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Abstract
Objectives: Pre-eclampsia is an important cause of maternal and fetal morbidity and mortality worldwide. Hyperhomocyst(e)inemia in pregnancy is associated with an increased risk of pre-eclampsia in most studies. Nutritional and genetic factors regulate homocyst(e)ine levels. A missense mutation 677 C→T in the gene for methylenetetrahydrofolate reductase (MTHFR) has been associated with an increased pre-eclampsia risk in some, although not most, previously studied populations.
Methods: To further understand the role of this polymorphism in the etiology of pre-eclampsia, we genotyped a total of 125 pre-eclamptics and 179 normotensive pregnant Peruvian women.
Results: The wild-type allele frequency among cases and controls was 54% and 58%, respectively. Twenty per cent of cases and 17% of controls were homozygous for the 677 C→T MTHFR genotype (T/T). After adjustment for confounding by covariates including maternal age, nulliparity, pre-pregnancy body mass index and use of prenatal vitamins, women homozygous for the 677 C→T MTHFR genotype (T/T) experienced a modest, statistically non-significant increased risk of pre-eclampsia (adjusted OR 1.6, 95% CI 0.7, 3.8). Maternal folate deficiency was associated with a statistically non-significant doubling in risk of pre-eclampsia in this population (adjusted OR 2.0, 95% CI 0.9, 4.3).
Conclusions: There was no evidence to suggest that pre-eclampsia risk is positively associated with the T/T genotype overall, or in the context of folate deficiency.