A 40-year-old obese white woman presented with scaly, brownish eruptions in both axillae of approximately 8 months’ duration. The lesions had started as small brownish papules that over time had slowly increased in size and had coalesced to form plaques. The lesions were odorless and asymptomatic. She had atopic dermatitis but was otherwise in good health. She was not on any medications. She did not recall any change in soap or detergent or any change in her deodorant. There was no family history of similar skin lesions.
The physical examination revealed 2 well-demarcated, linear, reddish brown, scaly, crusted hyperkeratotic plaques, 1 on each axillary area. Her height was 154 cm, her weight was 70 kg, and her body mass index was 29.5 kg/m2 (normal value, < 25 kg/m2). The rest of the physical examination findings were normal. In particular, there was no involvement of other intertriginous sites.
A culture of material from one of the lesions confirmed the clinical impression of impetigo. When patients do not respond to appropriate impetigo therapy, consider candidiasis, which can mimic impetigo. Excoriated and factitial lesions typically are more eroded and feature blood crusting rather than the serum crusting noted in this eruption. A contact dermatitis generally does not erupt as several small, discrete lesions.
Prevalence: Axillary granular parakeratosis is a rare condition, although the exact prevalence is not known. Scheinfeld and Mones reviewed the diagnosis of 363,343 specimens submitted to the Ackerman Academy of Dermatopathology in New York between July 1, 1999, and December 31, 2003. Eighteen (0.005%) specimens were diagnosed with granular parakeratosis. The condition most commonly is observed in individuals between 40 and 50 years of age, although children also can be affected. The female-to-male ratio is between approximately 5 to 1 and 25 to 1. There is no known predilection for race or ethnicity.
Etiopathogenesis: The exact etiopathogenesis is not known. Some authors believe that granular parakeratosis results from a basic defect in processing profilaggrin to filaggrin, resulting in a failure to degrade keratohyaline granules. Other authors suggest that the condition is an allergic contact or irritant reaction. The use of antiperspirants and deodorants has been implicated.2,8 Other predisposing factors include genetic predisposition, obesity, atopic dermatitis, occlusive environment, friction, and hyperhidrosis.
Histopathology: Histologic features include hyperkeratosis, compact parakeratosis, acanthosis, papillomatosis, and retention of basophilic keratohyaline granules within a thickened stratum corneum, often with a perivascular infiltrate consisting of lymphocytes and histiocytes. The granular appearance of the stratum corneum is due to the retention of basophilic keratohyaline granules, hence its name.
Clinical Manifestations: Initially, the lesions present as small, reddish-brown keratotic papules in the axillae. These papules can coalesce to form crusted, hyperkeratotic, well-demarcated plaques, with a cobblestone “stuck-on” appearance. The lesions may be discrete, confluent, or reticulated. The plaques may be covered by scale or crust, and satellite papules also may be present. The condition may be unilateral or bilateral. The lesions usually are asymptomatic but at times may be pruritic, painful, or burning.
Diagnosis and Laboratory Investigations: The diagnosis often can be made clinically. A Wood lamp can be used to rule out erythrasma. A potassium hydroxide wet-mount examination of skin scrapings can be performed to rule out a fungal infection. Cytologic examination of superficial scrapings from the lesion can be used to demonstrate retention of keratohyaline granules and preservation of cell nuclei within stratum corneum keratinocytes. Referral to a dermatologist should be considered if the diagnosis is in doubt. Histologic examination is required for definitive diagnosis.
Differential Diagnosis: The differential diagnosis includes acanthosis nigricans, intertrigo, erythrasma, contact dermatitis, confluent and reticulated papillomatosis, fungal infection, nummular eczema, granuloma annulare, linear epidermal nevus, seborrheic keratosis, verruca plana, inverse lichen planus, inverse psoriasis, pemphigus vulgaris, pemphigus vegetans, Hailey-Hailey disease, Bowen disease, Darier disease, and Dowling-Degos disease.
Complications: Axillary granular parakeratosis does not lead to any systemic disease. However, it can be cosmetically and socially embarrassing.
Prognosis: Although the condition may run a chronic and relapsing course, it also may resolve on its own.
Management: Underlying causes such as obesity should be treated if possible. For patients who desire treatment for cosmetic or symptomatic reasons, treatment options include topical corticosteroids, topical calcineurin inhibitors (tacrolimus, pimecrolimus), topical retinoids (tretinoin, tazarotene), topical vitamin D3 analogues (calcipotriol, calcipotriene), topical keratolytics (lactic acid, salicylic acid, urea), topical ammonium lactate, oral retinoids (isotretinoin, acitretin), cryotherapy, botulinum toxin injections, or ablative lasers. Individual cases have responded to a variety of these treatment modalities. However, there is no optimal treatment for this condition, and there have been no controlled trials.
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