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Human Genetics : Volume 124, Issue 1, August 2008

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Reduced folate carrier 80A→G polymorphism, plasma folate, and risk of placental abruption

Content Provider	Springer Nature Link
Author	Ananth, Cande V. Peltier, Morgan R. Moore, Dirk F. Kinzler, Wendy L. Leclerc, Daniel Rozen, Rima R.
Copyright Year	2008
Abstract	Folate deficiency and maternal smoking are strong risk factors for placental abruption. We assessed whether the reduced folate carrier [NM_194255.1: c.80A→G (i.e., p.His27Arg)] (RFC-1) polymorphism was associated with placental abruption, and evaluated if maternal smoking modified the association between plasma folate and abruption. Data were derived from the New Jersey-Placental Abruption Study—a multicenter, case-control study of placental abruption (2002–2007). Maternal DNA was assayed for the RFC-1 c.80A→G polymorphism using a PCR-dependent diagnostic test. Maternal folate (nmol/l) was assessed from maternal plasma, collected immediately following delivery. Due to assay limitations, folate levels at ≥60 nmol/l were truncated at 60 nmol/l. Therefore, case–control differences in folate were assessed from censored log-normal regression models following adjustment for potential confounders. Distribution of the mutant allele (G) of the RFC-1 c.80A→G polymorphism was similar between cases (52.3%; n = 196) and controls (50.5%; n = 191), as was the homozygous mutant (G/G) genotype (OR 1.1, 95% CI 0.6–2.2). In a sub-sample of 136 cases and 140 controls, maternal plasma folate levels (mean ± standard error) corrected for assay detection limits were similar between placental abruption cases (63.6 ± 5.1 nmol/l) and controls (58.3 ± 4.7 nmol/l; P = 0.270), and maternal smoking did not modify this relationship (interaction P = 0.169). We did not detect any association between the RFC-1 c.80A→G polymorphism and placental abruption, nor was an association between plasma folate and abruption risk evident. These findings may be the consequence of high prevalence of prenatal multivitamin and folate supplementation in this population (over 80%). It is therefore not surprising that folate deficiency may be rare and that the RFC-1 c.80A→G polymorphism is less biologically significant for placental abruption.
Starting Page	137
Ending Page	145
Page Count	9
File Format	PDF
ISSN	03406717
Journal	Human Genetics
Volume Number	124
Issue Number	2
e-ISSN	14321203
Language	English
Publisher	Springer-Verlag
Publisher Date	2008-07-16
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Human Genetics Metabolic Diseases Gene Function Molecular Medicine
Content Type	Text
Resource Type	Article
Subject	Genetics Genetics (clinical)

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