Cande V Ananth1, Carl A Nath, Claire Philipp. 1. Division of Epidemiology and Biostatistics, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08901-1977, USA. cande.ananth@umdnj.edu
Abstract
OBJECTIVE: To examine the association between maternal thrombophilia associated with anticoagulation (proteins C and S and activated protein C resistance ratio, APCR) and risk of placental abruption. METHODS: Data were derived from a case-control study - The New Jersey-Placental Abruption Study (2002-2007). Maternal blood was collected from abruption cases and controls and was assayed for the thrombophilias. Decreased protein C, S and APCR was defined as values <5% and <10% among controls. RESULTS: Of a total of 132 cases and 127 controls, 3 were heterozygous for the factor V Leiden mutation (1 case and 2 controls). Mean (± standard deviation) protein C (114.2 ± 25.6 vs. 121.4 ± 27.6; P=0.009), protein S (39.9 ± 18.4 vs. 35.7 ± 15.2; P=0.043) and APCR (2.86 ± 0.29 vs. 2.88 ± 0.27; P=0.039) were different between cases and controls. Abruption cases were associated with an odds ratio of 3.2 (95% CI 1.2, 9.9) in relation to decreased protein C (<Fifth centile). Decreases in both protein S and APCR ratio were not associated with abruption. CONCLUSIONS: A decrease in protein C was associated with an increased risk for abruption, suggesting an important role for the physiologic anticoagulant system in the etiology of placental abruption.
OBJECTIVE: To examine the association between maternal thrombophilia associated with anticoagulation (proteins C and S and activated protein C resistance ratio, APCR) and risk of placental abruption. METHODS: Data were derived from a case-control study - The New Jersey-Placental Abruption Study (2002-2007). Maternal blood was collected from abruption cases and controls and was assayed for the thrombophilias. Decreased protein C, S and APCR was defined as values <5% and <10% among controls. RESULTS: Of a total of 132 cases and 127 controls, 3 were heterozygous for the factor V Leiden mutation (1 case and 2 controls). Mean (± standard deviation) protein C (114.2 ± 25.6 vs. 121.4 ± 27.6; P=0.009), protein S (39.9 ± 18.4 vs. 35.7 ± 15.2; P=0.043) and APCR (2.86 ± 0.29 vs. 2.88 ± 0.27; P=0.039) were different between cases and controls. Abruption cases were associated with an odds ratio of 3.2 (95% CI 1.2, 9.9) in relation to decreased protein C (<Fifth centile). Decreases in both protein S and APCR ratio were not associated with abruption. CONCLUSIONS: A decrease in protein C was associated with an increased risk for abruption, suggesting an important role for the physiologic anticoagulant system in the etiology of placental abruption.
Authors: F Franchi; E Biguzzi; I Cetin; F Facchetti; T Radaelli; M Bozzo; G Pardi; E M Faioni Journal: Br J Haematol Date: 2001-09 Impact factor: 6.998
Authors: Alfonso Buil; José Manuel Soria; Juan Carlos Souto; Laura Almasy; Mark Lathrop; John Blangero; Jordi Fontcuberta Journal: Arterioscler Thromb Vasc Biol Date: 2004-05-13 Impact factor: 8.311