Association of MTHFR 677C>T polymorphism with IUGR and placental abruption risk: A systematic review and meta-analysis

Eur J Obstet Gynecol Reprod Biol. 2021 Jan:256:130-139. doi: 10.1016/j.ejogrb.2020.11.016. Epub 2020 Nov 11.

Abstract

Objective: The effects of the MTHFR 677C > T polymorphism on the intrauterine growth restriction (IUGR) and placental abruption risk have been evaluated in some studies. However, those studies results were conflicting and ambiguous. Therefore, we carried out the current meta-analysis to evaluate the association of MTHFR 677C > T polymorphism with risk of IUGR and placental abruption from all eligible studies.

Methods: An electronic search of the PubMed, Embase, Scopus and CNKI databases was performed up to February 25, 2020.

Results: A total of 25 case-control studies including eight studies with 687 cases and 2336 controls for IUGR and 17 studies with 1574 cases and 5758 controls for placental abruption were selected. The analysis results indicated that MTHFR 677C > T polymorphism was associated with an increased risk of IUGR and placental abruption in global population. When stratified by ethnicity a significant association between the MTHFR 677C > T polymorphism and IUGR risk was found in Caucasians and Africans. However, there was no a significant association between the MTHFR 677C > T polymorphism and placental abruption risk by ethnicity.

Conclusions: Our pooled data indicated that the MTHFR 677C > T polymorphism might play a role in development of IUGR and placental abruption.

Keywords: IUGR; MTHFR Gene; Meta-analysis; Placental abruption; Polymorphism; Susceptibility.

Publication types

  • Meta-Analysis
  • Systematic Review

MeSH terms

  • Abruptio Placentae / genetics*
  • Female
  • Fetal Growth Retardation / genetics*
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Methylenetetrahydrofolate Reductase (NADPH2) / genetics*
  • Polymorphism, Single Nucleotide
  • Pregnancy

Substances

  • MTHFR protein, human
  • Methylenetetrahydrofolate Reductase (NADPH2)