Grover's disease, also known as transient acantholytic dermatosis, was first described by Grover nearly 40 years ago. It's an idiopathic pruritic eruption of small vesicles and erythematous papules, classically on the central chest. Although it can resolve on its own, some patients endure multiple recurrences for years.
Most patients are over age 50, with most cases occurring in the 5th and 6th decades. It may be more common in Caucasians and in males. Grover's disease has been linked to several forms of dermatitis such as contact, asteatotic (dry skin), and atopic. Cases may spike in the winter.
The pathogenesis of Grover’s disease is largely unknown. It can be provoked and aggravated by heat, especially sweating (see Table 1). Friction and dry skin also make this condition worse. Hospitalization with bedrest longer than two weeks is a classic trigger. Excess sunlight may also aggravate Grover’s disease.
Grover’s disease chiefly involves the trunk, particularly the central chest, upper abdomen, and upper back. Rarely, proximal upper extremities are affected.
In these locations, there are numerous discrete erythematous or skin-coloured fragile vesicles and papules. Lesions quickly become crusted and hyperkeratotic papules, especially after scratching.
Patients often complain of severe itch, sometimes affecting sleep. Pruritus can be more severe than the cutaneous findings would suggest, but occasionally lesions are asymptomatic.
Grover’s disease can be acute or chronic, lasting from weeks to months. In some patients, lesions may persist or recur over years.
Grover’s disease should be distinguished from other causes of erythematous non-follicular papules such as miliaria (occlusion of sweat glands). It can be hard to discern whether lesions are follicular or not, so folliculitis may have to be considered. Other differential causes of pruritic erythema include scabies and bites. Rare causes of crusted lesions on the central chest include Darier’s disease, Galli-Galli disease and pemphigus foliaceus.
Grover’s disease is mainly a clinical diagnosis. Further tests are rarely needed. A biopsy can be diagnostic but it may be hard to distinguish Grover’s from Darier’s, and pemphigus. In Grover’s, however, direct immunofluorescence (DIF) testing will be negative. DIF requires a separate biopsy from perilesional skin and involves checking for the presence of self-reactive antibodies. Routine histological findings in Grover’s disease include acantholysis — separation and rounding up of keratinocytes — with dyskeratosis, abnormal keratinization of keratinocytes in the epidermis.
Treatment of Grover’s disease can be challenging, but in many cases simple behavioural modifications and topical agents can provide relief (see Table 2).
Instruct patients to avoid overheating and excessive sun exposure. Fevers should be controlled. Grover’s has been known to resolve upon hospital discharge, as bed rest under occlusive sheets is a common trigger.
Pruritus and any associated dry skin can be managed by avoiding harsh soaps and excessive bathing. Patients should bathe in lukewarm water, applying moisturizers afterwards and frequently throughout the day. Topical ointments or creams containing •% menthol or •% camphor are soothing. Wet compresses can also be tried. Antihistamines help relieve symptoms of pruritus.
Also, consider topical corticosteroids. Mid-potency steroids — e.g. betamethasone valerate 0.1% — are good initial options, especially to reduce itch. Topical immunomodulators — e.g. topical pimecrolimus and tacrolimus — can also help, without the atrophy associated with prolonged steroid use.
Another option includes topical calcipotriol unguent twice daily for 3-4 weeks. Try alternating with topical steroids to improve efficacy and decrease irritation. Topical retinoids are rarely used due to skin irritation.
If topical agents aren’t helping and symptoms are severe, a short course of oral corticosteroids is sometimes used to provide initial relief. Although they may suppress itch and inflammation, expect recurrences and rebound upon discontinuation. Systemic retinoids are reserved for resistant cases. They need careful monitoring, though, as side effects range from dry skin, eyes, and mucous membranes to more severe adverse reactions such as teratogenicity, hepatotoxicity, elevated triglycerides, and pseudotumour cerebri. One option might be isotretinoin 40 mg p.o. daily for 1-3 months.
Other possible options for treating severe cases include dapsone, though efficacy is questionable. Phototherapy — e.g. Psoralens plus ultra-violet A light, two treatments weekly, for 2-3 months — may be effective, but can initially worsen the disease.
John Kraft, Md, is in his third year of the Dermatology Residency Program at the University of Toronto.