1. Severe bullous pemphigoid associated with pembrolizumab therapy for metastatic melanoma with complete regression
- Author
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Gil Bar-Sela, O. Rofe, Reuven Bergman, Christian D. Sadik, Zohar Keidar, and Tanya Sezin
- Subjects
Pemphigoid ,Skin Neoplasms ,Ipilimumab ,Antineoplastic Agents ,Dermatology ,Pembrolizumab ,medicine.disease_cause ,Antibodies, Monoclonal, Humanized ,Autoimmunity ,030207 dermatology & venereal diseases ,03 medical and health sciences ,0302 clinical medicine ,Pemphigoid, Bullous ,medicine ,Humans ,Melanoma ,Autoimmune disease ,business.industry ,Autoantibody ,Middle Aged ,medicine.disease ,030220 oncology & carcinogenesis ,Immunology ,Female ,Bullous pemphigoid ,business ,medicine.drug - Abstract
Bullous pemphigoid (BP) is considered to be a humorally mediated autoimmune disease, but autoreactive T-cells and T-regulatory cells (Tregs) have also been implicated in this disease. Tregs and the programmed death-1 (PD-1) : programmed death ligand (PD-L) pathway are both critical in terminating immune response, and elimination of either can result in breakdown of tolerance and development of autoimmunity. We report a patient with metastatic malignant melanoma (MM), who underwent pembrolizumab (anti-PD-1) therapy following unsuccessful treatment with ipilimumab [anti-cytotoxic T-lymphocyte-associated protein (CTLA)-4]. The patient developed BP with increasing serum titres of anti-BP180 IgG autoantibodies and increasing disease severity during pembrolizumab therapy. High doses of corticosteroids and methotrexate were needed to control the BP. Following the termination of pembrolizumab therapy, imaging showed complete regression of all metastatic sites. This result may indicate a crucial role for T-cell suppressive activity in controlling and preventing BP.
- Published
- 2016