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Blood, 15 August 2008, Vol. 112, No. 4, pp. 1085-1090. Prepublished online as a Blood First Edition Paper on June 9, 2008; DOI 10.1182/blood-2007-11-123091. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-11-123091v1 112/4/1085    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Santilli, F. Articles by Davì, G. Search for Related Content PubMed PubMed Citation Articles by Santilli, F. Articles by Davì, G. Related Collections Hemostasis, Thrombosis, and Vascular Biology Neoplasia Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Circulating endothelial progenitor cells and residual in vivo thromboxane biosynthesis in low-dose aspirin-treated polycythemia vera patients Francesca Santilli1, Mario Romano1, Antonio Recchiuti1, Alfredo Dragani2, Angela Falco1, Gianfranco Lessiani1, Francesca Fioritoni2, Stefano Lattanzio1, Domenico Mattoscio1, Raimondo De Cristofaro3, Bianca Rocca1, and Giovanni Davì1,2 1 Center of Excellence on Aging, G. d'Annunzio University Foundation, Chieti; 2 Department of Hematology, Pescara Hospital, Pescara; and 3 Hemostasis Research Center, Catholic University School of Medicine, Rome, Italy Polycythemia vera (PV) is associated with high morbidity and mortality for thrombosis. We hypothesized that in PV altered sensitivity to aspirin might be related to dysfunction of the endothelial repair and/or of the nitric oxide (NO) system. Urinary thromboxane (TX) A2 metabolite (TXM), endothelial colony-forming cells (ECFCs), plasma asymmetric dimethylarginine (ADMA) and von Willebrand factor (VWF) were measured in 37 PV patients on low-dose aspirin and 12 healthy controls. Patients showed an approximately 2-fold increase in median TXM and plasma ADMA levels (P < .001), while ECFC numbers were reduced by approximately 7-fold (P < .001) as compared with nonaspirinated control. These differences were more pronounced in patients with previous thrombosis. An 8-week course of aspirin did not affect ECFCs in 6 controls. VWF and TXM correlated directly with ADMA, and inversely with ECFCs. By multiple regression analysis, lower ECFC quartiles (beta = –0.39; SE = 0.17; P = .028) and higher VWF levels (beta = 0.338, SE = 0.002, P = .034) were independent predictors of higher TXM quartiles (R2 = 0.39). Serum TXB2, measured in 22 patients, was approximat-ly 10-fold higher than aspirin-treated controls. PV patients appear to have an unbalanced ECFC/NO axis, and an apparent altered sensitivity of platelet TXA2 production, all potentially contributing to aspirin-insensitive TXM formation. Thus, additional antithrombotic strategies may be beneficial in PV. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Sozer, M. I. Fiel, T. Schiano, M. Xu, J. Mascarenhas, and R. Hoffman The presence of JAK2V617F mutation in the liver endothelial cells of patients with Budd-Chiari syndrome Blood, May 21, 2009; 113(21): 5246 - 5249. [Abstract] [Full Text] [PDF]

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