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Related Collections Hemostasis, Thrombosis, and Vascular Biology Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 January 2002, Vol. 99, No. 2, pp. 437-442 CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS Factor V Leiden: a genetic risk factor for thrombotic microangiopathy in patients with normal von Willebrand factor-cleaving protease activity Thomas J. Raife, Steven R. Lentz, Bonnie S. Atkinson, Sara K. Vesely, and Martin J. Hessner From The Blood Center of Southeastern Wisconsin, Milwaukee; the University of Iowa Department of Internal Medicine, Iowa City; and the University of Oklahoma Departments of Internal Medicine and Biostatistics and Epidemiology, Norman. Thrombotic microangiopathy (TM) is associated with abnormalities of von Willebrand factor-cleaving protease (VWCP) and other hemostatic factors. This study hypothesized that TM patients might have genetically determined thrombotic risk factors that predispose them to aberrant microvascular thrombosis. DNA samples from 30 white and 12 African American adult TM patients were analyzed for genetic alleles associated with vascular thrombosis, and plasma samples were analyzed for levels of VWCP activity. DNA was analyzed by using allele-specific polymerase chain reaction for factor V 1691A (Leiden), factor II 20 210A, methylenetetrahydrofolate reductase 667T, type 1 plasminogen activator inhibitor 4G/5G, and platelet GPIa 807T. Patients were segregated by race (white or African American) and plasma level of VWCP activity (normal or deficient). The prevalence of factor V Leiden was significantly increased among the white TM patients that had normal VWCP activity: 4 (36%) of 11 patients compared with 6 (3%) of 186 white control subjects possessed the factor V Leiden allele (P < .001; odds ratio, 17.1; 95% confidence interval, 5.4-54.0). No factor V Leiden alleles were detected in 19 white TM patients with intermediate or deficient levels of VWCP activity or in any of 12 African American patients. The prevalence of other thrombosis-associated alleles did not differ between TM patients and control subjects. These findings suggest that factor V Leiden may be a pathogenic risk factor in TM patients that have normal VWCP activity. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. J. Raife, W. Cao, B. S. Atkinson, B. Bedell, R. R. Montgomery, S. R. Lentz, G. F. Johnson, and X. L. Zheng Leukocyte proteases cleave von Willebrand factor at or near the ADAMTS13 cleavage site Blood, August 20, 2009; 114(8): 1666 - 1674. [Abstract] [Full Text] [PDF] C. Sucker, M. Schmitz, G. R. Hetzel, B. Grabensee, B. Maruhn-Debowski, L. Ostojic, R. E. Scharf, and R. B. Zotz Are Prothrombotic Variants of Platelet Glycoprotein Receptor Polymorphisms Involved in the Pathogenesis of Thrombotic Microangiopathies? Clinical and Applied Thrombosis/Hemostasis, August 1, 2009; 15(4): 402 - 407. [Abstract] [PDF] C. Sucker, C. Kurschat, F. Farokhzad, G. R. Hetzel, B. Grabensee, B. Maruhn-Debowski, R. Loncar, R. E. Scharf, and R. B. Zotz The TT Genotype of the C677T Polymorphism in the Methylentetrahydrofolate Reductase as a Risk Factor in Thrombotic Microangiopathies: Results From a Pilot Study Clinical and Applied Thrombosis/Hemostasis, June 1, 2009; 15(3): 283 - 288. [Abstract] [PDF] C. Sucker, C. Kurschat, G. R. Hetzel, B. Grabensee, B. Maruhn-Debowski, R. Loncar, L. Ostojic, R. E. Scharf, and R. B. Zotz The G1691A Mutation of the Factor V Gene (Factor V Leiden) and the G20210A Mutation of the Prothrombin Gene as Risk Factors in Thrombotic Microangiopathies Clinical and Applied Thrombosis/Hemostasis, June 1, 2009; 15(3): 360 - 363. [Abstract] [PDF] S. A. Levey, R. S. Bajwa, M. M. Picken, J. I. Clark, K. Barton, and D. J. Leehey Thrombotic microangiopathy associated with sunitinib, a VEGF inhibitor, in a patient with factor V Leiden mutation NDT Plus, June 1, 2008; 1(3): 154 - 156. [Full Text] [PDF] C. L. Bennett, B. Kim, A. Zakarija, N. Bandarenko, D. K. Pandey, C. G. Buffie, J. M. McKoy, A. D. Tevar, J. F. Cursio, P. R. Yarnold, et al. Two Mechanistic Pathways for Thienopyridine-Associated Thrombotic Thrombocytopenic Purpura: A Report From the SERF-TTP Research Group and the RADAR Project J. Am. Coll. Cardiol., September 18, 2007; 50(12): 1138 - 1143. [Abstract] [Full Text] [PDF] J. A. K. Hovinga, S. Krieg, J.-D. Studt, I. Sulzer, and B. Lammle Factor V Leiden Is Not a Risk Factor for Thrombotic Microangiopathies without Severe ADAMTS13 Deficiency. Blood (ASH Annual Meeting Abstracts), November 16, 2004; 104(11): 850 - 850. [Abstract] J. N. George and S. K. Vesely ADAMTS13 and TTP: the clot thickens Blood, June 1, 2004; 103(11): 3997 - 3998. [Full Text] [PDF] S. K. Vesely, J. N. George, B. Lammle, J.-D. Studt, L. Alberio, M. A. El-Harake, and G. E. Raskob ADAMTS13 activity in thrombotic thrombocytopenic purpura-hemolytic uremic syndrome: relation to presenting features and clinical outcomes in a prospective cohort of 142 patients Blood, July 1, 2003; 102(1): 60 - 68. [Abstract] [Full Text] [PDF] J. N. George, J. E. Sadler, and B. Lammle Platelets: Thrombotic Thrombocytopenic Purpura Hematology, January 1, 2002; 2002(1): 315 - 334. [Abstract] [Full Text]

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