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Successful treatment of bullous pemphigoid with omalizumab as corticosteroid‐sparing agent: report of two cases and review of literature
Author(s) -
Balakirski G.,
Alkhateeb A.,
Merk H.F.,
Leverkus M.,
Megahed M.
Publication year - 2016
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/jdv.13758
Subject(s) - omalizumab , medicine , bullous pemphigoid , immunoglobulin e , autoantibody , immunology , monoclonal antibody , antibody , pathogenesis , pemphigoid , monoclonal , autoimmune disease , disease , dermatology , pathology
Background Bullous pemphigoid ( BP ) is an autoimmune blistering disease that is characterized by formation of subepidermal bullae due to functional disturbance of the hemidesmosomal proteins on the keratinocytes at the basal membrane zone. In recent years, several studies have emphasized the important role of IgE autoantibodies in the pathogenesis of BP . Consequently, a therapeutic approach using IgE depleting antibodies, such as a humanized monoclonal anti‐IgE antibody (e.g. omalizumab) may represent a new option for treatment of this autoimmune disease. Methods In this paper, we report about the successful treatment of BP with omalizumab in two patients and provide a review of the current literature on the relationship between IgE antibodies and this autoimmune blistering disease. Results Two patients with therapy‐resistant BP were treated with humanized monoclonal anti‐IgE antibody omalizumab 300 mg subcutaneously every 3 weeks as corticosteroid‐sparing agent. Under this therapy, both patients experienced a significant improvement of skin condition and almost complete resolution of pruritus. The treatment was well tolerated. Conclusion Until recently IgG autoantibodies against the basal membrane proteins BP 180 und BP 230 were considered to be causative in the pathogenesis of BP . However, new in vitro studies as well as data from experimental mouse models have indicated that in addition to specific IgG, also IgE antibodies against BP 180 and BP 230 play a role in the development of this disease. Based on these new findings, new treatment modalities of BP became possible.