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By Manisha Patel and Steve Feldman, M.D., Ph.D.
A52-year-old Caucasian male presented with a history of an intense pruritic eruption, which began after he started exercising. When asked, he reported he hadn’t experienced any fever, chills, upper respiratory symptoms or arthralgias. Upon examination, we found scattered, discrete lesions limited to his trunk. In addition to typical seborrheic keratoses and cherry angiomata, small reddish papules with scale were present (see photo). Biopsy results confirmed our diagnosis of Grover’s disease. Diagnosing the Condition A diagnosis of Grover’s disease requires histological findings. The diagnosis is best supported by the presence of several different patterns of acantholysis in the same biopsy, occupying very small, circumscribed foci. Immunofluorescence and immuno-histochemical studies haven’t demonstrated consistent patterns of positivity in the disease nor elucidated the etiology. Pathology The microscopic appearance of the skin eruptions suggests that disordered keratinization plays an important role in the pathogenesis of this disorder. In patients with Grover’s disease, you’ll see the characteristic epidermal change of acantholysis — the separation of individual epidermal keratinocytes from their neighbors. Chalet et al. described four main patterns of acantholysis: - Darier-White/keratosis follicularis-type lesion. Separation occurs in a suprabasal location, and the epidermis exhibits marked dyskeratosis. - Pemphigus-like lesion. Acantholysis predominately occurs in the suprabasal location. - Hailey-Hailey/familial benign chronic pemphigus-like lesion. Separation occurs throughout most layers of the stratum malpighii, resulting in the formation of small intraepidermal clefts. - Spongiotic lesion with acantholytic cells. Dermal changes include superficial perivascular infiltrate of lymphocytes and histiocytes and occasional scattered eosinophils. Treatment In mild cases, patients can often see improvement by avoiding heat- and sweat-inducing activities. In addition, class II topical glucocorticoids under occlusion and antipruritics are often effective. Severe cases generally respond to systemic glucocorticoids, however relapse is frequent once steroid therapy ends. Severe cases have been successfully treated with synthetic retinoids and PUVA therapy.

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