Case Report: Carfilzomib-induced Thrombotic Microangiopathy With Complement Activation Treated Successfully With Eculizumab

Thrombotic microangiopathy (TMA) is a group of disorders characterized by endothelial injury, leading to activation of coagulation cascade, consumptive coagulopathy, thrombocytopenia, and hemolytic anemia. TMA causes end-organ damage such as renal and central nervous system dysfunction related to small vessel thrombosis and resultant ischemia.1 The pathogenesis of TMA is primarily divided into 4 major pathways: (1) autoantibody against ADAMTS13 leading to thrombotic thrombocytopenic purpura (TTP); (2) atypical hemolytic uremic syndrome (HUS) mediated by complement activation related to inherited mutations in the complement-related genes such as complement factor H; (3) Shiga toxin-mediated TMA resulting from direct endothelial toxicity by the toxin; and (4) drug-mediated TMA.

Source: Clinical Lymphoma, Myeloma and Leukemia - February 2, 2020 Category: Hematology Authors: Divaya Bhutani, Amer Assal, Markus Y. Mapara, Samantha Prinzing, Suzanne Lentzsch Tags: Case Report Source Type: research