Clinical laboratory · 2025
Correlation of Aldehyde Dehydrogenase 2 rs671 Polymorphism with Susceptibility to Acute Pancreatitis.
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Jiang Zhouqian, Zhou Wenjian, Chen Chaoguang, Yi Wenyan, Zhao Chengfei
Аннотация
BACKGROUND: This study aimed to investigate the correlation between the single nucleotide polymorphism (SNP) of the aldehyde dehydrogenase 2 (ALDH2) gene rs671 locus and susceptibility to acute pancreatitis (AP).
METHODS: A total of 58 AP patients were enrolled as the study group, and 51 healthy individuals from the outpatient physical examination center during the same time period were selected as the healthy control group. ALDH2 gene polymorphism was detected in both groups using the Fascan 48S multi-channel fluorescence quantitative analyzer. Blood lipid levels, age, gender, habitual alcohol consumption, and AP episodes were analyzed. Genetic linkage was assessed using the Hardy-Weinberg equilibrium test. Logistic regression and SPSS 25.0 were employed to evaluate associations between ALDH2 rs671 polymorphism, clinical factors, and AP risk.
RESULTS: The proportion of hyperlipidemia was significantly higher in the AP group compared to the healthy con-trol group (p < 0.05). ALDH2 rs671 polymorphism frequencies differed markedly between AP patients and healthy controls (p < 0.05). Subgroup analysis revealed that AP patients carrying the mutant ALDH2 rs671 genotype exhibited a lower proportion of habitual alcohol consumption compared to wild-type carriers (OR = 4.375, 95% CI: 1.178 - 16.250; p < 0.05). No significant differences were observed in age or gender distribution between groups (all p > 0.05).
CONCLUSIONS: The ALDH2 rs671 locus mutation is an independent risk factor influencing AP susceptibility. Patients with this mutation may exhibit altered alcohol metabolism pathways, contributing to AP pathogenesis. Further mechanistic studies are warranted to explore therapeutic implications.
METHODS: A total of 58 AP patients were enrolled as the study group, and 51 healthy individuals from the outpatient physical examination center during the same time period were selected as the healthy control group. ALDH2 gene polymorphism was detected in both groups using the Fascan 48S multi-channel fluorescence quantitative analyzer. Blood lipid levels, age, gender, habitual alcohol consumption, and AP episodes were analyzed. Genetic linkage was assessed using the Hardy-Weinberg equilibrium test. Logistic regression and SPSS 25.0 were employed to evaluate associations between ALDH2 rs671 polymorphism, clinical factors, and AP risk.
RESULTS: The proportion of hyperlipidemia was significantly higher in the AP group compared to the healthy con-trol group (p < 0.05). ALDH2 rs671 polymorphism frequencies differed markedly between AP patients and healthy controls (p < 0.05). Subgroup analysis revealed that AP patients carrying the mutant ALDH2 rs671 genotype exhibited a lower proportion of habitual alcohol consumption compared to wild-type carriers (OR = 4.375, 95% CI: 1.178 - 16.250; p < 0.05). No significant differences were observed in age or gender distribution between groups (all p > 0.05).
CONCLUSIONS: The ALDH2 rs671 locus mutation is an independent risk factor influencing AP susceptibility. Patients with this mutation may exhibit altered alcohol metabolism pathways, contributing to AP pathogenesis. Further mechanistic studies are warranted to explore therapeutic implications.