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NDT Advance Access originally published online on January 9, 2006
Nephrology Dialysis Transplantation 2006 21(3):577-579; doi:10.1093/ndt/gfk042
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Editorial Comment

A new treatment for TTP?

Fadi Fakhouri, Benjamin Deroure and Aurélie Hummel

Service de Néphrologie, Hôpital Necker, AP-HP, Université Paris V-René Descartes, Paris, France

Correspondence and offprint requests to: Fadi Fakhouri. Email: fakhouri@necker.fr

Keywords: monoclonal antibody; rituximab; thrombotic thrombocytopenic purpura (TTP)

The first 10% of the full text of this article appears below.



   Pathophysiology of TTP
 
Thrombotic thrombocytopenic purpura (TTP) is a life-threatening disease that mainly affects adult patients. It is characterized by microangiopathic haemolytic anaemia, thrombocytopenia, neurological disturbances and renal failure [1]. These symptoms are related to the presence of von Willebrand factor (VWF)-rich platelet thrombi in the arterioles and capillaries.

The VWF, a multimeric plasma glycoprotein secreted mainly by endothelial cells, is crucial for both platelet adhesion and aggregation, especially at the high shear rates in the microvasculature. The VWF is secreted in the form of high molecular weight multimers with a high potency to aggregate platelets. Thus, the size of VWF multimers is physiologically regulated in vivo by a specific metalloprotease, The ADAMTS13 (A Desintegrin And Metalloprotease with a ThromboSpondin-like . . . [Full Text of this Article]



   Therapeutic considerations
 


   Treatment of relapses with rituximab
 


   Prevention of relapsing TTP
 

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