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Idiopathic Thrombocytopenic Purpura: A Rare Syndrome with Alemtuzumab, Review of Monitoring Protocol

Alemtuzumab, a humanized monoclonal antibody that targets surface molecule CD52, causes rapid and complete depletion of circulating T- and B-lymphocytes through antibody-dependent cell-mediated and complement-mediated cytotoxicity. Alemtuzumab has demonstrated superior efficacy compared to subcutane...

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Detalles Bibliográficos
Autores principales: Sarvepalli, Deepika, Rashid, Mamoon Ur, Ullah, Waqas, Zafar, Yousaf, Khan, Muzammil
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6823085/
https://www.ncbi.nlm.nih.gov/pubmed/31720183
http://dx.doi.org/10.7759/cureus.5715
Descripción
Sumario:Alemtuzumab, a humanized monoclonal antibody that targets surface molecule CD52, causes rapid and complete depletion of circulating T- and B-lymphocytes through antibody-dependent cell-mediated and complement-mediated cytotoxicity. Alemtuzumab has demonstrated superior efficacy compared to subcutaneous interferon beta-1a (SC IFNB-1a) in patients with multiple sclerosis (MS). Alemtuzumab treatment causes a rare and distinct form of secondary immune thrombocytopenic purpura (ITP), characterized by delayed onset, responsiveness to conventional therapies, and prolonged remission following treatment. In phase two and three clinical trials, the incidence of ITP was higher with alemtuzumab treatment compared to the patients receiving SC IFNB-1a. Here we report a case of ITP occurring two years after the first treatment with alemtuzumab. The patient recovered completely after a timely diagnosis and adequate treatment. Rigorous patient education and careful complete blood count (CBC) monitoring by the physician are critical for early identification and treatment of this potentially fatal disorder.