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Blood, 15 June 2007, Vol. 109, No. 12, pp. 5104-5111. Prepublished online as a Blood First Edition Paper on January 30, 2007; DOI 10.1182/blood-2006-12-038968. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-12-038968v1 109/12/5104    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 Finazzi, G. Articles by Barbui, T. Search for Related Content PubMed PubMed Citation Articles by Finazzi, G. Articles by Barbui, T. Related Collections Neoplasia Red Cells How I Treat Free Research Articles Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HOW I TREAT How I treat patients with polycythemia vera Guido Finazzi, and Tiziano Barbui Department of Hematology, Ospedali Riuniti di Bergamo, Italy The clinical course of polycythemia vera (PV) is marked by a high incidence of thrombotic complications; fibrotic and leukemic disease transformations are additional causes of morbidity and mortality. Major predictors of vascular events are increasing age and previous thrombosis; leukocytosis and high JAK2 V617F allele burden are currently being investigated for additional prognostic value in this regard. Myelosuppressive drugs can reduce the rate of thrombosis, but there is concern that their use raises the risk of transformation into acute leukemia. To tackle this dilemma, a risk-oriented management strategy is recommended. Low-risk patients should be treated with phlebotomy and low-dose aspirin. Cytotoxic therapy is indicated in high-risk patients, and the drug of choice is hydroxyurea because of its efficacy in preventing thrombosis and low leukemogenicity. Interferon-alpha should be reserved for selected categories of patients due to high cost and toxicity. The demonstration of JAK2 V617F mutation in the vast majority of PV patients opens the avenue for the development of promising new molecularly targeted drugs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Barbui, A. Carobbio, A. Rambaldi, and G. Finazzi Perspectives on thrombosis in essential thrombocythemia and polycythemia vera: is leukocytosis a causative factor? Blood, July 23, 2009; 114(4): 759 - 763. [Abstract] [Full Text] [PDF] A. M. Vannucchi, P. Guglielmelli, and A. Tefferi Advances in Understanding and Management of Myeloproliferative Neoplasms CA Cancer J Clin, May 1, 2009; 59(3): 171 - 191. [Abstract] [Full Text] [PDF] V. Seaman, A. Jumaan, E. Yanni, B. Lewis, J. Neyer, P. Roda, M. Xu, and R. Hoffman Use of Molecular Testing to Identify a Cluster of Patients with Polycythemia Vera in Eastern Pennsylvania Cancer Epidemiol. Biomarkers Prev., February 1, 2009; 18(2): 534 - 540. [Abstract] [Full Text] [PDF] J.-J. Kiladjian, B. Cassinat, S. Chevret, P. Turlure, N. Cambier, M. Roussel, S. Bellucci, B. Grandchamp, C. Chomienne, and P. Fenaux Pegylated interferon-alfa-2a induces complete hematologic and molecular responses with low toxicity in polycythemia vera Blood, October 15, 2008; 112(8): 3065 - 3072. [Abstract] [Full Text] [PDF] R. Landolfi and L. Di Gennaro Prevention of thrombosis in polycythemia vera and essential thrombocythemia Haematologica, March 1, 2008; 93(3): 331 - 335. [Full Text] [PDF] A. M. Vannucchi and T. Barbui Thrombocytosis and Thrombosis Hematology, January 1, 2007; 2007(1): 363 - 370. [Abstract] [Full Text] [PDF]

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