Placental pathology in thrombophilia: establishing clinico-pathological correlations.

Women with thrombophilia are at an increased risk of not only venous thromboembolism, but various other complications including intrauterine foetal growth retardation, pre-eclampsia and foetal loss. Both inherited and acquired thrombophilias contribute to thrombotic events and their adverse outcome in pregnancy. The major inherited thrombophilias include deficiencies of antithrombin, protein C, protein S, factor V Leiden, prothrombin G20210A gene polymorphism and hyperhomocystinaemia associated with methylene tetrahydrofolate reductase (MTHFR) C 677 T mutation. Acquired thrombophilias are mostly associated with antiphospholipid antibodies-both lupus anticoagulants and anticardiolipin antibodies. A recent systematic review of 25 studies revealed a positive association between early pregnancy loss and thrombophilia. Data from late pregnancy loss analysed from 15 studies also showed significant association. The association was even stronger between thrombophilia and recurrent foetal loss. The most frequently encountered heritable thrombophilias leading to pregnancy loss were factor V Leiden, hyperhomocystinaemia, prothrombin G20210A and protein S deficiency. The only Indian study on thrombophilia and unexplained pregnancy loss was reported by Vora et al recently where 381 women were screened for heritable and acquired thrombophilia markers; 183 women had 2 and 198 women had >3 pregnancy losses. The strongest association was observed with anticardiolipin antibodies (P<0.001) followed by annexin V, lupus anticoagulant and anti β2 glycoprotein 1 (β2GP1). Amongst heritable thrombophilias the risk of pregnancy loss was highest with protein S deficiency, followed by protein C deficiency. A combination of >2 heritable factors was observed in 10.8 per cent and presence of both acquired and heritable risk factors in 20.7 per cent of patients. Placental pathology in thrombophilia: establishing clinico-pathological correlations