Thrombosis [16] H.-U. Pauer, T. Voigt-Tschirschwitz, B. Hinney et al., “Analyzes of three common thrombophilic gene mutations in German women with recurrent abortions,” Acta Obstetricia et Gyneco- logica Scandinavica, vol. 82, no. 10, pp. 942–947, 2003. [17] W. H. Kutteh, V. M. Park, and S. R. Deitcher, “Hypercoagu- lable state mutation analysis in white patients with early ﬁrst- trimester recurrent pregnancy loss,” Fertility and Sterility, vol. 71, no. 6, pp. 1048–1053, 1999. [18] W. Pickering, K. Marriott, and L. Regan, “G20210A prothrom- bin gene mutation: prevalence in a recurrent miscarriage pop- ulation,” Clinical and Applied Thrombosis/Hemostasis, vol. 7, no. 1, pp. 25–28, 2001. [19] H. Carp, O. Salomon, D. Seidman, R. Dardik, N. Rosenberg, and A. Inbal, “Prevalence of genetic markers for thrombo- philia in recurrent pregnancy loss,” Human Reproduction, vol. 17, no. 6, pp. 1633–1637, 2002. [20] P. W. Friederich, B. J. Sanson, P. Simioni et al., “Frequency of pregnancy-related venous thromboembolism in anticoagulant factor-deﬁcient women: implications for prophylaxis,” Annals of Internal Medicine, vol. 125, no. 12, pp. 955–960, 1996. [21] L. Regan and R. Rai, “Thrombophilia and pregnancy loss,” Journal of Reproductive Immunology, vol. 55, no. 1-2, pp. 163– 180, 2002. [22] M. J. Kupferminc, “Thrombophilia and pregnancy,” Current Pharmaceutical Design, vol. 11, no. 6, pp. 735–748, 2005. [23] G. Bedoya, P. Montoya, J. Garc´ıa et al., “Admixture dynam- ics in Hispanics: a shift in the nuclear genetic ancestry of a South American population isolate,” Proceedings of the Nation- al Academy of Sciences of the United States of America, vol. 103, no. 19, pp. 7234–7239, 2006. [24] L. G. Carvajal-Carmona, I. D. Soto, N. Pineda et al., “Strong Amerind/white sex bias and a possible Sephardic contribution among the founders of a population in Northwest Colombia,” American Journal of Human Genetics, vol. 67, no. 5, pp. 1287– 1295, 2000. [25] F. H. Herrmann, M. Koesling, W. Schro¨der et al., “Prevalence of factor V Leiden mutation in various populations,” Genetic Epidemiology, vol. 14, no. 4, pp. 403–411, 1997. [26] M. J. Kupferminc, A. Eldor, N. Steinman et al., “Increased frequency of genetic thrombophilia in women with compli- cations of pregnancy,” New England Journal of Medicine, vol. 340, no. 1, pp. 9–13, 1999. [27] R. P. Murphy, C. Donoghue, R. J. Nallen et al., “Prospec- tive evaluation of the risk conferred by factor V Leiden and thermolabile methylenetetrahydrofolate reductase polymor- phisms in pregnancy,” Arteriosclerosis, Thrombosis, and Vascu- lar Biology, vol. 20, no. 1, pp. 266–270, 2000. [28] A. Raziel, Y. Kornberg, S. Friedler, M. Schachter, B. A. Sela, and R. Ron-El, “Hypercoagulable thrombophilic defects and hyperhomocysteinemia in patients with recurrent pregnancy loss,” American Journal of Reproductive Immunology, vol. 45, no. 2, pp. 65–71, 2001. [29] P. M. Ridker, J. P. Miletich, C. H. Hennekens, and J. E. Buring, “Ethnic distribution of factor V Leiden in 4047 men and women: implications for venous thromboembolism screen- ing,” Journal of the American Medical Association, vol. 277, no. 16, pp. 1305–1307, 1997. [30] S. R. Poort, F. R. Rosendaal, P. H. Reitsma, and R. M. Bertina, “A common genetic variation in the 3 -untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis,” Blood, vol. 88, no. 10, pp. 3698–3703, 1996. [31] H. Mandel, B. Brenner, M. Berant et al., “Coexistence of hereditary homocystinuria and Factor V Leiden—eﬀect on 5 thrombosis,” New England Journal of Medicine, vol. 334, no. 12, pp. 763–768, 1996. [32] A. Pe´rez, N. Rodr´ıguez, J. Gil, and G. Ram´ırez, “Taman˜o de muestra. In. (Bogota´, Pontiﬁcia Universidad Javeriana. Facul- tad de Medicina. Unidad de Epidemiolog´ıa Cl´ınica y Bioesta- d´ıstica.), p Programa sistematizado para el ca´lculo del taman˜o de la muestra y el poder en disen˜os de investigacio´ n,” 2001. [33] SPSS 15.0 Command Syntax Reference, SPSS Inc., Chicago, Ill, USA, for Windows, 2006. [34] A. G. Dean, J. A. Dean, D. Coulombier et al., “EPI 6 STAT CALC,” in Epi Info Version 6: A Word Processing, Database, and Statistics Program for Epidemiology on Microcomputers, Atlanta, Ga, USA, 1994. [35] O. Camacho Vanegas, B. Giusti, C. M. Restrepo Fernandez, R. Abbate, and G. Pepe, “Frequency of factor V (FV) Leiden and C677T methylenetetrahydrofolate reductase (MTHFR) muta- tions in Colombians,” Thrombosis and Haemostasis, vol. 79, no. 4, pp. 883–884, 1998. [36] A. Varela, A. Bilbao, C. F. Garcia et al., “Prevalencia de la mutacion del factor V de la coagulacion (factor V Leiden) en donantes de banco de sangre en cuatro ciudades colombianas,” Acta M´edica Colombiana, vol. 25, pp. 2–5, 2000. [37] J. D. Torres Herna´ndez, H. Cardona, L. A´lvarez et al., “Inher- ited thrombophilia is associated with deep vein thrombosis in a Colombian population,” American Journal of Hematology, vol. 81, no. 12, pp. 933–937, 2006. [38] A. Roman-Gonzalez, H. Cardona, W. Cardona-Maya et al., “The ﬁrst homozygous family for prothrombin G20210A pol- ymorphism reported in Latin America,” Clinical and Applied Thrombosis/Hemostasis, vol. 15, no. 1, pp. 113–116, 2009. [39] I. Krabbendam, A. Franx, M. L. Bots, R. Fijnheer, and H. W. Bruinse, “Thrombophilias and recurrent pregnancy loss: a critical appraisal of the literature,” European Journal of Obs- tetrics Gynecology and Reproductive Biology, vol. 118, no. 2, pp. 143–153, 2005. [40] E. Nurk, G. S. Tell, H. Refsum, P. M. Ueland, and S. E. Vollset, “Factor V Leiden, pregnancy complications and adverse out- comes. The Hordaland Homocysteine Study,” Quarterly Jour- nal of Medicine, vol. 99, no. 5, pp. 289–298, 2006. [41] J. Balasch, J. C. Reverter, F. Fa´bregues et al., “First-trimester repeated abortion is not associated with activated protein C resistance,” Human Reproduction, vol. 12, no. 5, pp. 1094– 1097, 1997. [42] D. S. Dizon-Townson, S. Kinney, D. Ware Branch, and K. Ward, “The factor V Leiden mutation is not a common cause of recurrent miscarriage,” Journal of Reproductive Immunology, vol. 34, no. 3, pp. 217–223, 1997. [43] Z. R. Holmes, L. Regan, I. Chilcott, and H. Cohen, “The C677T MTHFR gene mutation is not predictive of risk for recurrent fetal loss,” British Journal of Haematology, vol. 105, no. 1, pp. 98–101, 1999. [44] A. Makino, T. Nakanishi, M. Sugiura-Ogasawara, Y. Ozaki, N. Suzumori, and K. Suzumori, “No association of C677T methylenetetrahydrofolate reductase and an endothelial nitric oxide synthase polymorphism with recurrent pregnancy loss,” American Journal of Reproductive Immunology, vol. 52, no. 1, pp. 60–66, 2004. [45] H. U. Pauer, J. Neesen, and B. Hinney, “Factor V Leiden and its relevance in patients with recurrent abortions [8],” American Journal of Obstetrics and Gynecology, vol. 178, no. 3, p. 629, 1998. [46] T. Ayadurai, S. Muniandy, and S. Z. Omar, “Thrombophilia investigation in Malaysian women with recurrent pregnancy