|April 2003 · Vol. 15, No. 4
Inherited 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.
Dr. 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.
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.
Observational studies suggest a role for heparin or folate supplementation in women with thrombophilia polymorphisms and prior adverse pregnancy outcomes.
Hyperhomocysteinemia, which sometimes develops from the influences of a polymorphism, has been linked to preeclampsia and may contribute to placental abruption and infarct.
The Leiden polymorphism of the factor V, with its greater propensity for thrombosis, occurs at increased frequency in women who experience habitual miscarriages.
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: