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Investigation of genetic risk factors for chronic adult diseases for association with preterm birth
Journal article   Open access   Peer reviewed

Investigation of genetic risk factors for chronic adult diseases for association with preterm birth

Nadia Falah, Jude McElroy, Victoria Snegovskikh, Charles J Lockwood, Errol Norwitz, Jeffey C Murray, Edward Kuczynski, Ramkumar Menon, Kari Teramo, Louis J Muglia, …
Human genetics, Vol.132(1), pp.57-67
01/2013
DOI: 10.1007/s00439-012-1223-x
PMCID: PMC3864772
PMID: 22972380
url
https://www.ncbi.nlm.nih.gov/pmc/articles/3864772View
Open Access

Abstract

Preterm birth (PTB) is the leading cause of infant mortality. PTB pathophysiology overlaps with those of adult cardiovascular, immune and metabolic disorders (CIMD), with mechanisms including inflammation, immunotolerance, thrombosis, and nutrient metabolism. Whereas many genetic factors for CIMD have been identified, progress in PTB has lagged. We hypothesized that highly validated genetic risk factors for CIMD may also be associated with PTB. We conducted case–control study of four female cohorts with spontaneous PTB (n = 673) versus term (n = 1119). Of 35 SNPs genotyped, there were 13 statistically significant associations (P<0.05), which were more than expected (binomial test; P = 0.02). In US White (307 cases/342 controls), the G allele of HLA-DQA1 (A/G) rs9272346 was protective for PTBin the initial discovery cohort (P = 0.02; OR = 0.65; 95 % CI 0.46, 0.94). This protective association replicated (P = 0.02; OR = 0.85; 95 % CI 0.75, 0.97) nominally in the Danish Cohort (883 cases, 959 controls), but lost significance upon multiple testing correction. We observed more statistically significant associations than expected, suggesting that chance is an unlikely explanation for one or more of the associations. Particularly, a protective association of the G allele of HLA-DQA1 was found in two independent cohorts, and in previous studies, this same allele was found to protect against type-1-diabetes (meta-analysis P value 5.52 × 10 −219 ). Previous investigations have implicated HLA phenotypic variation in recurrent fetal loss and in chronic chorioamnionitis. Given the limited sample size in his study, we suggest larger studies to further investigate possible HLA genetic involvement in PTB.

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