A 34-year-old white woman.
The patient was seen in consultation regarding a 1-month history of erythematous papules and bullae on the palms and soles. Associated intense pruritus was noted. Initial treatment with an over-the-counter antifungal cream was unsuccessful. The eruption worsened despite treatment with a first-generation cephalosporin and acyclovir, as provided by her primary care physician. There were no reported exposures to toxins, irritants, or potential allergens. The patient was on no other medications, vitamins, or supplements.
On examination, the patient demonstrated tense vesicular lesions on the lateral aspects of the digits of the hands and feet and also on the palmoplantar surfaces (Figure 1). These vesicles terminated abruptly at the wrists and ankles (Figure 2). There was little involvement of the dorsal surfaces. No targetoid lesions were noted. The conjunctiva and oral and genital mucosa were within normal limits. No other cutaneous abnormalities were noted on examination.

Figure 1. Courtesy of Whitney A. High, MD

Figure 2. Courtesy of Whitney A. High, MD
The most likely diagnosis is dyshidrotic dermatitis/pompholyx. Dyshidrotic dermatitis was first described by Tilbury Fox in 1873.[1] Typically, dyshidrotic dermatitis produces chronic hand dermatitis, often with the formation of minute vesicles on the lateral aspects of the digits ("tapioca pearls"). Despite the name, aberrant sweat gland function is not involved.
In 1876, Sir Jonathon Hutchinson described essentially the same condition but in a more explosive form and called the condition "pompholyx."[2] Some experts prefer to use the term "pompholyx" in reference to abrupt, primarily vesicular disease. Other experts use the terms "dyshidrotic dermatitis" and "pompholyx" interchangeably, fully embracing the spectrum of disease.
In the chronic form, dyshidrotic dermatitis is a relatively common condition. A large investigation in Sweden documented a prevalence of 0.05% in the general population.[3] In patients with existing hand dermatitis, dyshidrotic dermatitis may comprise 3% to 20% of all cases.[3,4]
Overall, hand dermatitis is more common in women, but dyshidrotic dermatitis may afflict men or women of any age. Classically, it has been taught that dyshidrotic dermatitis is more prevalent among those with atopy.[5] Other investigators have recently contested this teaching, finding no association with atopy above that expected in the general population.[6]
The diagnosis of dyshidrotic dermatitis may be made using the history and clinical characteristics. It is characterized by symmetric vesicular eruptions on the palms, soles, or lateral aspects of the digits. Either the palms, the soles, or both surfaces may be involved. Sharp circumscription at the wrists or ankles is common. Associated pruritus is intense. A waxing and waning course is common. Those with severe eruptions consisting of large bullae often experience less frequent exacerbations.[7]
A biopsy is not often necessary to make the diagnosis. If a biopsy is performed, the primary pathologic process identified is that of spongiotic dermatitis with an associated superficial perivascular lymphocytic infiltrate. The vesicular nature of the eruption is merely the phenotypic expression of severe spongiosis (epidermal edema) on acral skin with a thickened stratum corneum.[8] Dyshidrotic dermatitis is not a vesicular eruption in the same sense as an autoimmune bullous dermatosis.
Multiple investigations have examined the relationship between dyshidrotic dermatitis and nickel allergy. Although some studies have demonstrated an increased rate of cutaneous allergy to nickel among those afflicted with dyshidrotic dermatitis,[5,9] other studies have not demonstrated this association.[6,10] Flares of dyshidrotic dermatitis have been associated with nickel ingestion, even among those without cutaneous sensitivity to nickel.[11] Indeed, nickel-free diets have been reported to improve dyshidrotic dermatitis in some patients.[12]
Bullous pemphigoid. Bullous pemphigoid can involve the palms and soles, but this disorder is more common among the elderly, especially in those with multiple comorbidities. Such a diagnosis would be unlikely in an otherwise healthy young woman. Bullous pemphigoid would also probably involve additional areas of the body and would not be likely to be confined to the palms and soles.
Erythema multiforme. Classic erythema multiforme consists of targetoid eruptions affecting distal acral skin. It represents an immunologic reaction, most commonly to infection with herpes simplex. While central vesiculation may occur with erythema multiforme, targetoid lesions are lacking in this case, as is evidence of an eruption of herpes simplex.
Pemphigus vulgaris. Pemphigus vulgaris is an intraepidermal blistering disorder that most commonly begins in the oral mucosa. Difficulty eating "sharp" solid foods (eg, tortilla chips) is often noted weeks before other skin lesions develop. Pemphigus vulgaris is also unlikely to involve only the palms and soles.
Stevens-Johnson syndrome. Stevens-Johnson syndrome is a blistering disorder that results in epidermal sloughing. Although the diagnostic criteria for Stevens-Johnson syndrome are not universally accepted, nearly all schemas require involvement of 1 or 2 mucous membranes. Stevens-Johnson syndrome would not likely be confined to acral skin.
Conservative treatment measures include the identification of any aggravating factors, such as coincidental exposure to irritants. Generous use of emollients is important for maintaining an effective skin barrier.[13] Hand moisturizers containing 1% dimethicone are particularly valuable in the management of dyshidrotic dermatitis.
Topical corticosteroids are used as first-line treatment for dyshidrotic dermatitis. Ointments are considered generally superior due to greater penetration and an absence of preservatives.[13] When treating the thick skin of the palms and soles, potent or superpotent agents are necessary, particularly early on, with tapering to mid-potency agents as control is achieved. Occlusion may be used initially to increase penetration of the topical agent.[14]
Topical immunomodulators, such as tacrolimus and pimecrolimus, have been reported to be successful in the treatment of dyshidrotic dermatitis; however, these agents may not be potent enough to treat severe cases or cases involving the particularly thick plantar surface.[15]
Abrupt and severe eruptions, classically referred to as pompholyx, may require oral corticosteroids. Starting doses of prednisone range from 40 to 100 mg/day, with tapering after control is achieved.[16] Although dramatic improvement is often noted, use of oral steroids is limited by significant side effects, including osteoporosis, cataract formation, hypertension, hyperglycemia, immunosuppression, and endocrine abnormalities.
Other medical treatments for severe and recalcitrant disease include methotrexate, azathioprine, cyclosporine, mycophenolate mofetil, dapsone, thalidomide, and biologic TNF-alpha inhibitors (eg, etanercept).
Radiotherapy with nonionizing radiation (ultraviolet A [UVA] and ultraviolet B [UVB]) or ionizing radiation (superficial x-ray, Grenz ray, and mega-voltage therapy) has been used in severe cases. Of these interventions, psoralen with UVA (PUVA) has been studied most thoroughly. Topical and oral psoralen may be used. Smokers may have a lower success rate with PUVA therapy using a topical psoralen.[17]
While controversial, a nickel-free diet has been demonstrated to improve dyshidrotic dermatitis and decrease recurrences in some patients. However, a nickel-free diet is quite restrictive and requires a highly motivated patient. For example, canned foods of any kind are not permitted on such a diet. Chelating agents, such as disulfiram and diethyldithiocarbamate, have also been used with some limited success.[18]
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Whitney A. High, MD
Assistant Professor of Dermatology and Dermatopathology, Department of Dermatology, University of Colorado Health Sciences Center, Denver, Colorado
Disclosure: Whitney A. High, MD, has disclosed no relevant financial relationships.
Kristin M. Richardson
Editorial Director, Diabetes & Endocrinology, Medscape
Disclosure: Kristin M. Richardson has disclosed no relevant financial relationships.