The clinical features of EBA are protean. The classic presentation is that of a noninflammatory mechanobullous disease characterized by the development of acral blisters that heal with atrophic scarring, milia, and hyperpigmentation or hypopigmentation. They are localized to trauma-prone surfaces such as elbows, knees, hands, and feet.1- 3 Acral involvement may be mutilating. Scalp involvement occurs in up to 20% of patients.1- 3 The inflammatory BP-like presentation is associated with widespread vesicles and bullae involving intertriginous and flexural areas that heal without atrophic scarring.1- 3 Epidermolysis bullosa acquisita may also present as mucous membrane pemphigoid or as Brunsting-Perry pemphigoid phenotype.3 The potential causes of erythroderma include psoriasis, atopic dermatitis, drug reactions, and cutaneous T-cell lymphoma. With the exception of pemphigus foliaceus, the other autoimmune bullous diseases of the skin have been only anecdotally implicated as cause of erythroderma. Specifically, single cases of erythrodermic BP have been described.4,5 Epidermolysis bullosa acquisita is potentially associated with a number of systemic diseases, including inflammatory bowel diseases,1,3 but our patient showed no evidence of any of these.