Bullous pemphigoid (BP) is an acquired, autoimmune, bullous disease that is characterized by autoantibodies against the 230-kDa bullous pemphigoid antigen within basal keratinocytes and the 180-kDa type XVII collagen within the basement membrane zone (BMZ) lying between the epidermis and dermis.1 In addition to skin blisters, patients with BP often experience pruritus and erythematous urticaria-like skin lesions.2 IgG is usually the predominant autoantibody in the plasma and skin of patients with BP.3 Nevertheless, most of these patients also have IgE autoantibodies against type XVII collagen, and these IgE autoantibodies have been shown to be pathogenic.2,4- 6 Herein, we report a case of a woman with pruritic BP and very high levels of IgE and eosinophils who was refractory to standard aggressive immunosuppressive regimens for BP but responded rapidly to systemic omalizumab, a biological agent that binds to and nullifies IgE.
Figure. Comparison of right hand prior to treatment. A, Treatment with omalizumab, showing multiple bullae. B, Four weeks after treatment.
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