Vesicular Palmoplantar Eczema

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Background

Vesicular palmoplantar eczema is a term used to describe a group of diseases characterized by a pruritic vesiculobullous eruption involving mainly the hands and feet. Clinical presentations range from acute dermatitis to more chronic relapsing and remitting disease patterns. The diversity of presentation has created challenges in classifying hand eczema. In an effort to meet these challenges, one publication assembled an algorithm for chronic hand eczema that was based on etiology, morphology and clinical features.[1]

Although considerable overlap exists in the various forms of vesicular palmoplantar eczema, the disease can be roughly divided into the following four distinct categories[2] :

Pompholyx (Greek for "blister" or "bubble") may be further subdivided into vesicular and bullous forms, in which patients present with acute severe eruptions of blisters over their palms and, less commonly, the soles.

Chronic vesiculosquamous eczema, also called dyshidrotic eczema, was initially thought to be caused by abnormal functioning of the sweat glands. This association has since been disproved, but the term dyshidrotic eczema is still used. Patients with this variant present with small (1-2 mm) vesicles on nonerythematous skin involving the inner sides of the fingers or on the palms and soles. The vesicles are pruritic, last 1-2 weeks, desquamate, and then recur at unpredictable intervals.[2]

The chronic hyperkeratotic variety involves mainly the central palms, where it causes thickening and fissures. This category is notoriously the most difficult to treat.[2]

An id reaction refers to a widespread eczematous eruption in response to a distal focus of infection. Common manifestations include a papulovesicular eruption with vesicles on the hands and feet secondary to a fungal infection (dermatophytid).[2]

Despite the wide range of clinical presentations, all four types of vesicular palmoplantar eczema are histologically characterized by features of dermatitis, such as spongiosis and exocytosis.

Pathophysiology

Vesicular palmoplantar eczema is often thought to have an unidentified intrinsic cause. Although many etiologic factors are described, the underlying pathology of vesicular palmoplantar eczema is unknown. One study examined the roles of aquaporin 3 and aquaporin 10, which are water/glycerol channel proteins located in the epidermis, and concluded that overexpression of these channels may play a role.[3]

Similarly, although certain triggers have been associated with the development or worsening of symptoms such as atopy, contact allergy, and psychological stress, how these triggers cause flares has not been elucidated.[2]

Vesicular palmoplantar eczema results in histologic evidence of dermatitis, such as spongiosis, which is often accompanied by lymphocytic infiltrates.

Etiology

The etiology of hand eczema is unknown, but most observers suggest that intrinsic changes in the skin are responsible for vesicular palmoplantar eczema. A 2012 study of an autosomal dominant form of pompholyx found a genetic linkage on chromosome 18.[4] Whether other forms have a similar genetic linkage is not clear. However, several exogenous factors have been implicated in the causation or worsening of vesicular palmoplantar eczema.

Coexisting atopy is common in patients with palmoplantar eczema. A study found a strong association between pompholyx and atopic status.[5] However, this is by no means the only causal relationship, because many patients have no history of atopy. In a univariate analysis, personal and family history of atopy, history of eczema, hyperhidrosis, and tinea pedis were the main factors associated with pompholyx cases.[6]

Emotional stress may also trigger episodes.

Seasonal changes seem to be directly related to relapses, in that episodes are most common in the spring and summer months. Warm weather has been known to initiate episodes, with several cases of photoinduced pompholyx reported. Although dysfunction of the sweat glands is no longer accepted as the cause of dyshidrotic eczema, increased sweating seems to exacerbate the condition, and many patients with palmar hyperhidrosis also have coexisting dyshidrotic eczema. Hyperhidrosis can be an aggravating factor in as many as 40% of patients with pompholyx eczema.[7]

Photosensitivity to ultraviolet (UV) A (UVA) has been reported as an etiologic factor in a small subset of patients with eczema.[8] This suggests that the worsening of the disease in summer months may be due to the increase in exposure to sunlight. On the other hand, UVA therapy is a widely accepted form of treatment for palmoplantar eczema.[9]

Sensitivity to certain metals, particularly nickel and cobalt, has been linked to vesicular palmoplantar eczema.It has been suggested that low zinc levels may play a role. A 2016 prospective case-noncase study examining serum levels of cadmium and zinc noted a significant decrease in zinc levels in cases of vesicular palmoplantar eczema as compared with the noncase group. The exact role of zinc in the pathogenesis of vesicular palmoplantar eczema remains unknown but may be related to the impact of deficient states on inflammation.[10]

Exogenous factors causing allergic contact pompholyx include balsams and cosmetic and hygiene products.[11]

A 2013 study showed an increase in immunoglobulin E (IgE) levels and vesicular palmar eczema after house dust mite exposure.[12]

Drugs responsible for inducing episodes include oral contraceptive pills and aspirin.

Palmoplantar eczema occurring after intravenous immunoglobulin (IVIG) therapy has been reported.[13]  A review of eczematous reactions linked with IVIG therapy cited pompholyx as occurring in 63.5% of the cases reported having an eczematous reaction.[9] Although most cases are seen in adults,[14] there have been occurrences in the pediatric population after IVIG administration for Kawasaki syndrome.[15]

The onset of palmoplantar eczema typically occurs within a few days of the first treatment and can recur when rechallenged. The mechanism of pompholyx induction is unknown but may be related to the dose, infusion rate, type of IVIG, and even possibly the underlying disease being treated.[16] The majority of IVIG-associated cases of vesicular eczema are observed in patients with neurologic disorders, including multiple sclerosis, Guillain-Barré syndrome, amyotrophic lateral sclerosis, motor neuron disease, and chronic inflammatory demyelinating polyradiculoneuropathy.[15]

Case reports have described palmoplantar pompholyx secondary to secukinumab therapy for psoriasis.[17, 18]

Fungal infections, particularly tinea pedis caused by Trichophyton rubrum, are most commonly implicated in id reactions. Bacterial infections play a role in both causation and in secondarily infecting lesions.

Cigarette smoking has been suggested as a pathogenetic factor in palmar eczema[19] and may also reduce the efficacy of topical therapy with psoralen and UVA (PUVA).[20]

HIV infection has been associated with pompholyx, with response to antiretroviral therapy; conversely, one case report described two HIV-positive patients who developed severe dyshidrotic eczema after starting antiretroviral treatment, probably as a consequence of an immune reconstitution inflammatory syndrome.[21, 22]

Epidemiology

US and international statistics

The frequency of vesicular palmoplantar eczema in the United States is unknown.

The worldwide incidence is also unknown, but vesicular palmoplantar eczema is probably responsible for 5-20% of all cases of eczema of the hand. The dyshidrotic pattern is most common.[23]  A 2012 study found that pompholyx accounted for 14% of all cases of hand eczema.[5]

Age- and sex-related demographics

Pompholyx most commonly occurs in patients aged 20-40 years, but it may occur in individuals of any age. Onset in patients younger than 10 years is unusual. The frequency of recurrent episodes of pompholyx decreases after middle age, though this is not true of the chronic vesicular and hyperkeratotic variants.

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

Prognosis

For mild cases of palmoplantar eczema, the prognosis is excellent. The more severe chronic hyperkeratotic variety of vesicular palmoplantar eczema (eczema tyloticum) often requires lifelong treatment and results in considerable disability.

Acute vesicular eczema (pompholyx) in both major and minor forms tends to occur intermittently or sporadically and becomes less common as patients age. Episodes are less frequent from middle age onward.[2]

For subacute and chronic forms of vesicular and hyperkeratotic eczema, which often persist for years, the prognosis is less satisfactory than it is for other forms.

Patient Education

For patient education resources, visit the Skin Conditions and Beauty Center. Also see the patient education article Eczema (Atopic Dermatitis).

History

The severity of vesicular palmoplantar eczema symptoms varies, ranging from mild discomfort to acute severe episodes. Patients rarely require hospitalization.

Classically, the eruption of vesicles is preceded by itching, burning, and prickling sensations in the palms and soles. Thereafter, small (1- to 2-mm) vesicles form, most commonly on the lateral sides of the fingers. In pompholyx, the central areas of the palms and soles may or may not be involved. Large vesicles can also develop and may coalesce to form confluent bullae. The lesions last for 2-3 weeks, after which spontaneous resolution generally occurs. Occasionally, large bullae may have to be aspirated. This phase is followed by desquamation.

Chronic forms typically recur, and episodes are more frequent during the spring and summer than in the fall and winter.

Physical Examination

Clinical signs depend on the stage and form of palmoplantar eczema.

Acute episodes of vesicular eczema are characterized by a sudden onset of small, clear vesicles or bullae that are said to be "sago grain‒like" or "tapiocalike" in appearance (see the image below). Vesicles and/or bullae are accompanied by severe, occasionally painful pruritus. Small vesicles may enlarge or become more confluent and present as large bullae (especially on the palms and soles). Vesicles and bullae subsequently dry out and resolve, usually without rupturing.



View Image

Pompholyx of the palms.

In most individuals, desquamation occurs 2-3 weeks after the onset of vesicles and bullae. In some patients, a milder recurrence follows the initial severe episode. Secondary infections (eg, impetigo, cellulitis, or lymphangitis) are possible in patients with recurrent hand eczema. Secondary nail changes (eg, dystrophic nails, irregular transverse ridging, pitting, thickening, discoloration) can also occur.

Subacute vesicular eczema tends to have a chronic relapsing course, with more vesiculation and more erythema in the acute phases than in later phases. Residual erythema or some dryness or scaling occurs in the less active phases. Fissures are common and painful sequelae.

The chronic hyperkeratotic variety results in severe itching accompanied by thickening and fissuring of the palm. This effect may decrease the mobility of the affected hand.

When id reactions occur on the hands, they typically involve the fingers and the palms. These reactions often resolve when the primary infection is treated.

Complications

Potential complications of vesicular palmoplantar eczema include secondary bacterial infections can occur, such as cellulitis, lymphedema, and, more rarely, bloodstream infection (BSI).[24]

Approach Considerations

The diagnosis of palmoplantar eczema is essentially a clinical one; however, studies may be helpful in excluding other disorders. The following may be considered:

Guidelines for diagnosis of hand eczema

A 2023 S2k guideline from a group of German medical societies made recommendations for the diagnosis of hand eczema (HE), including the following[27] :

Laboratory Studies

There are no laboratory studies specific to vesicular palmoplantar eczema. However, immunoglobulin E (IgE) levels may be elevated in patients with atopic dermatitis.[2]

Histologic Findings

Histologic features of vesicular palmoplantar eczema vary according to the stage of evolution of the disease. Usually, evidence suggests intracellular edema or spongiosis, lymphocytic infiltration of the epidermis, and intraepidermal vesicles or bullae in acutely affected persons. In chronically affected persons, spongiosis is present and often associated with epithelial proliferation and/or hyperkeratosis or psoriasiform epidermal hyperplasia. Dermis is often edematous, with a mixed perivascular inflammatory cell infiltrate.

Distinguishing between palmoplantar pustulosis and pompholyx can be challenging because the two conditions have similar histologic features. Studies aimed at differentiating the two entities have found thinning of rete ridges, foci of parakeratosis, and irregular epidermal hyperplasia to be more often associated with pompholyx.[28] A comparison of inflammatory mediator expression between pompholyx and palmoplantar pustulosis found that mRNA expression of granzyme B was increased in pompholyx, whereas expression of interleukin (IL)-8, and IL-17α was increased in palmoplantar pustulosis.[29] These may serve as immunologic markers in distinguishing palmoplantar pustulosis from pompholyx.

Approach Considerations

Several modalities of therapy are available for the treatment and control of vesicular palmoplantar eczema. The dyshidrotic eczema severity index (DASI), a standardized severity scale for palmoplantar eczema, has made it easier to compare the efficacy of various therapies in controlled clinical trials.[30]

Therapy should be chosen according to the type and severity of the condition. Whenever possible, eliminate known triggers. If pruritus is a problem, antihistamines (eg. hydroxyzine) can relieve some symptoms.

Guidelines for treatment of hand eczema

A 2023 S2k guideline from a group of German medical societies made recommendations for the treatment of hand eczema (HE), including the following[27] :

Medical Care

Topical therapy

First-line topical therapy for vesicular palmoplantar eczema includes high-potency glucocorticoids; second-line therapeutic options include topical calcineurin inhibitors, adjunctive keratolytics, calcipotriene, retinoids, and various combinations thereof.[2]

Topical high-potency glucocorticoids (eg, betamethasone dipropionate and clobetasol propionate) are the agents of choice. Ointment preparations are less irritating and can enhance drug delivery. Application of these medications under plastic and vinyl occlusion enhances their efficacy. However, this method may predispose the patient to secondary infection and to both local and systemic adverse effects of corticosteroids; therefore, it should be used only intermittently and never in the presence of coexisting infection.

Mild vesicular palmoplantar eczema may be controlled with the use of less potent corticosteroids (eg, betamethasone valerate, triamcinolone, or mometasone cream or ointment).

In the hyperkeratotic form of hand eczema, topical keratolytic agents such as salicylic acid and tar agents may be useful adjunctive therapies.

Acute, severe episodes of pompholyx benefit from rest, bland applications of wet soaks and compresses, and drying agents such as Burow solution. Occasionally, large blisters may have to be aspirated.

Topical calcineurin inhibitors (eg, topical tacrolimus 0.1% ointment and pimecrolimus) have been shown to be as effective as mometasone furoate in treating chronic relapsing eczema of the hands.[31] They may be used as steroid-sparing agents to treat resistant palmar eczema, with minimal systemic absorption or systemic effect.[32] When plantar eczema is being treated, other agents should be considered, because calcineurin inhibitor therapy is less effective on the soles of the feet than on the hands. The use of occlusion has also been shown to increase the efficacy of these agents.

A small open-label study demonstrated the efficacy of topical vitamin D3 derivatives (ie, calcipotriol and maxacalcitol) for the control of hyperkeratotic palmoplantar eczema.[33]

Systemic therapy

Systemic therapy for vesicular palmoplantar eczema includes steroids, immunosuppressive agents (eg, azathioprine[34] and cyclosporine), retinoids (eg, acitretin and alitretinoin), and psoralen plus ultraviolet (UV) A (PUVA).

Systemic glucocorticoids or intralesional steroids may be considered in acute episodes of vesicular palmoplantar eczema when local therapy fails. These agents are not helpful for long-term treatment, because of their potential for severe adverse effects.

Cyclosporine, mycophenolate mofetil, and methotrexate either alone or in combination with steroids may be used for severe, recalcitrant cases of vesicular palmoplantar eczema.[35, 36] They have also been tried as steroid-sparing agents in chronic relapsing eczema.

For hyperkeratotic eczema, aromatic retinoids (eg, acitretin), which help control hyperkeratosis, may be considered. These agents are best used in relatively low doses because of their adverse effects. Therapy may have to be continued indefinitely and is often accompanied by topical occlusive therapy with combined or alternating steroids and keratolytics (5-20% salicylic acid) or tar preparations.

Increasingly, the retinoid alitretinoin has been shown to be an effective and well-tolerated therapy for severe hand eczema.[37, 38] In a multicenter randomized controlled trial (RCT) examining severe chronic hand eczema, it was found to be superior to placebo, with 48% of patients achieving full or almost full resolution of signs and symptoms.[39] A 2012 observational study noted alitretinoin improved vesicular eczema in 47.9% of patients.[40]

An open-label study showed significant improvement with alitretinoin in dosages starting at 10 mg/day (increased to 30 mg/day as tolerated).[41] A later chart review showed alitretinoin to be a safe and tolerated medication in real-world practice for chronic hand dermatitis, which included hyperkeratotic and dyshidrotic hand eczema.[42]

In a case study, the use of etanercept yielded a 4-month remission of vesicular palmoplantar eczema, which was followed by relapse.[43]

Dupilumab, a monoclonal antibody used in the treatment moderate-to-severe atopic dermatitis, has shown positive results in case reports for dyshidrosis as well as hand dermatitis.[44, 45, 46, 47, 48]  A 2025 systematic review of dupilumab in chronic hand eczema by Asamoah found that it consistently improved symptoms and that improvements were observed across several subtypes of eczema.[49] ​  A systematic review and meta-analysis by Riva et al also documented effectiveness.[50] Determination of long-term effectiveness, optimal dosing strategies, and cost-effectiveness requires further research.

A case report by Parmar et al described successful treatment of severe dyshidrotic palmoplantar eczema with tralokinumab.[51]

A case report by Kiszla et al described successful treatment of dyshidrotic eczema with the Janus kinase (JAK) inhibitor upadacitinib.[52]

Phototherapy

Phototherapy—in particular, PUVA—is effective in dyshidrotic eczema for controlling disease and maintaining remission[53] ; however, the use of psoralen has been shown to pose a carcinogenic risk to the skin. Although UVA-1 is conventionally combined with psoralen for its photosensitizing effects, it has also shown success in treating palmoplantar eczema when used alone, with the advantage of avoiding the risk associated with psoralen.[54, 24]

PUVA can be administered orally or topically. In a study comparing the effectiveness of the two modalities, dyshidrotic eczema responded well to both oral and topical (bath) treatment, whereas hyperkeratotic eczema showed significantly better clearance with oral therapy than with topical (bath) PUVA.[55]

Narrowband UVB therapy has been shown to be as efficacious as PUVA therapy for dyshidrotic and "dry" types of hand eczema and can be used as an alternative to PUVA, with fewer adverse effects.[56] In accordance with the known immunosuppressive effect of UV radiation, one case report noted resolution of dyshidrotic eczema symptoms with repeated sunlight exposures (though recurrences were not reduced).[57]

Relatively few reports have described the role of narrowband UVB therapy in hyperkeratotic hand eczema. However, narrowband UVB has been used with some success in other hyperkeratotic disorders (eg, palmoplantar psoriasis). In a study comparing PUVA therapy with narrowband UVB therapy for palmoplantar psoriasis, significant improvement was achieved with both modalities, but PUVA was superior to narrowband UVB in reducing clinical severity scores.[58] Because UVA radiation penetrates more deeply into the skin than UVB radiation does, PUVA may be superior to UVB modalities for hyperkeratotic hand eczema.

Other therapies

Other reported treatment options for vesicular palmoplantar eczema have included intradermal injections of botulinum toxin A, x-ray therapy, iontophoresis, sympathectomy,[39] disulfiram (for nickel-induced disease), and (for patients with obstructive sleep apnea [OSA]) continuous positive airway pressure (CPAP).[59]

Botulinum toxin A is a potent neurotoxin that blocks the autonomic cholinergic fibers.[60, 61] In a small (N = 8) controlled left-right hand comparison study, it was shown to improve symptoms of itching and vesicular formation.[62] This therapy may be used alone or in combination with topical steroids. However, its mechanism of action in reducing the severity of palmoplantar eczema is disputed.

One proposed mechanism is disruption of the afferent nerve supply of the skin, which may reduce sweating, because sweat is known to exacerbate the condition. Another mechanism is the possible effect of the toxin on afferent nerve fibers. Blockade of the inflammatory process and inhibition of neuropeptides such as substance P via toxic effects may explain the reduction of pruritus in treated patients.

The inflammatory cells functioning in eczema are highly radiosensitive, and for this reason, x-ray irradiation has been employed to treat some patients with resistant chronic eczema of the hand when other treatments have not been successful. Grenz (Bucky) rays and superficial radiotherapy (RT) were popular treatments for chronic severe hand eczema in the 1980s; however, they have since decreased in popularity, more because of a lack of availability than because of the risk of carcinogenesis.

Superficial RT appears to have a higher success rate than Grenz ray therapy because of its deeper penetration into the skin.[63] One study reported excellent results with the use of superficial RT for palmoplantar eczema, though others have not.[64, 65] In any case, the potential risk associated with RT for a benign non-life-threatening disease must be recognized, and care must be taken to confirm via dosimetry that the maximum safe cumulative lifetime dose is not exceeded. One case report found external-beam megavoltage RT to be successful in treating this condition.

Disulfiram may be administered as a nickel-chelating agent in patients with known nickel sensitivity, but it should not be used in thiuram-sensitive patients.

A case report by Matin et al described a patient with OSA and dyshidrotic palmar eczema whose dermatitis resolved after being placed on a CPAP machine.[66] The authors speculated the resolution of the eczema may reflect the effects of increased tissue oxygenation and decreased circulating inflammatory factors associated with better sleep quality.

A case report by Markantoni et al showed improvement of relapsing dyshidrotic eczema when coexisting hyperhidrosis was treated with the anticholinergic oxybutynin.[67]

Id reactions tend to resolve with treatment of the primary infection. If secondary infection is suspected, systemic antibiotics should be considered. Suspicious lesions should be cultured.

Crisaborole is a small boron-based molecule that inhibits phosphodiesterase 4 (PDE4) and decreases intracellular cyclic adenosine monophosphate (cAMP). It leads to lowered release of cytokines and decreased inflammation. It has been demonstrated to have efficacy in the treatment of mild-to-moderate atopic dermatitis.[68] Its efficacy in vesicular palmoplantar eczema has not been established.

Diet

Maintaining a low-cobalt diet has been suggested as a means of decreasing the number of dyshidrotic eczema flares.[69]

Patients with established nickel sensitivity may benefit from nickel-free diets.

Prevention

Elimination of known exacerbating factors, though often difficult to accomplish, is crucial in preventing relapses of vesicular palmoplantar eczema.

Regular use of hand emollients and avoidance of frequent contact with irritants are important measrues for preventing flareups of vesicular palmoplantar eczema. In one study (N = 120), contact allergy was found to be responsible for 67.5% of cases of pompholyx eczema.[11]  All patients should be considered for patch testing to identify relevant allergens.

 

Consultations

Patients whose disease is not easily managed should be referred to a dermatologist because vesicular palmoplantar eczema is likely to be a lifelong disease (albeit intermittent in some patients).

Patients in whom a contact allergen is the suspected cause or who do not improve with therapy should be referred to a dermatologist for consideration of a patch test.[11]

Guidelines Summary

The following organizations have released guidelines for the management of hand eczema. Key diagnostic and treatment recommendations have been reviewed and integrated throughout the article:

Alitretinoin topical (Panretin)

Clinical Context: 

Tacrolimus ointment (Protopic)

Clinical Context: 

Pimecrolimus (Elidel)

Clinical Context: 

Prednisone (Deltasone, Prednisone Intensol, Rayos)

Clinical Context: 

Betamethasone topical (Alphatrex, BetaVal, Dermabet)

Clinical Context: 

Clobetasol (Clobex, Clobex Spray, Cormax)

Clinical Context: 

Halobetasol topical (Bryhali, Lexette, Ultravate)

Clinical Context: 

Mometasone topical (Elocon)

Clinical Context: 

Triamcinolone topical (Kenalog Orabase, Kenalog topical, Pediaderm TA)

Clinical Context: 

Azathioprine (Azasan, Imuran)

Clinical Context: 

Cyclosporine (Gengraf, Neoral, Sandimmune)

Clinical Context: 

Methotrexate (Jylamvo, Otrexup, Rasuvo)

Clinical Context: 

Mycophenolate (CellCept, MMF, Myfortic)

Clinical Context: 

Dupilumab (Dupixent)

Clinical Context: 

OnabotulinumtoxinA (Botulinum toxin, Botox, Botox Cosmetic)

Clinical Context: 

Methoxsalen (8MOP, Oxsoralen, Oxsoralen Ultra)

Clinical Context: 

Disulfiram (Antabuse)

Clinical Context: 

Acitretin (Soriatane (DSC))

Clinical Context: 

What is vesicular palmoplantar eczema?What is the pathophysiology of vesicular palmoplantar eczema?What is the prevalence of vesicular palmoplantar eczema in the US?What is the global prevalence of vesicular palmoplantar eczema?What are the sexual predilections of vesicular palmoplantar eczema?Which age groups have the highest prevalence of vesicular palmoplantar eczema?What is the prognosis of vesicular palmoplantar eczema?What causes vesicular palmoplantar eczema?Which clinical history findings are characteristic of vesicular palmoplantar eczema?Which physical findings are characteristic of vesicular palmoplantar eczema?What are the possible complications of vesicular palmoplantar eczema?Which conditions are included in the differential diagnoses of vesicular palmoplantar eczema?What are the differential diagnoses for Vesicular Palmoplantar Eczema?How is vesicular palmoplantar eczema diagnosed?Which histologic findings are characteristic of vesicular palmoplantar eczema?How is vesicular palmoplantar eczema treated?How are vesicular palmoplantar eczema flare-ups prevented?What is the role of topical therapy in the treatment of vesicular palmoplantar eczema?What is the role of systemic medications in the treatment of vesicular palmoplantar eczema?What is the role of phototherapy in the treatment of vesicular palmoplantar eczema?What potential treatments for vesicular palmoplantar eczema have been reported?What is the role of botulinum toxin A in the treatment of vesicular palmoplantar eczema?What is the role of x-ray irradiation in the treatment of vesicular palmoplantar eczema?What is the role of disulfiram in the treatment of vesicular palmoplantar eczema?What is the role of CPAP in the treatment of vesicular palmoplantar eczema?What is the role of antibiotics in the treatment of vesicular palmoplantar eczema?What is the role of crisaborole in the treatment of vesicular palmoplantar eczema?Which dietary modifications are used in the treatment of vesicular palmoplantar eczema?How is relapse of vesicular palmoplantar eczema prevented?Which specialist consultations are beneficial to patients with vesicular palmoplantar eczema?Which organizations have issued guidelines on vesicular palmoplantar eczema?What is the goal of drug treatment for vesicular palmoplantar eczema?Which medications in the drug class Psoralens are used in the treatment of Vesicular Palmoplantar Eczema?Which medications in the drug class Neuromuscular Blockers, Botulinum Toxins are used in the treatment of Vesicular Palmoplantar Eczema?Which medications in the drug class Interleukin Inhibitors are used in the treatment of Vesicular Palmoplantar Eczema?Which medications in the drug class Immunosuppressants are used in the treatment of Vesicular Palmoplantar Eczema?Which medications in the drug class Corticosteroids, Topical are used in the treatment of Vesicular Palmoplantar Eczema?Which medications in the drug class Corticosteroids are used in the treatment of Vesicular Palmoplantar Eczema?Which medications in the drug class Calcineurin Inhibitors are used in the treatment of Vesicular Palmoplantar Eczema?Which medications in the drug class Antineoplastics, Retinoids are used in the treatment of Vesicular Palmoplantar Eczema?

Author

Jessica Dunkley, MD, MHSc, CCFP, Resident Physician, Department of Dermatology, University of British Columbia Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Wingfield Rehmus, MD, MPH, Dermatologist, BC Children's Hospital, Vancouver, British Columbia

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Abbvie; Valeant Canada<br/> Received honoraria from Valeant Canada for advisory board; Received honoraria from Pierre Fabre for advisory board; Received honoraria from Mustella for advisory board; Received honoraria from Abbvie for advisory board.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven R Feldman, MD, PhD, Professor, Departments of Dermatology, Pathology and Public Health Sciences, and Molecular Medicine and Translational Science, Wake Forest Baptist Health; Director, Center for Dermatology Research, Director of Industry Relations, Department of Dermatology, Wake Forest University School of Medicine

Disclosure: Received honoraria from Amgen for consulting; Received honoraria from Abbvie for consulting; Received honoraria from Galderma for speaking and teaching; Received consulting fee from Lilly for consulting; Received ownership interest from www.DrScore.com for management position; Received ownership interest from Causa Reseasrch for management position; Received grant/research funds from Janssen for consulting; Received honoraria from Pfizer for speaking and teaching; Received consulting fee from No.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Carol E Cheng, MD, Assistant Clinical Professor of Dermatology, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Elaine Dupuis, MD, MBA, Resident Physician, Section of Dermatology, Department of Medicine, University of Calgary Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

References

  1. Molin S, Diepgen TL, Ruzicka T, Prinz JC. Diagnosing chronic hand eczema by an algorithm: a tool for classification in clinical practice. Clin Exp Dermatol. 2011 Aug. 36 (6):595-601. [View Abstract]
  2. Doshi DN, Cheng CE, Kimball AB. Vesicular palmoplantar eczema. Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K, eds. Fitzpatrick's Dermatology in General Medicine. 8th ed. New York: McGraw-Hill; 2012. Chap 16.
  3. Soler DC, Bai X, Ortega L, Pethukova T, Nedorost ST, Popkin DL, et al. The key role of aquaporin 3 and aquaporin 10 in the pathogenesis of pompholyx. Med Hypotheses. 2015 May. 84 (5):498-503. [View Abstract]
  4. Chen JJ, Liang YH, Zhou FS, Yang S, Wang J, Wang PG, et al. The gene for a rare autosomal dominant form of pompholyx maps to chromosome 18q22.1-18q22.3. J Invest Dermatol. 2006 Feb. 126 (2):300-4. [View Abstract]
  5. Handa S, Kaur I, Gupta T, Jindal R. Hand eczema: correlation of morphologic patterns, atopy, contact sensitization and disease severity. Indian J Dermatol Venereol Leprol. 2012 Mar-Apr. 78 (2):153-8. [View Abstract]
  6. Pitché P, Boukari M, Tchangai-Walla K. [Factors associated with palmoplantar or plantar pompholyx: a case-control study]. Ann Dermatol Venereol. 2006 Feb. 133 (2):139-43. [View Abstract]
  7. Nalluri R, Rhodes LE. Photoaggravated pompholyx. Photodermatol Photoimmunol Photomed. 2016 May. 32 (3):168-70. [View Abstract]
  8. Man I, Ibbotson SH, Ferguson J. Photoinduced pompholyx: a report of 5 cases. J Am Acad Dermatol. 2004 Jan. 50 (1):55-60. [View Abstract]
  9. Gerstenblith MR, Antony AK, Junkins-Hopkins JM, Abuav R. Pompholyx and eczematous reactions associated with intravenous immunoglobulin therapy. J Am Acad Dermatol. 2012 Feb. 66 (2):312-6. [View Abstract]
  10. Suvirya S, Thakur A, Pandey SS, Tripathi SK, Dwivedi DK. Altered Levels of Serum Zinc and Cadmium in Patients with Chronic Vesiculobullous Hand and Feet Dermatitis. Dermatol Res Pract. 2016. 2016:3284937. [View Abstract]
  11. Guillet MH, Wierzbicka E, Guillet S, Dagregorio G, Guillet G. A 3-year causative study of pompholyx in 120 patients. Arch Dermatol. 2007 Dec. 143 (12):1504-8. [View Abstract]
  12. Schuttelaar ML, Coenraads PJ, Huizinga J, De Monchy JG, Vermeulen KM. Increase in vesicular hand eczema after house dust mite inhalation provocation: a double-blind, placebo-controlled, cross-over study. Contact Dermatitis. 2013 Feb. 68 (2):76-85. [View Abstract]
  13. Uyttendaele H, Obadiah J, Grossman M. Dyshidrotic-like spongiotic dermatitis after intravenous immunoglobulin therapy. J Drugs Dermatol. 2003 Jun. 2 (3):337-41. [View Abstract]
  14. Kotan D, Erdem T, Acar BA, Boluk A. Dyshidrotic eczema associated with the use of IVIg. BMJ Case Rep. 2013 Feb 15. 2013:[View Abstract]
  15. Shiraishi T, Yamamoto T. Severe dyshidrotic eczema after intravenous immunoglobulin therapy for Kawasaki syndrome. Pediatr Dermatol. 2013 May-Jun. 30 (3):e30-1. [View Abstract]
  16. Brazzelli V, Grassi S, Savasta S, Ruffinazzi G, Carugno A, Barbaccia V, et al. Pompholyx of the hands after intravenous immunoglobulin therapy for clinically isolated syndrome: a paediatric case. Int J Immunopathol Pharmacol. 2014 Jan-Mar. 27 (1):127-30. [View Abstract]
  17. Peera M, Smith A. Palmoplantar pompholyx secondary to interleukin 17A inhibitor therapy for psoriasis: A case series. JAAD Case Rep. 2021 Jul. 13:46-48. [View Abstract]
  18. Eichhoff G. Secukinumab-induced pompholyx in a psoriasis patient. Dermatol Online J. 2020 Apr 15. 26 (4):[View Abstract]
  19. Meding B, Alderling M, Wrangsjö K. Tobacco smoking and hand eczema: a population-based study. Br J Dermatol. 2010 Oct. 163 (4):752-6. [View Abstract]
  20. Douwes KE, Karrer S, Abels C, Landthaler M, Szeimies RM. Does smoking influence the efficacy of bath-PUVA therapy in chronic palmoplantar eczema?. Photodermatol Photoimmunol Photomed. 2000 Feb. 16 (1):25-9. [View Abstract]
  21. Colebunders R, Zolfo M, Lynen L. Severe dyshidrosis in two patients with HIV infection shortly after starting highly active antiretroviral treatment. Dermatol Online J. 2005 Aug 1. 11 (2):31. [View Abstract]
  22. MacConnachie AA, Smith CC. Pompholyx eczema as a manifestation of HIV infection, response to antiretroviral therapy. Acta Derm Venereol. 2007. 87 (4):378-9. [View Abstract]
  23. Gill J, Pratt M. A Severe Case of Recalcitrant Pompholyx. J Cutan Med Surg. 2015 Sep-Oct. 19 (5):494-7. [View Abstract]
  24. Petering H, Breuer C, Herbst R, Kapp A, Werfel T. Comparison of localized high-dose UVA1 irradiation versus topical cream psoralen-UVA for treatment of chronic vesicular dyshidrotic eczema. J Am Acad Dermatol. 2004 Jan. 50 (1):68-72. [View Abstract]
  25. Burke O, Beer J, Elman SA. Mycosis Fungoides Palmaris et Plantaris Mimicking "Dyshidrotic Eczema": A Case Report. J Drugs Dermatol. 2024 Jul 1. 23 (7):569-570. [View Abstract]
  26. Solomon A, Cosgarea R, Ruzicka T, Braun-Falco M. Palmoplantar eczema as initial sign of mycosis fungoides. J Eur Acad Dermatol Venereol. 2016 Nov. 30 (11):e124-e125. [View Abstract]
  27. [Guideline] Bauer A, Brans R, Brehler R, Büttner M, Dickel H, Elsner P, et al. S2k guideline diagnosis, prevention, and therapy of hand eczema. J Dtsch Dermatol Ges. 2023 Sep. 21 (9):1054-1074. [View Abstract]
  28. Yoon SY, Park HS, Lee JH, Cho S. Histological differentiation between palmoplantar pustulosis and pompholyx. J Eur Acad Dermatol Venereol. 2013 Jul. 27 (7):889-93. [View Abstract]
  29. Kim DY, Kim JY, Kim TG, Kwon JE, Sohn H, Park J, et al. A comparison of inflammatory mediator expression between palmoplantar pustulosis and pompholyx. J Eur Acad Dermatol Venereol. 2013 Dec. 27 (12):1559-65. [View Abstract]
  30. Vocks E, Plötz SG, Ring J. The Dyshidrotic Eczema Area and Severity Index - A score developed for the assessment of dyshidrotic eczema. Dermatology. 1999. 198 (3):265-9. [View Abstract]
  31. Schnopp C, Remling R, Möhrenschlager M, Weigl L, Ring J, Abeck D. Topical tacrolimus (FK506) and mometasone furoate in treatment of dyshidrotic palmar eczema: a randomized, observer-blinded trial. J Am Acad Dermatol. 2002 Jan. 46 (1):73-7. [View Abstract]
  32. Schurmeyer-Horst F, Luger TA, Bohm M. Long-term efficacy of occlusive therapy with topical pimecrolimus in severe dyshidrosiform hand and foot eczema. Dermatology. 2007. 214 (1):99-100. [View Abstract]
  33. Egawa K. Topical vitamin D3 derivatives in treating hyperkeratotic palmoplantar eczema: a report of five patients. J Dermatol. 2005 May. 32 (5):381-6. [View Abstract]
  34. Scerri L. Azathioprine in dermatological practice. An overview with special emphasis on its use in non-bullous inflammatory dermatoses. Adv Exp Med Biol. 1999. 455:343-8. [View Abstract]
  35. Egan CA, Rallis TM, Meadows KP, Krueger GG. Low-dose oral methotrexate treatment for recalcitrant palmoplantar pompholyx. J Am Acad Dermatol. 1999 Apr. 40 (4):612-4. [View Abstract]
  36. Pickenäcker A, Luger TA, Schwarz T. Dyshidrotic eczema treated with mycophenolate mofetil. Arch Dermatol. 1998 Mar. 134 (3):378-9. [View Abstract]
  37. Diepgen TL, Pfarr E, Zimmermann T. Efficacy and tolerability of alitretinoin for chronic hand eczema under daily practice conditions: results of the TOCCATA open study comprising 680 patients. Acta Derm Venereol. 2012 May. 92 (3):251-5. [View Abstract]
  38. Lakshmi C, Srinivas CR. Hand eczema: an update. Indian J Dermatol Venereol Leprol. 2012 Sep-Oct. 78 (5):569-82. [View Abstract]
  39. Ruzicka T, Lynde CW, Jemec GB, Diepgen T, Berth-Jones J, Coenraads PJ, et al. Efficacy and safety of oral alitretinoin (9-cis retinoic acid) in patients with severe chronic hand eczema refractory to topical corticosteroids: results of a randomized, double-blind, placebo-controlled, multicentre trial. Br J Dermatol. 2008 Apr. 158 (4):808-17. [View Abstract]
  40. Diepgen TL, Pfarr E, Zimmermann T. Efficacy and tolerability of alitretinoin for chronic hand eczema under daily practice conditions: results of the TOCCATA open study comprising 680 patients. Acta Derm Venereol. 2012 May. 92 (3):251-5. [View Abstract]
  41. Tan J, Maari C, Nigen S, Bolduc C, Bissonnette R. Open-label exploratory study of acitretin for the treatment of severe chronic hand dermatitis. J Dermatolog Treat. 2015. 26 (4):373-5. [View Abstract]
  42. Crowley EL, Sayeau RL, Gooderham MJ. An Update on the Use of Alitretinoin for Chronic Hand Dermatitis in a Dermatology Practice Setting. J Cutan Med Surg. 2018 Jan/Feb. 22 (1):102-103. [View Abstract]
  43. Ogden S, Clayton TH, Goodfield MJ. Recalcitrant hand pompholyx: variable response to etanercept. Clin Exp Dermatol. 2006 Jan. 31 (1):145-6. [View Abstract]
  44. Zirwas MJ. Dupilumab for hand eczema. J Am Acad Dermatol. 2018 Jul. 79 (1):167-169. [View Abstract]
  45. Weston GK, Hooper J, Strober BE. Dupilumab in the Treatment of Dyshidrosis: A Report of Two Cases. J Drugs Dermatol. 2018 Mar 1. 17 (3):355-356. [View Abstract]
  46. Oosterhaven JAF, Romeijn GLE, Schuttelaar MLA. Dupilumab Treatment of Very Severe Refractory Atopic Hand Eczema. JAMA Dermatol. 2018 Aug 1. 154 (8):969-970. [View Abstract]
  47. Nanda S, Nagrani N, MacQuhae F, Nichols A. A Case of Complete Resolution of Severe Plantar Dyshidrotic Eczema With Dupilumab. J Drugs Dermatol. 2019 Feb 1. 18 (2):211-212. [View Abstract]
  48. Gall RA, Peters JD, Brinker AJ. Two Cases of Recalcitrant Dyshidrotic Eczema Treated With Dupilumab. J Drugs Dermatol. 2021 May 1. 20 (5):558-559. [View Abstract]
  49. Asamoah N, Branyiczky MK, Almuqrin A, Alkhayal F, Sakka N, Bednar D, et al. Efficacy and safety of dupilumab in chronic hand eczema: a systematic review. Arch Dermatol Res. 2025 Feb 20. 317 (1):441. [View Abstract]
  50. Riva HR, Yoon T, Hendricks AJ, Malick H, Chisholm CD, Housewright CD, et al. Dupilumab for Chronic Hand Eczema: A Systematic Review and Meta-Analysis. Dermatitis. 2024 Nov 6. [View Abstract]
  51. Parmar NV, Hammadi AA. Successful treatment of dyshidrotic palmoplantar eczema with tralokinumab. Australas J Dermatol. 2024 Sep. 65 (6):e176-e177. [View Abstract]
  52. Kiszla BM, Orlowski TJ, Kole LCS. Efficacy and tolerance of upadacitinib in the treatment of dyshidrotic eczema. JAAD Case Rep. 2023 Aug. 38:141-143. [View Abstract]
  53. Bretterklieber A, Legat FJ, Wolf P, Hofer A. Retrospective long-term follow-up in patients with chronic palmoplantar dermatoses after good response to bath PUVA therapy. J Dtsch Dermatol Ges. 2012 Nov. 10 (11):814-8. [View Abstract]
  54. Behrens S, von Kobyletzki G, Gruss C, Reuther T, Altmeyer P, Kerscher M. PUVA-bath photochemotherapy (PUVA-soak therapy) of recalcitrant dermatoses of the palms and soles. Photodermatol Photoimmunol Photomed. 1999 Apr. 15 (2):47-51. [View Abstract]
  55. Tzaneva S, Kittler H, Thallinger C, Hönigsmann H, Tanew A. Oral vs. bath PUVA using 8-methoxypsoralen for chronic palmoplantar eczema. Photodermatol Photoimmunol Photomed. 2009 Apr. 25 (2):101-5. [View Abstract]
  56. Sezer E, Etikan I. Local narrowband UVB phototherapy vs. local PUVA in the treatment of chronic hand eczema. Photodermatol Photoimmunol Photomed. 2007 Feb. 23 (1):10-4. [View Abstract]
  57. Letić M. Use of sunlight to treat dyshidrotic eczema. JAMA Dermatol. 2013 May. 149 (5):634-5. [View Abstract]
  58. Sezer E, Erbil AH, Kurumlu Z, Taştan HB, Etikan I. Comparison of the efficacy of local narrowband ultraviolet B (NB-UVB) phototherapy versus psoralen plus ultraviolet A (PUVA) paint for palmoplantar psoriasis. J Dermatol. 2007 Jul. 34 (7):435-40. [View Abstract]
  59. Robertson L. New and existing therapeutic options for hand eczema. Skin Therapy Lett. 2009 Mar. 14 (3):1-5. [View Abstract]
  60. Swartling C, Naver H, Lindberg M, Anveden I. Treatment of dyshidrotic hand dermatitis with intradermal botulinum toxin. J Am Acad Dermatol. 2002 Nov. 47 (5):667-71. [View Abstract]
  61. Kontochristopoulos G, Gregoriou S, Agiasofitou E, Nikolakis G, Rigopoulos D, Katsambas A. Letter: regression of relapsing dyshidrotic eczema after treatment of concomitant hyperhidrosis with botulinum toxin-A. Dermatol Surg. 2007 Oct. 33 (10):1289-90. [View Abstract]
  62. Wollina U, Karamfilov T. Adjuvant botulinum toxin A in dyshidrotic hand eczema: a controlled prospective pilot study with left-right comparison. J Eur Acad Dermatol Venereol. 2002 Jan. 16 (1):40-2. [View Abstract]
  63. Fairris GM, Jones DH, Mack DP, Rowell NR. Conventional superficial X-ray versus Grenz ray therapy in the treatment of constitutional eczema of the hands. Br J Dermatol. 1985 Mar. 112 (3):339-41. [View Abstract]
  64. Cartwright PH, Rowell NR. Comparison of Grenz rays versus placebo in the treatment of chronic hand eczema. Br J Dermatol. 1987 Jul. 117 (1):73-6. [View Abstract]
  65. Lindelöf B, Wrangsjö K, Lidén S. A double-blind study of Grenz ray therapy in chronic eczema of the hands. Br J Dermatol. 1987 Jul. 117 (1):77-80. [View Abstract]
  66. Matin A, Bliwise DL, Wellman JJ, Ewing HA, Rasmuson P. Resolution of dyshidrotic dermatitis of the hand after treatment with continuous positive airway pressure for obstructive sleep apnea. South Med J. 2002 Feb. 95 (2):253-4. [View Abstract]
  67. Markantoni V, Kouris A, Armyra K, Vavouli C, Kontochristopoulos G. Remarkable improvement of relapsing dyshidrotic eczema after treatment of coexistant hyperhidrosis with oxybutynin. Dermatol Ther. 2014 Nov-Dec. 27 (6):365-8. [View Abstract]
  68. Paller AS, Tom WL, Lebwohl MG, Blumenthal RL, Boguniewicz M, Call RS, et al. Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. J Am Acad Dermatol. 2016 Sep. 75 (3):494-503.e6. [View Abstract]
  69. Stuckert J, Nedorost S. Low-cobalt diet for dyshidrotic eczema patients. Contact Dermatitis. 2008 Dec. 59 (6):361-5. [View Abstract]

Pompholyx of the palms.

Pompholyx of the palms.