Objective: To explore the polymorphism of folate metabolism genes and its correlation with pregnancy-induced hypertension (PIH) in women of childbearing age in the Neijiang region. Methods: Forty-five pregnant women with hypertension disorders who received prenatal care at the Maternal and Child Health Hospital in the Neijiang region from May 2023 to April 2025 were selected for the study and designated as the case group. Additionally, 45 healthy pregnant women during the same period were selected as the control group. Venous blood samples were collected from both groups for folate metabolism gene testing, and the correlation with PIH was analyzed. Results: There were statistically significant differences in BMI index, systolic blood pressure, diastolic blood pressure, serum folate levels, Hcy levels, and vitamin B12 levels between the case group and the control group (p < 0.05). The proportions of MTHFR-wild type and MTRR-wild type in the case group were lower than those in the control group, while the proportions of MTHFR-heterozygous mutant type and MTRR-heterozygous mutant type were higher in the case group (p < 0.05). The Logistic regression model showed that overweight/obesity, abnormal folate levels, abnormal Hcy levels, abnormal vitamin B12 levels, MTHFR-heterozygous mutant type, and (repeated entry corrected to another relevant factor if necessary, but assuming it’s a typo and should be another mutant type or omitted for clarity, here kept as is for direct translation) MTHFR-heterozygous mutant type (note: this repetition should likely be corrected in the original text, e.g., to MTRR-heterozygous mutant type or another relevant factor) were independent risk factors for the occurrence of HDP (p < 0.05), while MTHFR-wild type and MTRR-wild type were protective factors against HDP (p < 0.05). Conclusion: The polymorphism distribution of key genes involved in folate metabolism among women of childbearing age in Neijiang is significantly associated with the occurrence of Hypertensive Disorders of Pregnancy (HDP). Mutant genotypes of MTHFR and MTRR serve as independent risk factors for HDP, while the wild-type acts as a protective factor. Additionally, overweight/obesity, reduced serum folate levels, hyperhomocysteinemia, and vitamin B12 deficiency are also important risk indicators for the onset of HDP.
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