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Thrombotic Thrombocytopenic Purpura: From the Bench to the Bedside, but Not Yet to the Community

James N. George, MD; and Sara K. Vesely, PhD
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From The University of Oklahoma Health Sciences Center; Oklahoma City, OK 73190

Requests for Single Reprints: James N. George, MD, Hematology-Oncology Section, The University of Oklahoma Health Sciences Center, 1100 N. Lindsay, Oklahoma City, OK 73104; e-mail, Jim-George@ouhsc.edu.

Current Author Addresses: Drs. George and Vesely: Hematology-Oncology Section, The University of Oklahoma Health Sciences Center, PO Box 26901, Oklahoma City, OK 73190.

Ann Intern Med. 2003;138(2):152-153. doi:10.7326/0003-4819-138-2-200301210-00018
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In the past 4 years, remarkable advances have been made in our understanding of the pathogenesis of thrombotic thrombocytopenic purpura (TTP). This condition is associated with a severe deficiency of von Willebrand factor–cleaving protease (14), now known as ADAMTS13 (5). This deficiency prevents normal processing of large von Willebrand factor multimers that are secreted from endothelial cells (6). Persistence of the large von Willebrand factor multimers in the circulation helps form microvascular platelet thrombi, the pathologic hallmark of TTP (6). Mutations of the ADAMTS13 gene may result in life-long recurrent episodes of TTP due to congenital deficiency of ADAMTS13 (7). Acquired ADAMTS13 deficiency can be caused by autoantibodies (13), as in the patient described by Zheng and colleagues in this issue (8).

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