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NDT Advance Access originally published online on September 12, 2006
Nephrology Dialysis Transplantation 2006 21(11):3038-3045; doi:10.1093/ndt/gfl507
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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

Gemcitabine-induced thrombotic microangiopathy: a systematic review

Hassane Izzedine1,*, Corinne Isnard-Bagnis1,*, Vincent Launay-Vacher1, Lucille Mercadal1, Isabelle Tostivint1, Olivier Rixe2, Isabelle Brocheriou3, Edward Bourry1, Svetlana Karie1, Samir Saeb4, Nadine Casimir5, Bertrand Billemont2 and Gilbert Deray1

1Department of Nephrology, 2Department of Clinical Oncology, 3Department of Pathology, 4Hemobiotherapy Federation and 5Department of Pharmacy, Pitie-Salpetriere Hospital, Paris, France

Correspondence and offprint requests to: Dr Hassane Izzedine and Corinne Isnard-Bagnis, Department of Nephrology, La Pitié-Salpêtrière Hospital, 47-80 Boulevard de l’Hôpital, Assistance Publique-Hopitaux de Paris, Pierre et Marie Curie University, 75013 Paris, France. Email: hassan.izzedine@psl.aphp.fr

Keywords: gemcitabine; haemolytic uraemic syndrome; thrombotic microangiopathy

The first 150 words of the full text of this article appear below.

Thrombotic microangiopathy (TMA) is a microvascular occlusive disorder characterized by predominantly platelet thrombi in the renal and/or systemic circulations. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are the clinical entities comprising TMA, with predominantly renal manifestations in the former, while the latter more often presents with systemic and neurological findings. In some cases, TMA includes de novo hypertension and pulmonary or central nervous system symptoms. TMA is a rare condition, which is severe and may be fatal.

Globally, two biological abnormalities explain TMA, namely: ADAMTS13 (A Disintegrin-like And Metalloprotease with ThromboSpondin type 1 repeats) deficiency and various complement component deficiencies. Studies aimed at determining these deficiencies in cases of chemotherapy-induced TMA were not systematically available in the articles reviewed.

Gemcitabine was approved by the US Food and Drug Administration (FDA) in 1996 for the treatment of patients with metastatic pancreatic cancer and is currently used for the treatment . . . [Full Text of this Article]



   Methods and patients
 
Criteria for diagnosis of thrombotic microangiopathy
Patient selection and protection of study participants
Cases
Case 1
Case 2
Case 3


   Results
 


   Discussion
 
Incidence
Time course between gemcitabine therapy and the development of HUS
Symptoms
Haematological findings
Renal findings
Hypertension
Outcome
Treatments
Pathogenesis
Perspectives and practice


   Conclusion
 

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