Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Clinical Trial
. 2010 Aug;116(2 Pt 1):355-364.
doi: 10.1097/AOG.0b013e3181e66d58.

Prevalence of parental thrombophilic defects after fetal death and relation to cause

Fleurisca J Korteweg  1 , Jan Jaap H M Erwich, Nienke Folkeringa, Albertus Timmer, Nic J G M Veeger, Joke M Ravisé, Jozien P Holm, Jan van der Meer
Affiliations
Free article
Clinical Trial

Prevalence of parental thrombophilic defects after fetal death and relation to cause

Fleurisca J Korteweg et al. Obstet Gynecol. 2010 Aug.
Free article

Abstract

Objective: To estimate whether parental thrombophilic defects after fetal death, either acquired or inherited, were more prevalent than in the normal population and to estimate associations between these thrombophilic defects and different fetal death causes.

Methods: In a multicenter, prospective cohort study of 750 fetal deaths, we tested couples for antithrombin, protein C, total and free protein S, and von Willebrand factor (vWF) plasma levels. Mothers' values were compared with reference values in gestational age-matched healthy pregnant women, and fathers were compared with healthy men. Prevalence of factor V Leiden, prothrombin G20210A mutation, and lupus anticoagulant were compared with the normal population. A panel classified death cause.

Results: More women with fetal death had decreased antithrombin (16.8%, P<.001) and protein C (4.0%, P=.03) and increased vWF (15.5%, P<.001) plasma levels than healthy pregnant women (2.5%). However, compared with normal ranges in the nonpregnant population, we only observed more women with increased vWF (12.4%, P<.001). More fathers had decreased free protein S (6.3%, P<.001) and elevated vWF (12.1%, P<.001) than healthy men (2.5%). Prevalence of inherited thrombophilias was not higher in couples with fetal death than in the population. Neither inherited nor acquired maternal or paternal thrombophilic defects were associated with the main cause of death. Of placental causes, abruption and infarction were associated with acquired maternal defects.

Conclusion: Except for vWF and paternal free protein S, acquired and inherited thrombophilic defects were not more prevalent after fetal death. Routine thrombophilia testing after fetal death is not advised.

Level of evidence: II.

PubMed Disclaimer

References

    1. Silver RM. Fetal death. Obstet Gynecol 2007;109:153–67.
    1. Infante-Rivard C, Rivard GE, Yotov WV, Genin E, Guiguet M, Weinberg C, et al. Absence of association of thrombophilia polymorphisms with intrauterine growth restriction. N Engl J Med 2002;347:19–25.
    1. Kupferminc MJ, Eldor A, Steinman N, Many A, Bar-Am A, Jaffa A, et al. Increased frequency of genetic thrombophilia in women with complications of pregnancy. N Engl J Med 1999;340:9–13.
    1. Khong TY, Hague WM. Biparental contribution to fetal thrombophilia in discordant twin intrauterine growth restriction. Am J Obstet Gynecol 2001;185:244–5.
    1. Middeldorp S. Thrombophilia and pregnancy complications: cause or association? J Thromb Haemost 2007;5(Suppl 1):276–82.

Publication types