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(Stroke. 2007;38:1636.)
© 2007 American Heart Association, Inc.
Research Reports |
From the Service of Angiology (D.P., D.H.), University Hospital, Lausanne, Switzerland; INSERM (C.M.B., N.A.), Centre de Recherche Cardiovasculaire, Hôpital Lariboisière, Paris, France; the Department of Internal Medicine (S.E.), University Hospital, Lausanne, Switzerland; the Department of Internal Medicine (P.P., D.H.), Hôpital Cantonal, Fribourg, Switzerland; and the Laboratory of Hemostasis (C.G.), University Hospital, Lausanne, Switzerland.
Correspondence to Dr Daniel Periard, Service of Angiology, PMU 07, Bugnon 44, Lausanne, Switzerland 1011. E-mail Daniel.Periard{at}chuv.ch
Background and Purpose— To evaluate whether cisplatin-induced stroke is mediated by vascular toxicity with release of prothrombotic endothelial and platelet-derived microparticles (MPs).
Methods— Endothelial (CD31+CD41–), platelets (CD31+CD41+) and prothrombotic (Annexin V+) circulating MPs were quantified by flow cytometry in 18 patients with cancer, before and 3 days after administration of cisplatin, and compared with 18 healthy controls. Thrombin-antithrombin complex and prothrombin fragments (F1+2) were measured as markers of the activation of the coagulation.
Results— In patients with cancer, baseline levels of circulating prothrombotic, endothelial and platelet-derived MPs were similar to healthy controls and decreased significantly after administration of cisplatin. High-baseline MPs levels were observed in 5 patients who received cisplatin for a second or third cycle. A high-baseline activation of the coagulation was observed in all patients without further increase after cisplatin infusion.
Conclusion— Cisplatin treatment is immediately followed by a decrease in circulating levels of endothelial and platelet-derived MPs. However, a transient increase in MPs is observed at the second and third infusion, and this may contribute to the cisplatin-induced stroke.
Key Words: brain infarction cancer & stroke cisplatin microparticles
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