A painful eruption in a woman with Darier disease

dyshidrosiform pemphigoid, antibodies to the hemidesmosomes of the basement membrane predominate; in BrunstingePerry cicatricial pemphigoid, the anchoring filament component laminin 332 is also reported. Localized, nonscarring bullous pemphigoid has been described to arise spontaneously and at areas of trauma. Nontraumatic bullae most commonly arise in the pretibial area and either remain localized or precede more generalized bullous pemphigoid. No localizing mechanism has been described, although speculation regarding vascular disease in the lower extremities has been proposed. Localized traumatic bullous pemphigoid has also been described as arising secondary to physical trauma and remaining limited to the site of injury, such as surgical sites, poorly healing wounds, amputation sites, and even as an isomorphic response in patients with chronic pruritus. Treatment of dyshidrosiform pemphigoid, like that of bullous pemphigoid, focuses on immunosuppressive therapy. Topical corticosteroids are regarded as the first-line therapy, with the addition of systemic corticosteroids, dapsone, mycophenolate mofetil, or azathioprine combination therapy as indicated. No clinical, laboratory, or histopathologic findings have been shown to be predictive of either the duration or extent of involvement in patients with localized or generalized bullous pemphigoid. Although half of patients with generalized bullous pemphigoid in 1 hospital series experienced clinical remission after 3 years, no similar studies regarding dyshidrosiform pemphigoid exist. In our patient’s case, a high potency topical corticosteroid applied twice daily was sufficient to obtain a clinical remission after 4 months of therapy. For this series, the recommended choices are: 1, b; 2, a; 3, c; 4, b.