AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Background

Transient acantholytic dermatosis is not an uncommon condition, but, surprisingly, it was not thoroughly characterized until Grover did so in 1970. While generally accepted to be a benign, self-limited disorder, it is often persistent and difficult to manage; hence, the description of transient is misleading. The presentation can be subtle, or it may closely resemble other pruritic dermatoses. A high index of suspicion for this disease is necessary if the diagnosis is to be made correctly. Furthermore, the histologic features of Grover disease closely resemble those of several other conditions that are clinically distinct, which may add to potential diagnostic confusion.

Pathophysiology

The etiology of Grover disease is unknown. However, a number of factors have been suggested as being potentially causal or exacerbating. The most frequent association is with heat or sweating, and the obstruction of sweat ducts has been postulated to be responsible. Many patients describe preceding exposure to sunlight, although exposure to artificial ultraviolet radiation has not been shown to reproduce the process. Grover disease seems to occur more frequently in patients with atopic dermatitis and asteatotic dermatitis, although many individuals with these conditions never develop it. Viral, bacterial, and other pathogens have also been proposed, but no causative role has been established. The exact pathogenesis has not been elucidated.

Frequency

United States

Exact numbers regarding the prevalence of the disease are not available. Because of the clinical similarities with other entities and variable histopathologic findings, the disease is underdiagnosed in nondermatologic settings and probably underdiagnosed overall.

Race

Grover disease most commonly affects middle-aged white men, although it may be seen in other ethnic groups, such as Hispanics and blacks.

Sex

Men are affected 3 times more often than women.

Age

Grover disease most commonly affects middle-aged men; however, it has been in reported in children.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

History

• One of the hallmarks of Grover disease is pruritus, and all individuals who are affected experience variable degrees of itching, sometimes severe in nature.
• The clinical appearance does not always correlate to the degree of pruritus; for example, some patients with limited cutaneous disease complain of severe itching, whereas others with many lesions have few or no symptoms.
• No systemic symptoms are associated with Grover disease, but oral lesions can develop that resemble aphthae and may be slightly painful.¹

Physical

• The process usually begins as an eruption of the skin on the anterior part of the chest, the upper part of the back, and the lower part of the rib cage (see Media Files 1-2).
• Patients who are severely affected may have disseminated disease affecting the neck, the shoulders, the arms, and the legs.
• The scalp is usually not affected, and the palms and the soles are almost always spared.
• Individual lesions are erythematous to red brown keratotic papules that remain discrete and do not usually tend to coalesce.
• Occasionally, lesions may be acneiform, vesicular, pustular, and rarely even bullous. Although the most common presentation is that of widespread scattered papules, unusual distributions, including zosteriform or unilateral, may occur.²

Causes

The etiology of Grover disease is unknown.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Other Problems to be Considered

Clinical differential diagnoses and their key differentiating features are listed below.
Dermatitis herpetiformis - Vesicular; pruritus more severe; extensor distribution
Folliculitis - Follicular papules; pustules if lesions intact
Arthropod reaction - Tendency to cluster; extremities and exposed sites usually involved
Papular urticaria (prurigo simplex) - Primarily excoriations; unreachable areas tend to be spared
Miliaria rubra - History of exacerbation with heat; often more nodular lesions
Papular drug eruption - Papules tend to coalesce into plaques; no sparing of extremities
Disseminated herpes simplex or herpes zoster - Vesicular; painful; history of immunosuppression
Scabies - Intractable itching, worse at night; wrists, finger webs, and axillae affected
Papular pityriasis rosea - Herald patch, less severe or absent pruritus, collarette of scale; seasonal incidence
Secondary syphilis - Usually scaly, with palmar lesions; pruritus is mild or absent

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Lab Studies

• A skin scraping with oil preparation to search for mites, ova, and scybala of scabies is warranted in any patient with pruritus and a rash.

Histologic Findings

The histology of Grover disease contains certain characteristic features, but for a precise diagnosis to be rendered, clinicopathologic correlation is needed (see Media Files 3-4). Typically, focal acantholysis and dyskeratosis are seen. Spongiosis is also commonly observed, and the presence of spongiosis and acantholysis in the same specimen should raise the possibility of Grover disease.

Five distinct histologic patterns of Grover disease have been described: (1) a pattern that simulates Hailey-Hailey disease; (2) a pattern that simulates Darier disease; (3) a pattern characterized mainly by spongiotic dermatitis; (4) a pattern that simulates pemphigus vulgaris; and (5) a pattern that simulates pemphigus foliaceus. Although one pattern may predominate, each pattern may be seen in different lesions from the same patient or, in some cases, within a single specimen. The key discriminating features are described below.

• Darier disease - Virtually identical; greater tendency to involve follicles; clinical correlation essential
• Linear acantholytic epidermal nevus - Virtually identical; clinical correlation essential
• Hailey-Hailey disease - Epidermis usually more hyperplastic; more diffuse involvement
• Pemphigus vulgaris - Broad zones of suprabasilar acantholysis; mucosal involvement; involvement of adnexal structures; often abundant eosinophils
• Primary spongiotic dermatitis (allergic contact dermatitis, nummular dermatitis) - Involvement of entire epidermis; psoriasiform hyperplasia
• Acantholytic solar keratosis - Atypical keratinocytic proliferation in lower portion of epidermis with cytologic atypia and mitoses; alternating orthokeratosis and parakeratosis; solar elastosis
• Solitary acantholytic keratosis - Epidermal hyperplasia; slight papillomatosis or digitation of epidermis; clinical correlation required
• Pemphigus foliaceus/erythematosus - Broad zone of subcorneal and subgranular acantholysis; involvement of adnexal structures; often eosinophils
• Warty dyskeratoma - Cup-shaped exoendophytic cystlike lesion; acantholytic and dyskeratotic cells lining cyst wall; pseudopapillae with acantholytic dyskeratosis lined by a single layer of basal cells
• Familial dyskeratotic comedones - Small cylindrical invagination with epithelial lining demonstrating acantholytic dyskeratosis

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Medical Care

• Potent topical corticosteroids may be effective in diminishing inflammation and in controlling itching.
• Menthol or pramoxine-containing lotions may also be helpful for itching.
• For refractory disease, retinoids, such as vitamin A 50,000 U 3 times a day for 2 weeks then daily for up to 12 weeks or isotretinoin 40 mg/day for 2-12 weeks, may be effective.³
• Oral corticosteroids, UV-B exposure, psoralen plus ultraviolet A light (PUVA), grenz radiation, and methotrexate (MTX) have all been reported to be effective in severely resistant cases. However, some cases are refractory to virtually all forms of therapy.

Diet

Grover disease is unaffected by diet.

Activity

Excess heat and sweating are frequently associated with an increase in the symptoms of Grover disease. Activities that cause these symptoms should be avoided.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Retinoids

These agents decrease the cohesiveness of abnormal hyperproliferative keratinocytes, and they may reduce the potential for malignant degeneration. They also affect keratinocyte differentiation.

Drug Category: Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

Drug Category: Antimetabolites

These agents regulate cell growth and differentiation.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Further Outpatient Care

• Initial care may be limited to midpotency topical corticosteroids and oral antihistamines. Atopic skin care measures should be recommended.
• Acitretin, calcipotriol, and UVA-1 have been described as useful in patients with disease that is difficult to manage.⁴

In/Out Patient Meds

• Fluocinonide gel 0.05% should be applied twice a day. Never apply to the face, the axillae, or the genital areas. Desoximetasone may be used in place of fluocinonide. High potency (class I) topical steroids, such as Temovate or Diprolene, are limited to 2 weeks' use. They can cause atrophy if used longer and, therefore, should be avoided.
• Hydroxyzine 10-30 mg can be used every 6 hours as needed for itching. As a substitute, Benadryl 25-50 mg may be used every 6 hours as needed. Both may cause drowsiness.

Deterrence/Prevention

• Patients should avoid activities that cause excessive heat, such as exercise and prolonged sun exposure. Patients should also avoid applying topical irritants.

Complications

• Lesions may resolve with postinflammatory pigmentary alteration or with no residual change. Scarring is usually minimal unless induced by excoriation.

Prognosis

• Generally, Grover disease is a self-limited disorder that resolves over weeks to months, but it can be persistent and may repeatedly recur for years.

Patient Education

• Grover disease is not curable, and the cause is unknown. Although the symptoms can frequently be controlled, some cases are refractory to treatment and difficult to manage.

MULTIMEDIA

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Media file 1:  A 54-year-old man with a pruritic eruption on the trunk. Notice the slight lichenification and significant erythema from rubbing that is localized to the central part of the torso. Also note the red-brown papules in the abdominal region.
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Media type:  Photo

Media file 2:  Closer view of the abdominal area (same patient as in Media File 1). Multiple, small, discrete, red-brown papules characteristic of Grover disease are present.
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Media type:  Photo

Media file 3:  Histopathology of Darier-type Grover disease. A focus of acantholytic dyskeratosis is present in the epidermis with slight epithelial hyperplasia and hyperkeratosis, a sign of rubbing as a consequence of the pruritic nature of the disease (hematoxylin and eosin, original magnification X40).
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Media type:  Photo

Media file 4:  Higher magnification reveals the acantholytic dyskeratosis to better advantage. Note the corps ronds and grains (hematoxylin and eosin, original magnification X400).
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Media type:  Photo

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

1. Kanzaki T, Hashimoto K. Transient acantholytic dermatosis with involvement of oral mucosa. J Cutan Pathol. Feb 1978;5(1):23-30. [Medline].
2. Liss WA, Norins AL. Zosteriform transient acantholytic dermatosis. J Am Acad Dermatol. Nov 1993;29(5 Pt 1):797-8. [Medline].
3. Helfman RJ. Grover's disease treated with isotretinoin. Report of four cases. J Am Acad Dermatol. Jun 1985;12(6):981-4. [Medline].
4. Miljkovic J, Marko PB. Grover's disease: successful treatment with acitretin and calcipotriol. Wien Klin Wochenschr. 2004;116 Suppl 2:81-3. [Medline].
5. Breuckmann F, Appelhans C, Altmeyer P, Kreuter A. Medium-dose ultraviolet A1 phototherapy in transient acantholytic dermatosis (Grover's disease). J Am Acad Dermatol. Jan 2005;52(1):169-70. [Medline].
6. Fantini F, Kovacs E, Scarabello A. Unilateral transient acantholytic dermatosis (Grover's disease) along Blaschko lines. J Am Acad Dermatol. Aug 2002;47(2):319-20. [Medline].
7. Grover RW. Transient acantholytic dermatosis. Arch Dermatol. Apr 1970;101(4):426-34. [Medline].
8. Streit M, Paredes BE, Braathen LR, Brand CU. [Transitory acantholytic dermatosis (Grover disease). An analysis of the clinical spectrum based on 21 histologically assessed cases]. Hautarzt. Apr 2000;51(4):244-9. [Medline].

Article Last Updated: Feb 22, 2007