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 four major pathways a) autoantibody against ADAMTS13 leading to TTP (thrombotic thrombocytopenic purpura), b) atypical HUS (hemolytic uremic syndrome) mediated by complement activation related to inherited mutations in the complement related genes such as complement factor H, c) Shiga toxin mediated TMA resulting from direct endothelial toxicity by the toxin, d) drug mediated TMA (1).

Source: Clinical Lymphoma, Myeloma and Leukemia - February 2, 2020 Category: Hematology Authors: D. Bhutani, A. Assal, M.Y. Mapara, S. Prinzing, S. Lentzsch Tags: Case Report Source Type: research