Question

Discussion

The answer is D: Grover’s disease. Grover’s disease, or transient acantholytic dermatosis, was first described in 1970.¹ It is characterized by pruritic papules and vesicles, usually occurring on the chest, back, and thighs. The lesions tend to be transient, lasting from days to weeks, but in some instances may persist for several years. The diagnosis is based on the histopathologic findings of focal acantholysis on skin biopsy.¹ A superficial dermal infiltrate of eosinophils, lymphocytes, and histiocytes also may be present.

Grover’s disease is more common in older white men. The etiology and pathogenesis remain unclear, but a number of local and systemic causes or triggers are linked with this condition. Often, the lesions have been initiated or exacerbated by sunlight.² The timing and distribution of the lesions suggest that ultraviolet radiation may be a trigger, but sunlight is not likely to be the sole mechanism because the condition is uncommon compared with other manifestations of solar damage. Excessive heat or sweating also may be a factor in the initiation of Grover’s disease.³

Associations with various malignancies have been suggested; however, this is more likely to be coincidental because of the typical age distribution of Grover’s disease.² This disease may be a reaction to cutaneous infections. Infectious etiologies that have been implicated are Malassezia furfur, Demodex folliculorum, and Sarcoptes scabiei.⁴ Currently, the role of these organisms in the development of Grover’s disease is highly speculative.

Statistically significant associations have been noted between transient acantholytic dermatosis and asteatotic eczema, allergic contact dermatitis, atopic dermatitis, and nonspecific irritation.⁵ The Koebner phenomenon (manifestation of skin disease at the site of skin damage) appears to account for most of these associations. These findings of nonspecific irritation leading to the appearance of new lesions suggest that the patient’s skin responds in a genetically determined fashion; however, a genetic basis for Grover’s disease has not been proven.²

The treatment of Grover’s disease usually is symptomatic because the disease often resolves spontaneously. Patients should be advised to avoid strenuous exercise and excessive exposure to ultraviolet radiation. Soothing baths with emollient bath oils or colloidal oatmeal are used to decrease the pruritus and may slow the formation of new lesions. Treatments of topical glucocorticoids under plastic occlusion are prescribed to relieve the pruritus.² If the eruption is severely pruritic and extensive, despite less aggressive therapy, systemic therapy with oral glucocorticoids may be indicated.² Phototherapy with ultraviolet B radiation or psoralen plus ultraviolet A also may be useful, although the mechanism is unknown.²

Grover’s disease can vary in clinical appearance, making the differential diagnosis potentially extensive. Because eruptions may appear similar to acne, impetigo, irritant dermatitis, herpes zoster, scabies, seborrheic dermatitis, or many other conditions, a reasonable suspicion for Grover’s disease often is needed to reach the diagnosis.² The lesions of candidiasis could present as erythematous papules and pustules; however, the distribution is usually in intertriginous areas or under areas of occlusion. In patients who have been bedridden, candidiasis should be considered. The lesions of a morbilliform drug eruption are characteristically maculopapular and not limited to the trunk. Furthermore, an association with a new medication would be typical.

The lesions of folliculitis may look similar to those of Grover’s disease because the distribution is often truncal. A biopsy would help differentiate the two diseases. Darier’s disease (keratosis follicularis) is a genetic skin disorder typically presenting in the teenage or young adult years as persistent eruptions of crusted papules. Often these are confluent and in a seborrheic distribution. Palmoplantar pits and nail abnormalities also are typical.⁶