eMedicine Specialties > Dermatology > Reactive & Inflammatory Dermatoses

Vesicular Palmoplantar Eczema

Author: Wingfield Rehmus, MD, MPH,
Coauthor(s): Carol E Cheng, Boston University School of Medicine
Contributor Information and Disclosures

Updated: Oct 30, 2009

Introduction

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 ("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.
  • 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 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. Similarly, although certain triggers have been associated with the development or worsening of symptoms, how these triggers cause flares has not been elucidated.

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

Frequency

United States

The frequency of vesicular palmoplantar eczema 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 of vesicular palmoplantar eczema often requires lifelong treatment and results in considerable disability.

Sex

The male-to-female ratio for vesicular palmoplantar eczema 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

History

The severity of vesicular palmoplantar eczema 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 vesicular palmoplantar eczema. An absence of erythema is often an important clinical feature in the acute and chronic forms.

Pompholyx of the palms.

Pompholyx of the palms.

Pompholyx of the palms.

Pompholyx of the palms.


  • Acute episodes are characterized by a sudden onset of small, clear vesicles or bullae that are said to be sagolike or tapiocalike 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 vesicular palmoplantar eczema. A study of an autosomal dominant form of pompholyx found a genetic linkage on chromosome 18.1 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.2

  • 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, 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.
    • Photosensitivity to ultraviolet A (UVA) has been reported as an etiologic factor in a small subset of patients with eczema.3,4 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.
  • Sensitivity to certain metals, particularly nickel and cobalt, has been linked to vesicular palmoplantar eczema.
  • Exogenous factors causing allergic contact pompholyx include balsams and cosmetic and hygiene products.5
  • Drugs responsible for inducing episodes include oral contraceptive pills and aspirin. Palmoplantar eczema occurring after intravenous immunoglobulin (IVIG) therapy is reported.6
  • Fungal infections, particularly tinea pedis, are most commonly implicated in id reactions. Bacterial infections play a role in both causation and in secondarily infecting lesions.
  • Cigarette smoking may reduce the efficacy of topical therapy with psoralen and UVA (PUVA) and has been itself, linked to pompholyx.
  • 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.7,8

More on Vesicular Palmoplantar Eczema

Overview: Vesicular Palmoplantar Eczema
Differential Diagnoses & Workup: Vesicular Palmoplantar Eczema
Treatment & Medication: Vesicular Palmoplantar Eczema
Follow-up: Vesicular Palmoplantar Eczema
Multimedia: Vesicular Palmoplantar Eczema
References

References

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Further Reading

Keywords

vesicular palmoplantar eczema, pompholyx, dyshidrotic eczema, vesicobullous dermatitis, dyshidrosis, subacute vesiculosquamous eczema, chronic relapsing vesiculosquamous eczema, hand eczema

Contributor Information and Disclosures

Author

Wingfield Rehmus, MD, MPH, 
Wingfield Rehmus, MD, MPH is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Carol E Cheng, Boston University School of Medicine
Disclosure: Nothing to disclose.

Medical Editor

James J Nordlund, MD, Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine
James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey J Miller, MD, Associate Professor of Dermatology, Penn State University College of Medicine; Staff Dermatologist, Penn State Milton S Hershey Medical Center
Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Association of Professors of Dermatology, North American Hair Research Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

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

Chief Editor

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

 
 
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