April 2003 · Vol. 15, No. 4Inherited thrombophilia and adverse pregnancy outcomes: What the evidence shows
Recent findings suggest that inherited thrombophilias lead to habitual fetal loss, preeclampsia, and placental abruption. Here, an expert examines the role of gene polymorphism-related clotting abnormalities in these outcomes and reviews studies of promising interventions.
LOUISE
WILKINS-HAUG,
MDDr. Wilkins-Haug is chief, division of reproductive genetics, department of obstetrics and gynecology; and director, Center for Fetal Medicine and Prenatal Genetics at Brigham and Women’s Hospital, Boston, Mass. She also is associate professor of obstetrics, gynecology, and reproductive biology, Harvard Medical School.
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KEY POINTS
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Because polymorphisms affecting thrombotic potential are frequent (2% to 20% of the general population), even a slightly increased risk of thrombosis affects a far greater number of pregnancies than complete deficiencies of clotting factor proteins S and C or antithrombin III.
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Observational studies suggest a role for heparin or folate supplementation in women with thrombophilia polymorphisms and prior adverse pregnancy outcomes.
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Hyperhomocysteinemia, which sometimes develops from the influences of a polymorphism, has been linked to preeclampsia and may contribute to placental abruption and infarct.
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The Leiden polymorphism of the factor V, with its greater propensity for thrombosis, occurs at increased frequency in women who experience habitual miscarriages.
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When obstetric histories of habitual or late fetal loss, preeclampsia, intrauterine growth retardation, and placental abruption or infarct suggest placental compromise, a search for thrombophilia is warranted. This article examines:
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