Inherited thrombophilia and pregnancy
- 1 April 1998
- journal article
- review article
- Published by Wolters Kluwer Health in Current Opinion in Obstetrics and Gynecology
- Vol. 10 (2) , 135-144
- https://doi.org/10.1097/00001703-199804000-00010
Abstract
Inherited thrombophilia is associated with an increased risk of thrombosis. Classically it consists of protein C and protein S deficiency, activated protein C resistance and antithrombin III deficiency. In pregnancy, in addition to thrombosis, inherited thrombophilia is associated with poor obstetric outcome, including recurrent miscarriage, late fetal loss, abruption and pre-eclampsia.Hyperhomocysteinaemia is a newly recognized cause of familial thrombophilia. It is likely that further causes such as prothrombin gene mutations will be added to the rapidly expanding list. The diagnosis of some forms of genetic thrombophilia must, however, be approached with caution during pregnancy, particularly protein S deficiency and activated protein C resistance.Keywords
This publication has 47 references indexed in Scilit:
- Changes in activated protein C resistance during normal pregnancyAmerican Journal of Obstetrics and Gynecology, 1997
- Ethnic distribution of factor V Leiden in 4047 men and women. Implications for venous thromboembolism screeningPublished by American Medical Association (AMA) ,1997
- Homozygous variant of antithrombin with lack of affinity for heparinBlood Coagulation & Fibrinolysis, 1996
- Comparison of protein S functional and antigenic assays in normal pregnancyAmerican Journal of Obstetrics and Gynecology, 1996
- Are we ready for factor V Leiden screening?The Lancet, 1996
- World distribution of factor V LeidenThe Lancet, 1995
- Long-term outcomes of deep-vein thrombosisArchives of internal medicine (1960), 1995
- Changes in protein C and protein S levels in normal pregnancyAmerican Journal of Obstetrics and Gynecology, 1995
- Prevalence of antithrombin deficiency in the healthy populationBritish Journal of Haematology, 1994
- Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C.Proceedings of the National Academy of Sciences, 1993