone in several patients followed in her practice. Note that topical calcineurin inhibitors can exacerbate irritant hand dermatitis.


OnabotulinumtoxinA injections may be helpful in some patients. OnabotulinumtoxinA 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 their Dyshidrotic Eczema Area and Severity Index scores and faster reductions of pruritus and vesiculation.[43] In another study, 7 of 10 vesicular pompholyx patients achieved good to very good responses after the injection of OnabotulinumtoxinA alone, with a reduction of pruritus.[44]

Immunosuppressive Agents

For severe refractory pompholyx, azathioprine, methotrexate,[45] mycophenolate mofetil, cyclosporine,[46] or etanercept may be helpful. In one study, etanercept was administered subcutaneously to a 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.[47] Consider measuring thiopurine methyltransferase levels, which may help to guide azathioprine therapy. Accurate dosing avoids toxicity and underdosing.

Nickel Chelators and Khellin

Nickel chelators, such as disulfiram (Antabuse), occasionally are used in nickel-sensitive patients who demonstrate a positive oral provocation test.[48]

Khellin, a furanochromone similar to methoxypsoralen, may be used in combination with photochemotherapy (sun exposure) for recalcitrant palmoplantar cases.[34] Khellin, unlike other psoralens, does not induce skin phototoxicity (erythema) and hyperpigmentation of healthy skin after UVA radiation therapy.


Alitretinoin (9-cis retinoic acid) activates the retinoid X receptor and all retinoic receptors. In one study, alitretinoin treatment produced significant clinical improvements in patients with chronic hand dermatitis, but it was not effective specifically against dyshidrotic eczema. The randomized, double-blind, placebo-controlled, multicenter trial involved 319 patients with chronic hand dermatitis (70 with pompholyx) that was refractory to standard therapy. Oral alitretinoin was administered at doses of 10 mg, 20 mg, or 40 mg once daily 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) in the patient group as a whole, no difference was noted in the patients with pompholyx compared with placebo.[43, 49]

However, evidence from another study indicated that alitretinoin is effective against dyshidrotic eczema In this investigation, 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.[50]

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,[51] photoaging,[52] pyogenic granuloma,[53] and cutaneous T-cell lymphoma.[54] Currently, alitretinoin 1% gel has not been used for the topical treatment of pompholyx.

Three phase III studies (1 open-label study and 2 double-blind, randomized, controlled trials) evaluated the safety[55] and efficacy[56] of once-daily oral alitretinoin at 10 mg or 30 mg versus placebo in 1032 patients with chronic hand eczema, including pompholyx, in whom treatment with potent topical corticosteroids had failed.

According to physician assessment, "clear" or "almost-clear" status was achieved in up to 48% of patients in the alitretinoin groups and 17% in the placebo group. Median percentage reduction in disease symptoms was 75%. Alitretinoin at 30 mg had faster responses (median 85 d) than did placebo (median 141 d). Among complete responders who relapsed, 80% in the alitretinoin groups responded to the same alitretinoin dose and 8-10% of patients in the placebo group responded to retreatment with placebo.

Common adverse effects included headache, flushing, erythema, and xerosis. Headache was the most common adverse effect with alitretinoin at 30 mg. Also in the treatment group, dry skin, dry eyes, dry mouth, dry lips, and cheilitis were reported in 10% of patients, compared with 4% of patients in the placebo group. Lipid abnormalities were similar to those seen with other retinoids.

A phase III trial--a randomized, double-blind (subject, investigator), placebo-controlled, parallel-assignment, safety/efficacy study--has been conducted on the treatment of chronic hand dermatitis (including pompholyx) using oral alitretinoin at 30 mg/d (1 capsule) for up to 24 weeks.[57] Results are not yet available.

Additional Agents

Potential agents for the treatment of pompholyx, such as topical bexarotene, systemic alitretinoin, leukotriene receptor antagonists, leukotriene synthesis inhibitors, phosphodiesterase-4 inhibitors, and monoclonal antibodies, have been 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).


For nickel-sensitive patients, consider a low-nickel diet for 3-4 weeks. However, 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.[17]

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.[3] Some patients have reported improvement by avoiding foods rich in heavy metal salts.

Medication Summary

Dyshidrotic eczema treatment can be quite challenging because of the severe inflammatory process that can be involved and because of frequent recurrences. Pharmacologic treatment begins with high-strength, topical corticosteroids. In recalcitrant cases, systemic corticosteroids are the next line of treatment. Two case reports also note some success with other immunosuppressants (eg, methotrexate, mycophenolate mofetil).

The long-term efficacy of occlusive therapy with pimecrolimus (Elidel), a topical calcineurin inhibitor, was reported in patients with severe dyshidrosiform hand and foot eczema.[42] However, the authors recommend caution in the extended use of calcineurin inhibitors.

In March 2005, the US Food and Drug Administration (FDA) issued a public health advisory to inform healthcare professionals and patients about a potential cancer risk from the use of pimecrolimus.[58, 59, 60] This concern is based on information from animal studies, case reports in a small number of patients, and knowledge of how drugs in this class work. Human studies of 10 years or longer may be needed to determine if pimecrolimus administration is linked to cancer. In the meantime, because this risk is uncertain, the FDA advises that pimecrolimus be used only in patients in whom other prescription treatments have failed or cannot be tolerated. This information reflects the FDA’s preliminary analysis of data concerning this drug.

Other treatment options include onabotulinumtoxinA injections and a topical form known as bexarotene gel, as well as plant-based pharmaceuticals; new types of anti-inflammatory oral drugs, such as leukotriene inhibitors and phosphodiesterase-4 (PDE4) inhibitors; and phototherapy with high-dose UVA-1 and UV-free phototherapy.[43]

Clobetasol (Temovate, Clobex, Cormax, Olux)

Clinical Context:  Clobetasol is for severe episodes. It is a class I superpotent topical steroid; it suppresses mitosis and increases the synthesis of proteins that decrease inflammation and cause vasoconstriction.

Fluocinonide (Vanos)

Clinical Context:  Fluocinonide is a class II steroid. It has high potency and, like all topical steroids, possesses anti-inflammatory, antipruritic, and vasoconstrictive properties.


Clinical Context:  This immunosuppressant is used in the treatment of autoimmune disorders. It is a potent anti-inflammatory agent that has salt-retaining properties and varied metabolic effects. Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) activity.

A glucocorticoid, prednisone is readily absorbed from gastrointestinal tract. It is used as second-line pharmacologic treatment for dyshidrotic eczema.

Betamethasone (Celestone, Diprolene, Luxiq)

Clinical Context:  Betamethasone is used for severe, acute episodes. It has a rapid onset (within 1 h) and a 72-hour duration. It can be administered for inflammatory dermatosis that is responsive to steroids. It decreases inflammation by suppressing the migration of PMN leukocytes and reversing capillary permeability.

Triamcinolone (Aristospan, Kenalog)

Clinical Context:  Triamcinolone is for inflammatory dermatosis that is responsive to steroids; it decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. This agent has a long duration (4-6 wk).

Class Summary

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

Topical corticosteroids are the first-line therapy. Steroid potency choice is based on the patient's response to treatment; however, the higher-strength steroids are usually necessary for disease control.

Tacrolimus topical (Protopic)

Clinical Context:  Tacrolimus topical is used for short-term treatment or for intermittent, long-term treatment in unresponsive or intolerant cases. It inhibits T-lymphocyte activation. Some patients may benefit from tacrolimus topical or pimecrolimus. Patients may achieve disease control with topical calcineurin inhibitors alone. Tacrolimus topical is available in a 0.03% and a 0.1% ointment.

Pimecrolimus cream (Elidel)

Clinical Context:  Pimecrolimus cream is used for short-term treatment or for intermittent, long-term treatment in unresponsive or intolerant cases. It is available in a 1% cream.

This was the first nonsteroid cream approved in the United States for mild to moderate atopic dermatitis. It is derived from ascomycin, a natural substance produced by the fungus Streptomyces hygroscopicus var. ascomyceticus. Pimecrolimus cream selectively inhibits the production and release of inflammatory cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids. Pimecrolimus cream is indicated only after other treatment options have failed.

Methotrexate (Rheumatrex, Trexall)

Clinical Context:  Methotrexate has an unknown mechanism of action in the treatment of inflammatory reactions; it may affect immune function. Methotrexate ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). It is an antimetabolite that inhibits deoxyribonucleic acid (DNA) synthesis and cell reproduction in malignant cells; it may suppress immune system. A satisfactory response is seen within 3-6 weeks following the administration of methotrexate. Adjust the dose gradually to attain a satisfactory response.

Azathioprine (Imuran, Azasan)

Clinical Context:  Azathioprine antagonizes purine metabolism and inhibits the synthesis of DNA, ribonucleic acid (RNA), and proteins. It may decrease the proliferation of immune cells, thus lowering autoimmune activity.

Cyclosporine (Neoral. Gengraf, Sandimmune)

Clinical Context:  Cyclosporine is a 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 the dosing on ideal body weight.

Class Summary

These agents are for the treatment of severe, acute episodes.


Clinical Context:  Dicloxacillin binds to 1 or more penicillin-binding proteins, which, in turn, inhibits the synthesis of bacterial cell walls. This agent is used for infections caused by penicillinase-producing staphylococci. It may be used to initiate therapy when staphylococcal infection is suspected

Cephalexin (Keflex)

Clinical Context:  Cephalexin is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms. The drug's primary activity is against skin flora; it is used for skin infections and for prophylaxis in minor procedures.

Erythromycin (E.E.S., Erythro RX, Ery-Tab)

Clinical Context:  Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl transfer RNA (tRNA) from ribosomes, causing RNA-dependent protein synthesis to arrest. It is used for the treatment of staphylococcal and streptococcal infections.

Age, weight, and the severity of infection determine the proper dosage in children. When twice-daily dosing is desired, one half of the total daily dose may be taken every 12 hours. Double the dose for more severe infections.

Class Summary

Antibiotics are used for dyshidrosis with secondary impetiginization.

Loratadine (Claritin, Alavert, Loradamed)

Clinical Context:  This is a nonsedating agent that selectively inhibits peripheral histamine H1 receptors.

Hydroxyzine (Vistaril)

Clinical Context:  Hydroxyzine antagonizes H1 receptors in the periphery. It has sedating qualities and may suppress histamine activity in the subcortical region of the central nervous system (CNS).

Pramoxine topical (Pramosone, Zypram, Epifoam)

Clinical Context:  This is a topical antihistamine and mild anti-inflammatory. It blocks nerve conduction and impulses by inhibiting the depolarization of neurons. This agent is available alone or as a 1% or 2.5% cream or ointment. It is available over the counter as Prax.

Class Summary

Antihistamines are used to treat pruritus associated with dyshidrosis. Desloratadine (Clarinex) is a long-acting, tricyclic histamine antagonist that is selective for the H1 receptor. It is a major metabolite of loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine. The dose for adults and children over age 12 years is 5 mg by mouth daily. Decrease the dose in hepatic impairment. Data are 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.

Disulfiram (Antabuse)

Clinical Context:  Disulfiram is a thiuram derivative that interferes with aldehyde dehydrogenase. It is for patients with severe, vesicular hand dermatitis who are highly allergic to nickel. The chelating effect of disulfiram helps to reduce the body's nickel burden in individuals who are allergic to nickel. Do not administer this drug if the patient has ingested alcohol within last 12 hours. Disulfiram is supplied as a 250-mg tablet.

Class Summary

These minimize the effects of nickel in eczema.


Sadegh Amini, MD, Dermatologist, Hollywood Dermatology; Voluntary Assistant Professor, Department of Dermatology and Cutaneous Surgery, University of Miami, Leonard M Miller School of Medicine; Staff Member, Department of Dermatology, Jackson Memorial Hospital

Disclosure: Nothing to disclose.


Anne E Burdick, MD, MPH, Professor of Dermatology, Director of Leprosy Program, Associate Dean for TeleHealth and Clinical Outreach, University of Miami, Leonard M Miller School of Medicine

Disclosure: Nothing to disclose.

Camila K Janniger, MD, Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, Rutgers New Jersey Medical School

Disclosure: Nothing to disclose.

Specialty Editors

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Disclosure: Nothing to disclose.

Paul Krusinski, MD, Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Naked Biome<br/>Received income in an amount equal to or greater than $250 from: Elsevier; WebMD<br/>StatPearls; Editor.

Additional Contributors

Kevin P Connelly, DO, Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University School of Medicine; Medical Director, Paws for Health Pet Visitation Program of the Richmond SPCA; Pediatric Emergency Physician, Emergency Consultants Inc, Chippenham Medical Center

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Ivan D Camacho, MD, Julie K Keck, MD, and James D Korb, MD, to the development and writing of the source articles.


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

Multiple tense vesicles on the palm.

Small tense vesicles on the fingers.

Small, discrete, coalesced vesicles on the dorsal hand.

Small, discrete, coalesced vesicles on the fingers.

Small discrete vesicles of the lateral fingers.

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. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.

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

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 palm. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.

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.

Small tense vesicles on the fingers.

Small, discrete, coalesced vesicles on the dorsal hand.

Small, discrete, coalesced vesicles on the fingers.

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.