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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 (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 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 Davi, G. Search for Related Content PubMed PubMed Citation Articles by Santilli, F. Articles by Davi, G. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 13, 2007 Accepted May 19, 2008 Circulating endothelial progenitor cells and residual in vivo thromboxane biosynthesis in low-dose aspirin-treated polycythemia vera patients Francesca Santilli, Mario Romano, Antonio Recchiuti, Alfredo Dragani, Angela Falco, Gianfranco Lessiani, Francesca Fioritoni, Stefano Lattanzio, Domenico Mattoscio, Raimondo De Cristofaro, Bianca Rocca, and Giovanni Davi* Center of Excellence on Aging, "G. D'Annunzio" University Foundation", Chieti, Italy Department of Haematology, Pescara Hospital, Pescara, Italy Heamostasis Research Center, Catholic University School of Medicine, Rome, Italy * Corresponding author; email: gdavi{at}unich.it. 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 a ~2-fold increase in median TXM and plasma ADMA levels (P<0.0001), while ECFCs number was reduced by ~7 fold (P<0.0001) as compared to non-aspirinated control. These differences were more pronounced in patients with previous thrombosis. Eight-week aspirin did not affect ECFCs in 6 controls. vWF and TXM correlated directly with ADMA, and inversely with ECFCs. By multiple regression analysis, lower ECFCs quartiles (Beta=-0.39; SE=0.17; P=0.028) and higher vWF levels (Beta=0.338, SE=0.002, P=0.034) were independent predictors of higher TXM quartiles (R2=0.39). Serum TXB2, measured in 22 patients, was ~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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