Placental Pathology in Thrombophilia: Establishing Clinico-Pathological Correlations (Commentary)

Placental Pathology in Thrombophilia: Establishing Clinico-Pathological Correlations (Commentary)

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. (1,2) 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. (3) Data from late pregnancy loss analysed from 15 studies also showed significant association. The association was even stronger between thrombophilia and recurrent foetal loss. (3) The most frequently encountered heritable thrombophilias leading to pregnancy loss were factor V Leiden, hyperhomocystinaemia, prothrombin G20210A and protein S deficiency. (4,5) The only Indian study on thrombophilia and unexplained pregnancy loss was reported by Vora et al (6) 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 [beta]2 glycoprotein 1 ([beta]2GP1). 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. (6) Histopathological examination of the placentas in women with recurrent pregnancy loss, intrauterine growth retardation and pre-eclampsia have revealed lesions due to vascular hypoperfusion. An organ once considered senescent after birth, usually discarded, is now increasingly being examined as an important diagnostic tool for maternal/foetal vasculopathies. The word placenta is derived from a Latin word meaning ‘flat cake’. It provides oxygen and nourishment to the foetus through regulation of maternal and foetal circulations. The cytotrophoblast separates both the circulations and extends into the decidua basalis to form villi. Maternal blood in the intervillous space allows gaseous and nutrient exchange. Foetal blood is separated from the cytotrophoblast by foetal endothelial cells. (7) Hence maternal blood flow in the placenta can be affected by both maternal and foetal thrombophilic gene mutations if the latter are expressed in the trophoblast.

Placental Pathology in Thrombophilia: Establishing Clinico-Pathological Correlations (Commentary)



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