AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

Vesicular palmoplantar eczema is a term used to describe a group of diseases characterized by vesiculobullous eruption involving mainly the hands and feet. Clinical presentations vary from acute dermatitis to more chronic relapsing and remitting disease patterns.

Although considerable overlap exists in the various forms of vesicular palmoplantar eczema, the disease can be divided into 4 distinct categories: pompholyx, subacute or chronic relapsing vesiculosquamous eczema, chronic vesiculohyperkeratotic or hyperkeratotic eczema, and id reactions.

Pompholyx may be further subdivided into vesicular and bullous forms in which patients present with acute eruptions of blisters over their palms and soles. Chronic vesiculosquamous eczema, also called dyshidrotic eczema, was initially thought to be caused by abnormal function of the sweat glands. This association has since been disproved, but the term dyshidrotic eczema is still used. Patients with this variant present with vesicles involving the inner sides of the fingers. The chronic hyperkeratotic variety involves mainly the central palms, where it causes thickening and fissures. This category is notoriously the most difficult to treat. An id reaction refers to vesicular eruption of the hands, caused by a distal focus of infection, with fungal infections being the most common.

Despite the wide range of clinical presentations, all 4 types 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 is unknown. Similarly, though certain triggers have been associated with the development or worsening of symptoms, how these triggers cause flares has not been elucidated.

The disease results in histologic evidence of dermatitis, such as spongiosis, which is often accompanied by lymphocytic infiltrates.

Frequency

United States

The frequency in the United States is unknown.

International

The true incidence is unknown, but vesicular palmoplantar eczema is probably responsible for 5-20% of all cases of eczema of the hand.

Mortality/Morbidity

Patients with mild cases of pompholyx have an excellent prognosis. The more severe chronic hyperkeratotic variety often requires lifelong treatment and results in considerable disability.

Sex

The male-to-female ratio is 1:1.

Age

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.

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

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

• 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 develop on the palms and soles 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.
• Palmoplantar eczema typically recurs, and episodes are more frequent during the spring and summer than in the fall and winter.
• 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.

Physical

Clinical signs depend on the stage of disease. An absence of erythema is often an important clinical feature in the acute and chronic forms.

• Acute episodes are characterized by a sudden onset of small, clear vesicles or bullae that are said to be sago-like or tapioca-like in appearance (see Media File 1).
• • 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.
• A form of microvesicular palmar eczema also occurs in association with dry nummular (discoid) eczema.
• Hyperkeratotic palmar eczema is characterized by highly itchy, hyperkeratotic palms. Fissures in the folds of the hands and fingers are common and painful. Fissures can limit use of the hands.
• • Typically, chronic eczema affects the central area of the palm or the palmar aspect of the hands and fingers.
  • Only occasionally are vesicles visible on clinical examination, but spongiosis is found on histology.
• When they occur on the hands, id reactions typically involve the lateral sides of the fingers. These reactions often resolve when the primary infection is treated.

Causes

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

• Coexisting atopy is common in patients with palmoplantar eczema. This is by no means the only causal relationship because many patients have no history of atopy.
• 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.
• • Although dysfunction of the sweat glands is no longer accepted as the cause of dyshidrotic eczema, increased sweating seems to exacerbate the condition.
  • Photosensitivity to ultraviolet A (UVA)-1 has been reported as an etiologic factor in a small subset of patients with eczema. Therefore, worsening of the disease in summer months may be due to the increase in exposure to sunlight. UVA therapy is a widely accepted form of treatment for palmoplantar eczema.
• Sensitivity to certain metals, particularly nickel, has been linked to the condition.
• Other exogenous factors include balsams and various allergens in general.
• Drugs responsible for inducing episodes include oral contraceptive pills and aspirin. Palmoplantar eczema occurring after intravenous immunoglobulin therapy is reported.
• Bacterial infections play a role in both causation and in secondarily infecting lesions. Fungal infections are most commonly implicated in id reactions.
• Cigarette smoking may reduce the efficacy of topical therapy with psoralen and UVA (PUVA).

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Allergy (eg, benzoisothiazolines)
N-Isopropyl-N-phenyl-4-phenylenediamine (IPPD)
Occult fungal infection
Palmoplantar pustular psoriasis
Pustular bacterid
Keratolysis exfoliativa (focal palmar peelings, desquamation en aires)
Protein contact dermatitis
Chronic acral dermatitis
Pemphigoid/pemphigoid gestationis
Dyshidrosiform bullous pemphigoid
Epidermolysis bullosa
Autoimmune progesterone dermatitis
Keratoderma climactericum

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab Studies

• The diagnosis of palmoplantar eczema is essentially a clinical one, and laboratory tests are not routinely performed. However, laboratory studies may be helpful in excluding other disorders.
• Elevated serum immunoglobulin E levels or positive results on prick tests may suggest an atopic tendency.
• Skin scrapings can be used to exclude the presence of a fungus.
• Skin swabs may exclude bacterial infection.

Other Tests

• Perform KOH staining of skin scrapings to rule out fungal infection, especially in hyperkeratotic forms of the disease.
• Swab and culture suspected lesions to exclude secondary bacterial infection.

Procedures

• Perform patch tests to exclude contact dermatitis or a systemic reaction to contact allergen.
• Perform biopsy to distinguish eczema from psoriasis or some forms of palmoplantar hyperkeratoses.

Histologic Findings

Histologic features vary according to the stage of the evolution of 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.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical Care

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

• Topical therapy
• • Topical therapy includes high-potency glucocorticoids, Burow solution (aluminum acetate 1%, or potassium permanganate solution (1:8000 dilution), tacrolimus FK506, and/or PUVA.
  • Topical high-potency glucocorticoids, such as betamethasone valerate and clobetasol propionate, are first-line therapies. Application of these medications under plastic and vinyl occlusion enhances their efficacy. However, this method may predispose the patient to secondary bacterial or fungal 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 disease may be controlled with the use of less potent corticosteroids such as fluocinonide. 
  • 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.
  • Newer agents, such as topical tacrolimus and pimecrolimus, are just as effective at mometasone furoate in the treatment of chronic relapsing eczema of the hands. These topical immunosuppressants may be used as steroid-sparing agents to treat resistant palmar eczema, with minimal systemic absorption or systemic effect. Use of other agents should be considered when plantar eczema is being treated, as this therapy is less effective on the soles of the feet than on the hands. The use of occlusion with these agents has been shown to increase the efficacy as well.
  • A recent open-label study demonstrated efficacy of topical vitamin D-3 derivatives (ie, calcipotriol, maxacalcitol) for the control of hyperkeratotic palmoplantar eczema.
• Systemic therapy
• • Systemic therapy includes steroids, immunosuppressive agents (eg, azathioprine, cyclosporine), retinoids (including acitretin), and/or PUVA.
  • Consider the use of systemic glucocorticoids or intralesional steroids in acute episodes 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. These agents 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.
  • The use of etanercept in a case study achieved a 4-month remission, which was followed by relapse.
• Other treatment options include treatment with intradermal injections of botulinum toxin A, X-ray therapy, and disulfiram (Antabuse).
• • Botulinum toxin A has been shown to improve symptoms of itching and vesicular formation in controlled left-right comparison studies. 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, which is known to exacerbate the condition.
  • X-ray irradiation has been used in some patients with resistant chronic eczema of the hand. Take care not to exceed the maximum safe cumulative lifetime dose by using dosimetry. External-beam mega-voltage radiation therapy was reportedly successful in treatment of this condition in 1 patient. Typically, ionizing radiation is not used to treat hand eczema.
  • Disulfiram may be administered as a nickel-chelating agent in patients with known nickel sensitivity.
• Id reactions tend to resolve with treatment of primary infection.
• Consider systemic antibiotics if secondary infection is suspected.
• • Guard against group A beta-hemolytic streptococcal infection in particular because cellulitis, lymphangitis, and septicemia may occur.
  • Culture suspicious lesions.

Consultations

Refer patients to a dermatologist because vesicular palmoplantar eczema is likely to be a lifelong disease (albeit intermittent in some patients).

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The goals of pharmacotherapy 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.

Drug Category: Corticosteroids

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

Drug Category: Systemic immunosuppressives

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

Drug Category: Retinoids

Beta-carotene derivatives have marked effects on keratinizing epithelia. Etretinate often helps control hyperkeratosis in hyperkeratotic palmar eczema. Therapy may have to be continued indefinitely. The incidence of adverse effects tends to be high.

Drug Category: Nickel-chelating agents

These drugs split into 2 molecules of sodium diethyldithiocarbamate after absorption, which in turn, chelates divalent metal ions (eg, Ni⁺⁺) and results in the increased urinary excretion of nickel. Effective in the treatment of vesicular palmoplantar dermatitis in nickel-hypersensitive patients whose eczema is aggravated by oral challenge with nickel.

Drug Category: Phototherapy

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 h before exposure to UV-A irradiation. The initial UV-A irradiation dose of 2.5 J/cm² is usually increased by 0.5 J/cm² for approximately 6 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 UV-A radiation.

Drug Category: Topical immunosuppressives

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.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Deterrence/Prevention

• Elimination of known exacerbating factors, though often difficult to accomplish, is crucial in preventing relapses.
• Patients with established nickel sensitivity may benefit from nickel-free diets.

Prognosis

• 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.
• 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 excellent patient education resources, visit eMedicine’s Skin, Hair, and Nails Center. Also, see eMedicine’s patient education article Eczema.

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to investigate for other possible diagnoses, such as contact dermatitis, palmoplantar pustular psoriasis, and pustular bacterid is a pitfall.
• Failure to inform patients about the potential atrophy of the skin and/or increased risk of secondary infection that occurs with prolonged application of potent topical steroids is another pitfall. Consider potential systemic adverse effects, such as hyperglycemia, osteoporosis, and weight gain in patients receiving long-term treatment with systemic steroids.
• Failure to monitor and inform patients with recurrent episodes of the possible long-term effects of immunosuppressive drugs (eg, liver and kidney damage, increased risks of neoplasia) is another pitfall.

Special Concerns

• Vesicular and hyperkeratotic eczema is a major cause of disability and may result in long periods of sick leave.
• Provide emotional support and psychological counseling to patients, with particular sensitivity to the concerns and needs of patients and their families in view of the chronic nature of the disease.

ACKNOWLEDGMENTS

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, (1) Spiros Gramvussakis, MD; (2) John D Wilkinson, MBBS, MRCS, FRCP; and (3) Raeesa W Mirza, MD, MBBS, to the development and writing of this article.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  Pompholyx of the palms.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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• Schnopp C, Remling R, Mohrenschlager 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. Jan 2002;46(1):73-7. [Medline].
• 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. [Medline].
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• Uyttendaele H, Obadiah J, Grossman M. Dyshidrotic-like spongiotic dermatitis after intravenous immunoglobulin therapy. J Drugs Dermatol. Jun 2003;2(3):337-41. [Medline].
• Vocks E, Plotz 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. [Medline].
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Article Last Updated: Aug 30, 2007