Skip Navigation



Mol. Hum. Reprod. Advance Access published online on February 4, 2005
Molecular Human Reproduction, doi:10.1093/molehr/gah151
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
11/3/207    most recent
gah151v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Sziller, I.
Right arrow Articles by Witkin, S. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sziller, I.
Right arrow Articles by Witkin, S. S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Molecular Human Reproduction © European Society of Human Reproduction and Embryology 2005; all rights reserved
Received October 13, 2004
Accepted January 7, 2005

Article

An A>G polymorphism at position -670 in the Fas (TNFRSF6) gene in pregnant women with pre-eclampsia and intrauterine growth restriction

Istvan Sziller 1, Daniel Nguyen 2, Amrita Halmos 1, Petronella Hupuczi 1, Zoltan Papp 1, and Steven S. Witkin 2*

1 First Department of Obstetrics and Gynecology, Semmelweis University Medical School, Budapest, Hungary
2 Division of Immunology and Infectious Diseases, Department of Obstetrics and Gynecology, Weill Medical College of Cornell University, New York, NY, USA

* To whom correspondence should be addressed.
Steven S. Witkin, E-mail: switkin{at}med.cornell.edu


  Abstract

Fas-mediated apoptosis of maternal lymphocytes during pregnancy has been postulated to prevent the development of pre-eclampsia. A single adenine (A) to guanine (G) polymorphism at position -670 in the Fas gene (TNFRSF6) results in decreased Fas synthesis. The association between this polymorphism and pre-eclampsia in Hungarian women was investigated. In a case-control study, buccal swabs from 38 pregnant women with pre-eclampsia and 89 normotensive controls were analysed for the TNFRSF6-670 polymorphism. Investigators were blinded to clinical outcomes. Maternal homozygosity for the TNFRSF6-670*A occurred in 33 (37.1%) normotensive pregnant women as compared to only 5 (16.1%) of 31 pre-eclamptic pregnant women who delivered at <37 weeks gestation (P=0.04). The carriage rate of the TNFRSF6-670*G variant was also higher among these patients (59.7%) than among normotensive controls (42.1%; P=0.01). There was no relation between the polymorphism and the pre-eclampsia diagnosed at ≥37 weeks. Among pre-eclamptic patients with an intrauterine growth restriction (IUGR) neonate, eight (57.2%) were TNFRSF6-670*G homozygous as opposed to 3 (17.6%) of 17 pre-eclamptics who did not have IUGR (P=0.03) and 19 (21.3%) normotensive controls (P=0.008). Carriage of the TNFRSF6-670 polymorphism in the neonate was not associated with pre-eclampsia or IUGR. Maternal possession of the TNFRSF6-670*G increases the risk for pre-eclampsia and pre-eclampsia-associated IUGR in women who deliver at <37 weeks.

Keywords: Fas; genetic polymorphism; intrauterine growth restriction; pre-eclampsia; TNFRSF6.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Pathol.Home page
L. K. Harris, R. J. Keogh, M. Wareing, P. N. Baker, J. E. Cartwright, J. D. Aplin, and G. S. J. Whitley
Invasive Trophoblasts Stimulate Vascular Smooth Muscle Cell Apoptosis by a Fas Ligand-Dependent Mechanism
Am. J. Pathol., November 1, 2006; 169(5): 1863 - 1874.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.