Increasing evidence for omalizumab in the treatment of bullous pemphigoid

Bullous pemphigoid (BP) is an acquired autoimmune blistering disease characterized by the formation of autoantibodies against hemidesmosomal antigens BP180 and BP230. Although IgG autoantibodies predominate within the plasma and skin of BP patients, some features of the disease cannot be explained solely by IgG-mediated mechanisms.1,2 IgE autoantibodies are also detectable in at least 75% of untreated BP patients and autoreactive IgE-mediated inflammation has been shown to contribute to the pathogenesis of BP.