ArticleEndocrine2024
Acute pancreatitis and metabolic syndrome: genetic correlations and causal associations.
Article in Endocrine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- Insulin resistance-related surrogate indices and recurrence of mild hypertriglyceridemic acute pancreatitis: a retrospective cohort study.Frontiers in nutrition · 2026Article
- Phospholipase D2: A biomarker implicated in various pancreatic diseases beyond acute pancreatitis.World journal of gastroenterology · 2025Article
- Triglyceride-glucose index and triglyceride-to-high-density lipoprotein cholesterol ratio in predicting severity of acute pancreatitis: a cross-sectional clinical study.BMC gastroenterology · 2025Article
- Two-Sample Bidirectional Mendelian Randomization Study With Causal Association Between Metabolic Syndrome and Cerebral Aneurysm.Brain and behavior · 2025Article
- The impact of hyperinsulinemia on short-term prognosis in patients with hypertriglyceridemia-induced acute pancreatitis.Frontiers in endocrinology · 2025Article
- Metabolic syndrome and acute pancreatitis: Current status and future prospects.World journal of gastroenterology · 2024Review
- Genetic Variability in theInternational journal of molecular sciences · 2024Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough there is a definite correlation between the Metabolic Syndrome (MetS) and Acute Pancreatitis (AP), cause is yet unknown. The current work combined linkage disequilibrium score (LDSC) regression and Mendelian randomization (MR) approaches to fill this important information gap.
methodsIn this study, we harnessed the power of publicly available gene-wide association databases (GWAS) to explore the intricate relationship between MetS and its components with AP. The cornerstone of our analysis was the Inverse-Variance Weighted (IVW) method, serving as our primary analytical tool. In addition to IVW, we complemented our investigation with several other robust MR methods, including MR-Egger, Weighted Median, Maximum Likelihood, and MR-PRESSO. By employing this diverse set of analytical approaches, we sought to ensure the comprehensiveness and robustness of our findings.
resultLDSC regression indicated a genetic correlation between MetS and AP. Univariate MR results indicated a genetic association between MetS (OR = 1.084; 95% CI, 1.005-1.170; P = 0.037), BMI (OR = 1.459; 95% CI, 1.325-1.606; P = 1.46E-14), WHR (OR = 1.189; 95% CI, 1.068-1.323; P = 1.56 E-03), TG (OR = 1.110; 95% CI, 1.001-1.231; P = 0.047), and FI (OR = 1.798; 95% CI, 1.245-2.595; P = 1.74E-03) were able to significantly increase the risk of AP. The results of multivariate MR analysis revealed that these causality associations still existed.
conclusionOur investigation has yielded compelling evidence that substantiates the presence of both a genetic correlation and a causal relationship between MetS and AP.
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