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Blood, 15 September 2007, Vol. 110, No. 6, pp. 1723-1729. Prepublished online as a Blood First Edition Paper on May 11, 2007; DOI 10.1182/blood-2006-10-053736. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-10-053736v1 110/6/1723    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Varki, A. Search for Related Content PubMed PubMed Citation Articles by Varki, A. Related Collections Reviews in Translational Hematology Free Research Articles Clinical Trials and Observations Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  REVIEW IN TRANSLATIONAL HEMATOLOGY Trousseau's syndrome: multiple definitions and multiple mechanisms Ajit Varki1 1 University of California, San Diego, La Jolla In 1865, Armand Trousseau noted that unexpected or migratory thrombophlebitis could be a forewarning of an occult visceral malignancy. An analysis by Sack and colleagues in 1977 extended the term Trousseau's syndrome to include chronic disseminated intravascular coagulopathy associated with microangiopathy, verrucous endocarditis, and arterial emboli in patients with cancer, often occurring with mucin-positive carcinomas. In recent times the term has been ascribed to various clinical situations, ranging all the way from these classic descriptions to any kind of coagulopathy occurring in the setting of any kind of malignancy. These multiple definitions of Trousseau's syndrome are partly the consequence of multiple pathophysiologic mechanisms that apparently contribute to the hypercoagulability associated with cancer. Even the classic syndrome probably represents a spectrum of disorders, ranging from exaggerated fluid-phased thrombosis dependent on prothrombotic agents such as tissue factor to a platelet- and endotheliumum-based selectin-dependent microangiopathy associated with mucin-producing carcinomas, along with thrombin and fibrin production. Also considered here are recent hypotheses about genetic pathways within tumor cells that might trigger these thrombotic phenomena, and the reasons why therapy with heparins of various kinds remain the preferred treatment, probably because of their salutary actions on several of the proposed pathologic mechanisms. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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