Skip Navigation



Mol. Hum. Reprod. Advance Access published online on October 13, 2006
Molecular Human Reproduction, doi:10.1093/molehr/gal084
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
12/12/771    most recent
gal084v1
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 Zammiti, W.
Right arrow Articles by Gris, J.-C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zammiti, W.
Right arrow Articles by Gris, J.-C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received August 8, 2006
Accepted September 7, 2006

Article

Association of -592C/A, -819C/T and -1082A/G interleukin-10 promoter polymorphisms with idiopathic recurrent spontaneous abortion

W. Zammiti 1, N. Mtiraoui 1, E. Cochery-Nouvellon 2, T. Mahjoub 1, W.Y. Almawi 3 *, and J.-C. Gris 2

1 Research unit of Haematological and Autoimmune diseases, Faculty of Pharmacy, Monastir, Center University, Montpellier, France
2 Faculty of Biological and Pharmaceutical Sciences, Montpellier-1 University, Montpellier, France
3 Department of Medical Biochemistry, Arabian Gulf University, Manama, Bahrain

* To whom correspondence should be addressed.
W.Y. Almawi, E-mail: wyalmawi{at}yahoo.co.uk


  Abstract

Increasing evidence supports a role for altered T helper 1 (Th1)-Th2 cytokine balance in idiopathic recurrent spontaneous abortion (RSA). The aim of this study was to investigate the association of the interleukin 10 (IL-10) promoter polymorphisms -592C/A, -819C/T and -1082A/G with RSA. Women (n = 350) with at least three consecutive spontaneous abortions (RSA cases) and 200 control women with at least two successful pregnancies were included. The frequency of the -819T allele [P = 0.05, odds ratio (OR) = 1.51], but not other single-nucleotide polymorphisms (SNPs), was higher among RSA patients. Complete linkage disequilibrium (LD) was seen between -592C and -819C and -1082G alleles, as well as between -592A and -819T and between -819C and -1082G alleles only among patients. Although the genotype frequencies (except for -819C/C) of the three polymorphisms were comparable between patients and controls, higher frequency of -592A/-819T/-1082A haplotype (OR = 4.01, 95% CI = 1.83-7.95) was seen in cases versus controls. Regression analysis indicated that, after adjusting for potential variables, -592C/A (OR = 3.32, 95% CI = 1.76-6.27) and -819C/T (OR = 5.06, 95% CI = 2.59-9.91) were associated with exclusively early but not exclusively late RSA, where negative association for both was noted. This supports the notion of involvement of IL-10-592C/A and -819C/T polymorphisms as inherited risk factors of idiopathic RSA.

Keywords: autoimmunity/autoantibodies/IL-10/recurrent abortion.
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
 Biol. Reprod.Home page
E. Cochery-Nouvellon, P. Nguyen, R. Attaoua, P. Cornillet-Lefebvre, E. Mercier, F. Vitry, and J.-C. Gris
Interleukin 10 Gene Promoter Polymorphisms in Women with Pregnancy Loss: Preferential Association with Embryonic Wastage
Biol Reprod, June 1, 2009; 80(6): 1115 - 1120.
[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.