Folic Acid Deficiency and Abrupt10 Placentae

Hall, Marion H.

doi:10.1111/j.1471-0528.1972.tb15787.x

Cited by 28 publications

(5 citation statements)

References 11 publications

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“…A meta-analysis reported a pooled odds ratio of 25.9 (95% CI 0.9–736.3) for abruption in relation to folate deficiency (Ray and Laskin 1999). Our study suggests that low folate levels are not a phenomenon that accompanies women with placental abruption—an observation that provides corroboration with some earlier reports (Alperin et al 1969; Hall 1972; Menon et al 1966; Whalley et al 1969). …”

Section: Discussionsupporting

confidence: 93%

“…Although some studies show increased risk of placental abruption among folate-deficient women (Hibbard 1964, 1975; Hibbard and Hibbard 1963; Ray and Laskin 1999; Streiff and Little 1967), others do not (Alperin et al 1969; Hall 1972; Menon et al 1966; Whalley et al 1969). Moreover, the mechanisms that underlie this association also remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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

Ananth

Peltier

Moore³

et al. 2008

Hum Genet

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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 JerseyPlacental Abruption Study-a multicenter, case-control study of placental abruption (2002)(2003)(2004)(2005)(2006)(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.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

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

Ananth

Peltier

Moore³

et al. 2008

Hum Genet

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“…An abnormal FIGLU test recurred in 73% of 200 women, including 18 of 27 retested in the first trimester. By contrast, Hall (1972) found no association between folate deficiency at first booking or at 30 weeks and placental abruption. Giles (1966) reported 335 cases of megaloblastic anaemia of pregnancy and the puerperium with no significant increase in fetal malformation rate.…”

Section: Discussionmentioning

confidence: 64%

Vitamin dificiencies and neural tube defects.

Smithells¹,

Sheppard²,

Schorah³

1976

Archives of Disease in Childhood

529

229

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944. Vitamin deficiencies and neural tube defects. Serum folate, red cell folate, white blood cell vitamin C, riboflavin saturation index, and serum vitamin A were determined during the first trimester of pregnancy in over 900 cases. For each of these there was a social class gradient. Social classes I + II showed the highest levels which differed significantly from other classes, except for serum folate.In 6 mothers who gave birth to infants with neural tube defects, first trimester serum folate, red cell folate, white blood cell vitamin C, and riboflavin values were lower than in controls. In spite of small numbers the differences were significant for red cell folate (P <0 001) and white blood cell vitamin C (P <0 05).These findings are compatible with the hypothesis that nutritional deficiencies are significant in the causation of congenital defects of the neural tube in man.

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“…Measuring serum and red cell folate levels, most investigators have found no relation between low levels and the occurrence of abruptio placentae (Alpern et al, 1969;Hall, 1972;Whalley et ai., 1969). One study reported that 100% of abruptio placentae patients had low red cell folate levels, while none of the normal delivery patients had low levels (Streiff and Little, 1967).…”

Section: Folatementioning

confidence: 97%