BACKGROUND AND OBJECTIVES: Inherited thrombophilia has been associated with fetal and maternal complications of pregnancy. It is reasonable to suppose that an imbalance of maternal hemostasis could lead to decreased fetal growth. DESIGN AND METHODS: We retrospectively investigated the birth-weight of neonates in relation to the presence of factor V G1691A and factor II A(20210) mutations in the mothers. Overall, 755 women (194 with a history of unexplained recurrent pregnancy loss, 202 with gestational hypertension with or without proteinuria, 359 with at least one uneventful pregnancy) and 1100 alive neonates were considered. RESULTS: Among 980 neonates from mothers without mutations, 136 (13.9%) weighed <2500 grams, whereas 34 out 123 (27.6%) neonates from mothers carrying the factor V G1691A or factor II A(20210) mutation were under this birth-weight (OR: 2.4, 95%CI: 1.5- 3.7). Adjusting for diagnosis, parity, and age, the risk of having a baby <2500 grams was 2.0 (95%CI: 1.1-3.6) in women carrying factor V G1691A or factor II A(20210) mutation. When we analyzed all the neonates according to growth centiles and the presence of a thrombophilic mutation in the mothers, we found 142 (14.5%) and 28 (22.8%) neonates under the 10th centile from mothers without and with thrombophilic mutations, respectively (OR: 1.7, 95%-CI: 1.1-2.7). Adjusting for confounding variables (diagnosis, parity and age), the association between thrombophilic mutations and <10th growth centile did not change (OR: 1.7, 95% CI: 1.0-3.0). INTERPRETATION AND CONCLUSIONS: Mothers carrying the factor V G1691A or factor II A(20210) mutation have a significantly higher risk of delivering neonates with a lower birth-weight.
BACKGROUND AND OBJECTIVES: Inherited thrombophilia has been associated with fetal and maternal complications of pregnancy. It is reasonable to suppose that an imbalance of maternal hemostasis could lead to decreased fetal growth. DESIGN AND METHODS: We retrospectively investigated the birth-weight of neonates in relation to the presence of factor V G1691A and factor II A(20210) mutations in the mothers. Overall, 755 women (194 with a history of unexplained recurrent pregnancy loss, 202 with gestational hypertension with or without proteinuria, 359 with at least one uneventful pregnancy) and 1100 alive neonates were considered. RESULTS: Among 980 neonates from mothers without mutations, 136 (13.9%) weighed <2500 grams, whereas 34 out 123 (27.6%) neonates from mothers carrying the factor V G1691A or factor II A(20210) mutation were under this birth-weight (OR: 2.4, 95%CI: 1.5- 3.7). Adjusting for diagnosis, parity, and age, the risk of having a baby <2500 grams was 2.0 (95%CI: 1.1-3.6) in women carrying factor V G1691A or factor II A(20210) mutation. When we analyzed all the neonates according to growth centiles and the presence of a thrombophilic mutation in the mothers, we found 142 (14.5%) and 28 (22.8%) neonates under the 10th centile from mothers without and with thrombophilic mutations, respectively (OR: 1.7, 95%-CI: 1.1-2.7). Adjusting for confounding variables (diagnosis, parity and age), the association between thrombophilic mutations and <10th growth centile did not change (OR: 1.7, 95% CI: 1.0-3.0). INTERPRETATION AND CONCLUSIONS: Mothers carrying the factor V G1691A or factor II A(20210) mutation have a significantly higher risk of delivering neonates with a lower birth-weight.