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Mol. Hum. Reprod. Advance Access published online on March 19, 2008
Molecular Human Reproduction, doi:10.1093/molehr/gan013
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© The Author 2008. 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

Paternal Contribution of H L A-G*0106 Significantly Increases Risk for Pre-Eclampsia in Multigravid Pregnancies

Chia Yee Tan1,*, Julia F.V. Ho1,*, Yap Seng Chong2, Annamalai Loganath2, Yiong Huak Chan3, Jeganathan Ravichandran4, Caroline G. Lee5,6,7 and Samuel S. Chong1,8,{dagger}

1Departments of Pediatrics,Yong Loo Lin School of Medicine, National University of Singapore, 119074, SINGAPORE 2Departments of Obstetrics & Gynecology Yong Loo Lin School of Medicine, National University of Singapore, 119074, SINGAPORE 3Biostatistics Unit, Yong Loo Lin School of Medicine, National University of Singapore, 117597, SINGAPORE 4Department of Obstetrics & Gynecology, Sultanah Aminah Hospital, Johor Bahru, Johor, 80100, MALAYSIA 5Departments of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, 119074, SINGAPORE 6Division of Medical Sciences, Humphrey Oei Institute of Cancer Research, National Cancer Center, 169610, SINGAPORE 7Duke-NUS Graduate Medical School, 169547, SINGAPORE 8Children's Medical Institute and Department of Laboratory Medicine, National University Hospital, 119074, SINGAPORE

{dagger} Address for correspondence: Samuel S. Chong, PhD, FACMG Department of Pediatrics, Yong Loo Lin School of Medicine National University of Singapore 5 Lower Kent Ridge Road, Singapore 119074, SINGAPORE 065-6772-4152 (phone), 065-6779-7486 (fax), paecs{at}nus.edu.sg

Pre-eclampsia (PE) is a leading cause of maternal and fetal mortality and morbidity. Structural or functional alterations of Human Leukocyte Antigen (HLA)-G present at the maternal-fetal interface may predispose women to PE. We tested the HLA-G gene for association with PE in a case-control study of 83 PE and 240 normotensive Malay women. HLA-G was amplified in a single-tube multiplex-PCR reaction and genotyped for 18 single nucleotide polymorphisms (SNPs) by multiplex-minisequencing. Case-control comparisons were performed, and associations with disease were expressed as odds ratios. Risk for PE was significantly associated with fetal allele G*0106 only in multigravid pregnancies (p=0.002, OR=5.0, 95%CI=1.8-13.8). Among multigravid pregnancies, the frequency of PE babies heterozygous or homozygous for G*0106 was also significantly higher compared to normal control babies (p=0.002. OR=5.4, 95%CI=1.9-15.4). Multivariate analyses with adjustment for factors associated with PE revealed similar results (p=0.003, OR=10.1, 95%CI=2.2-46.8). Additionally, a significantly higher frequency of fetal-maternal G*0106 genotype mismatch was observed in pre-eclamptic compared to normal multigravid pregnancies (p=0.001, OR=9.6, 95%CI=2.4-38.7). Thus paternal HLA-G G*0106 contribution significantly increases risk for PE in multigravidas who do not carry this allele, potentially mediated by a gradual maternal alloimmune response to repeated exposure to the paternal HLA-G variant.

Key Words: pregnancy/placenta/pre-eclampsia/HLA-G/haplotype

* Both authors contributed equally to this work.

Submitted on November 28, 2007; resubmitted on February 11, 2008; accepted on February 19, 2008.


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