Vesicular Palmoplantar Eczema

Updated: Oct 08, 2021
Author: Jessica Dunkley, MD, MHSc, CCFP; Chief Editor: Dirk M Elston, MD 



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 vary from acute dermatitis to more chronic relapsing and remitting disease patterns. The diversity of presentation has created challenges in classifying hand eczema. A 2011 publication assembled an algorithm for chronic hand eczema 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 four distinct categories: pompholyx, subacute or chronic relapsing vesiculosquamous eczema, chronic vesiculohyperkeratotic or hyperkeratotic eczema, and Id reactions.[2]

Pompholyx ("blister" or "bubble" in Greek) 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.


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 of Palmoplantar Eczema

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.[5]

Coexisting atopy is common in patients with palmoplantar eczema. A study found a strong association between pompholyx and atopic status.[6] 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.[7]

Emotional stress may also trigger episodes.

Seasonal changes seem to be directly related to relapses, as episodes are most common in the spring and summer months. Warm weather has been known to initiate episodes, with several cases reporting photo-induced pompholyx. 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 up to 40% of patients with pompholyx eczema.[8] Photosensitivity to ultraviolet A (UVA) has been reported as an etiologic factor in a small subset of patients with eczema.[9] Therefore, worsening of the disease in summer months may be due to the increase in exposure to sunlight. Conversely, UVA therapy is a widely accepted form of treatment for palmoplantar eczema.[10]

Sensitivity to certain metals, particularly nickel and cobalt, has been linked to vesicular palmoplantar eczema. Low zinc levels have been proposed to play a role. A 2016 prospective case-noncase study examining serum levels of cadmium and zinc noted a significant decrease in zinc levels in patients with vesicular palmoplantar eczema 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.[11]

Exogenous factors causing allergic contact pompholyx include balsams and cosmetic and hygiene products.[12]

A 2013 study showed an increase in IgE levels and vesicular palmar eczema after house dust mite exposure.[13]

Drugs responsible for inducing episodes include oral contraceptive pills and aspirin. Palmoplantar eczema occurring after intravenous immunoglobulin (IVIG) therapy is reported.[14]  Case reports have described palmoplantar pompholyx secondary to secukinumab therapy for psoriasis.[15, 16]

A review of eczematous reactions linked with intravenous immunoglobulin (IVIG) therapy cited pompholyx as occurring in 63.5% of the cases reported having an eczematous reaction.[10] While most cases are seen in adults,[17] there have been occurrences in the pediatric population after IVIG administration for Kawasaki syndrome.[18] The onset of palmoplantar eczema typically occurs within a few days of the first treatment and can reoccur 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.[19] The majority of IVIG-associated cases of vesicular eczema are observed in patients with neurologic disorders, including multiple sclerosis, Guillen-Barre syndrome, amyotrophic lateral sclerosis, motor neuron disease, and chronic inflammatory demyelinating polyradiculoneuropathy.[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[20, 21] and may also reduce the efficacy of topical therapy with psoralen and UVA (PUVA).[22]

HIV infection has been associated with pompholyx, with response to antiretroviral therapy; conversely, one case report describes of 2 HIV-positive patients who developed severe dyshidrotic eczema after starting antiretroviral treatment, thought to be due to an immune reconstitution inflammatory syndrome.[23, 24]



United States

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


The true incidence is 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[25] ; a 2012 study found pompholyx accounted for 14% of all cases of hand eczema.[6]


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


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, although this is not true of chronic vesicular and hyperkeratotic variants.


Patients with mild cases of palmoplantar eczema have an excellent prognosis. 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]

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

Patient Education

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




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

Classically, itching, burning, and prickling sensations of the palms and soles precede the eruption of vesicles. 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 need 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. 

Pompholyx of the palms. Pompholyx of the palms.

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


Secondary bacterial infections can occur, such as cellulitis, lymphedema, and, more rarely, septicemia.[26]



Diagnostic Considerations

The differential diagnosis for hand eczema can be broad. Consider other causes of dermatitis, papulosquamous disorders such as psoriasis, bullous diseases, drug reactions (eg, bullous and eczematous forms), infestations, and infections (especially with dermatophytes). Less common entities that can mimic hand dermatitis include mycosis fungoides[27, 28, 29] and keratodermas.

Differential Diagnoses



Approach Considerations

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

  • KOH staining of skin scrapings to rule out fungal infection, especially in hyperkeratotic forms of the disease

  • Swab and culture of suspected lesions to exclude secondary bacterial infection if infection is suspected

  • A biopsy to distinguish eczema from psoriasis or some forms of palmoplantar hyperkeratoses

  • Patch testing to exclude contact dermatitis or a systemic reaction to contact allergen

  • Allergy testing may suggest an atopic tendency

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

Histologic Findings

Histologic features vary according to the stage of the evolution vesicular palmoplantar eczema. 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, as they share similar histological features. Recent studies have looked at differentiating the two entities and found thinning of rete ridges, foci of parakeratosis, and irregular epidermal hyperplasia to be more often associated with pompholyx.[30] Further, a comparison of inflammatory mediator expression between pompholyx and palmoplantar pustulosis found increased mRNA expression of granzyme B in pompholyx. In contrast, interleukin (IL)–8, and IL-17α were increased in palmoplantar pustulosis.[31] These may serve as immunologic markers in distinguishing palmoplantar pustulosis from pompholyx.



Medical Care

Several modalities of therapy are available for the treatment and control of vesicular palmoplantar eczema. 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.

Preventative measures

Regular use of hand emollients and avoidance of frequent contact with irritants are important means to prevent flare-ups of vesicular palmoplantar eczema. Contact allergy has been noted in one study to be responsible for 67.5% of pompholyx eczema, and all patients should be considered for patch testing to identify relevant allergens.[12]

Topical therapy

First-line topical therapy for vesicular palmoplantar eczema includes high-potency glucocorticoids followed by second-line topical therapy options such as topical calcineurin inhibitors, adjunctive keratolytics, calcipotriene, and/or retinoids.[2]

Topical high-potency glucocorticoids, such as betamethasone dipropionate and clobetasol propionate, are first-line therapies. Ointment preparations are less irritating and can enhance drug delivery. As well, 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 should never be used in the presence of coexisting infection.

Patients with mild vesicular palmoplantar eczema may be controlled with the use of less potent corticosteroids such as betamethasone valerate, triamcinolone, or mometasone cream or ointment.

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

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

Topical calcineurin inhibitors, such as topical tacrolimus 0.1% ointment and pimecrolimus, have been shown to be as effective as mometasone furoate in the treatment of chronic relapsing eczema of the hands.[32] These topical immunomodulators may be used as steroid-sparing agents to treat resistant palmar eczema, with minimal systemic absorption or systemic effect.[33] Use of other agents should be considered when plantar eczema is being treated because this therapy is less effective on the soles of the feet than on the hands. The use of occlusion with these agents has also been shown to increase their efficacy.

A small open-label study demonstrated efficacy of topical vitamin D-3 derivatives (ie, calcipotriol, maxacalcitol) for the control of hyperkeratotic palmoplantar eczema.[34]

Systemic therapy

Systemic therapy includes steroids, immunosuppressive agents (eg, azathioprine,[35] cyclosporine), retinoids (eg, acitretin, alitretinoin), and PUVA.

Consider the use of systemic glucocorticoids or intralesional steroids in acute episodes of vesicular palmoplantar eczema when local therapy fails. These agents are not helpful for long-term treatment because of a 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.[36, 37] These therapies have also been tried as steroid-sparing agents in chronic relapsing eczema.

For hyperkeratotic eczema, consider the use of aromatic retinoids, such as acitretin, which help control hyperkeratosis. These agents are best used in relatively low doses because of adverse effects. Therapy may need to be continued indefinitely in cases of hyperkeratotic eczema 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 a favorable option for severe hand eczema. Oral alitretinoin has been shown to be an effective and well-tolerated therapy for treatment of severe hand eczema.[38, 39] One randomized, double-blind, placebo-controlled multicenter trial examining severe chronic hand eczema found alitretinoin superior to placebo, with 48% of patients achieving full or almost full resolution of signs and symptoms.[40] A 2012 observational study noted alitretinoin improved vesicular eczema in 47.9% of patients.[41] An open-label study showed significant improvement with alitretinoin at doses starting at 10 mg daily (increased to 30 mg daily as tolerated).[42] A more recent 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.[43]

The use of etanercept in a case study achieved a 4-month remission of vesicular palmoplantar eczema, which was followed by relapse.[44]

Dupilumab, a novel monoclonal antibody therapy for moderate-to-severe atopic dermatitis, has shown positive results in case reports for dyshidrosis as well as hand dermatitis.[45, 46, 47, 48, 49]


Phototherapy, in particular PUVA, has been shown to be effective in dyshidrotic eczema for disease control and maintaining remission.[50] However, the use of psoralen has been associated with carcinogenic risk of the skin. Although conventionally used with psoralen for its photosensitizing effects, UVA-1 alone has also shown success in treating palmoplantar eczema, with the advantage that it does not require psoralen.[51, 26] PUVA can be administered orally or topically. In a study comparing the effectiveness of the 2 modalities, dyshidrotic eczema responded well to both oral and topical (bath) treatment, while hyperkeratotic eczema cleared significantly better with oral therapy than with topical (bath) PUVA.[52]  

Narrowband UVB therapy has been shown to be equally 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.[53] As UV radiation has an immunosuppressive effect, one case noted resolution of dyshidrotic eczema symptoms with repeated sunlight exposures (although recurrences were not reduced).[54] Only a few reports describe the role of narrowband UVB therapy in hyperkeratotic hand eczema. However, narrowband UVB has been used with some success in other hyperkeratotic disorders like palmoplantar psoriasis. One study comparing PUVA therapy with narrowband UVB for palmoplantar psoriasis demonstrated significant improvement with both modalities. However, PUVA was superior to narrowband UVB in reducing clinical severity scores.[55] PUVA may be superior to UVB modalities for hyperkeratotic hand eczema because of the deeper penetration of UVA rays into the skin.

Other therapies

Other treatment options[56] for vesicular palmoplantar eczema that have been reported include treatment with intradermal injections of botulinum toxin A, x-ray therapy, iontophoresis, sympathectomy,[40] disulfiram for nickel-induced disease, and, in patients with obstructive sleep apnea, continuous positive airway pressure (CPAP).

Botulinum toxin A is a potent neurotoxin that blocks the autonomic cholinergic fibers.[57, 58] It has been shown to improve symptoms of itching and vesicular formation in a controlled left-right hand comparison study with 8 subjects.[59] This therapy may be used alone or in combination with topical steroids. However, the mechanism of action in reducing the severity of palmoplantar eczema is disputed. Some proposed mechanisms are a 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. One case report showed improvement of relapsing dyshidrotic eczema with treatment of coexisting hyperhidrosis with the anticholinergic oxybutynin.[60]

The inflammatory cells functioning in eczema are highly radiosensitive, and, therefore, x-ray irradiation has been used in some patients with resistant chronic eczema of the hand when other treatments have not been successful. Grenz rays and superficial radiotherapy were popular treatments for chronic severe hand eczema in the 1980s; however, they have currently decreased in popularity, mostly because of a lack of availability than because of the risk for potential carcinogenesis. Superficial radiation therapy appears to have a higher success rate than grenz ray therapy because of its deeper penetration into the skin.[61] One study revealed excellent results with the use of superficial radiation for palmoplantar eczema, while others have not.[62, 63] However, the potential risk of irradiation for a benign non–life-threatening disease must be recognized, and care must be taken not to exceed the maximum safe cumulative lifetime dose by using dosimetry. External-beam megavoltage radiation therapy was reportedly successful in treatment of this condition in one patient.

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

One case report describes a patient with obstructive sleep apnea and dyshidrotic palmar eczema whose dermatitis resolved after being placed on a CPAP machine. 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.[64]

Id reactions tend to resolve with treatment of the primary infection. Consider systemic antibiotics if secondary infection is suspected, and culture suspicious lesions.

Crisaborole is a novel boron-based small molecule that inhibits phosphodiesterase 4 and decreases intracellular cyclic adenosine monophosphate. 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.[65] Its efficacy in vesicular palmoplantar eczema has not been established.


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

If a contact allergen is suspected or if they do not improve with therapy, patients should be referred to a dermatologist for consideration of a patch test.[12]


Maintaining a low-cobalt diet has been suggested to decrease the number of dyshidrotic eczema flares.[66]

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


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



Guidelines Summary

The European Society of Contact Dermatitis published guidelines in the Journal of the German Society of Dermatology for diagnosis, prevention, and treatment of hand eczema, which include information on pompholyx.[67]



Medication Summary

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

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.[68]


Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the immune response of the body to diverse stimuli.

Betamethasone dipropionate topical (Diprolene)

Betamethasone dipropionate topical is for inflammatory dermatoses responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It affects the production of lymphokines and has inhibitory effect on Langerhans cells.

Clobetasol (Temovate, Olux-E, Temovate E, Cormax)

Clobetasol is a class I superpotent topical steroid; it suppresses mitosis and increases the synthesis of proteins that decrease inflammation and cause vasoconstriction.

Halobetasol (Ultravate)

Halobetasol is a class 1, superpotent topical steroid. It has antiinflammatory, antipruritic, and vasoconstrictive activity.


Prednisone is an immunosuppressant used to treat autoimmune disorders; it may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. It stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.

Calcineurin Inhibitors

Class Summary

Topical immunosuppressive agents, such as tacrolimus, have been successfully used to decrease the severity of chronic palmar eczema. These drugs may be used as steroid-sparing agents.

Tacrolimus topical (Protopic)

Tacrolimus topical reduces itching and inflammation by suppressing the release of cytokines from T cells; it inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha (all involved in early T-cell activation). Tacrolimus topical may inhibit the release of preformed mediators from skin mast cells and basophils; it may down-regulate FCeRI expression on Langerhans cells. It can be used in patients as young as 2 years. Drugs of this class more expensive than topical corticosteroids.  Tacrolimus is available in an ointment formulation.

Pimecrolimus (Elidel)

Pimecrolimus is a calcineurin inhibitor that has an anti-inflammatory effect through decreasing cytokine production. It leads to decreased expression of IL-3, IL-4, IL-5, and TNFα, and it inhibits mast cell and neutrophil activation. It is available in a cream formulation.


Class Summary

Beta-carotene derivatives have marked effects on keratinizing epithelia. Oral alitretinoin has been shown to be an effective and well-tolerated therapy for treatment of severe hand eczema.


Alitretinoin topical (Panretin)

Alitretinoin is a retinoic acid derivative. Its mechanism of action is thought to be through modulation of the immune system with reduction of inflammatory mediators involved in eczematous reactions. Alitretinoin is category X in pregnancy. Patients should avoid becoming pregnant for up to 2 years after drug administration.


Class Summary

These agents are used for severe acute episodes and as steroid-sparing agents in the chronic forms of the disease.

Azathioprine (Azasan, Imuran)

Azathioprine antagonizes purine metabolism and inhibits the synthesis of DNA, RNA, and proteins. It may decrease the proliferation of immune cells, resulting in low autoimmune activity. It is used in transplant recipients and some autoimmune conditions.

Cyclosporine (Gengraf, Neoral, Sandimmune)

Cyclosporine is a calcineurin inhibitor. It is a potent immunosuppressant and  is nonmyelotoxic but markedly nephrotoxic. It is widely used in organ and tissue transplantation and skin diseases (eg, psoriasis, atopic dermatitis).

Methotrexate (Rheumatrex, Trexall)

Methotrexate is an antimetabolite; it inhibits the enzyme dihydrofolate reductase, which is essential for purine and pyrimidine synthesis. It has an unknown mechanism of anti-inflammatory action. Folinic acid after methotrexate administration helps prevent methotrexate-induced mucositis or myelosuppression.

Mycophenolate (CellCept, Myfortic)

Mycophenolate is an immunosuppressant used to prevent acute rejection of renal or cardiac transplants. It inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis by lymphocytes, inhibiting their proliferation. It inhibits antibody production.


Class Summary

These drugs split into two molecules of sodium diethyldithiocarbamate after absorption, which, in turn, chelates divalent metal ions (eg, Ni++) and results in the increased urinary excretion of nickel. They are effective in the treatment of vesicular palmoplantar dermatitis in nickel-hypersensitive patients whose eczema is aggravated by an oral challenge with nickel.

Disulfiram (Antabuse)

Disulfiram is a thiuram derivative that interferes with aldehyde dehydrogenase. The chelating effect is helpful in reducing the nickel burden in patients allergic to nickel.

Dermatologics, Other

Class Summary

PUVA therapy is used to treat many skin conditions, including psoriasis, eczema, urticaria, mycosis fungoides, vitiligo, and palmoplantar pustular dermatoses.

The drug 8-methoxypsoralen (8-MOP) is taken 2 hours before exposure to UVA irradiation. The initial UVA irradiation dose of 0.5 J/cm2 is usually increased by 0.5 J/cm2 for approximately six treatments, then by 1 J/cm2 per treatment for a total of 25-35 treatments.

Local bath-PUVA therapy has been successful in treating palmoplantar eczema and psoriasis. Compared with systemic PUVA, local-bath therapy has several advantages, particularly the absence of phototoxicity, severe hyperpigmentation, and protracted photosensitivity. The drug 8-MOP in a 0.15% alcoholic solution is added to tap water (37°C) at a concentration of 1 mg 8-MOP/L (0.0001%). After a 15-minute bath, the palms or soles are exposed to UVA radiation.

Methoxsalen (Oxsoralen-Ultra, Uvadex, 8-MOP)

Methoxsalen inhibits mitosis by covalently binding to pyrimidine bases in DNA when photoactivated by UVA.

Interleukin Inhibitors

Dupilumab (Dupixent)

Dupilumab is a human monoclonal antibody against the IL-4 receptor alpha subunit. It is FDA approved for moderate-to-severe atopic dermatitis.


Questions & Answers


What is vesicular palmoplantar eczema?

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What are the differential diagnoses for Vesicular Palmoplantar Eczema?


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Which medications in the drug class Interleukin Inhibitors are used in the treatment of Vesicular Palmoplantar Eczema?

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