Yi Guo

Background Bile reflux gastritis (BRG) may lead to precancerous lesions of gastric cancer and gastric cancer. Although ursodeoxycholic acid (UDCA) has been used to treat BRG, its clinical efficacy remains unknown. Therefore, we systematically evaluated the efficacy and safety of UDCA compared with conventional therapy for BRG. Methods We selected candidate studies and generated a forest plot to evaluate outcomes. Metaregression analysis was conducted to identify possible explanations for heterogeneity. Study quality was evaluated using the Cochrane Risk of Bias 2 tool and the Newcastle–Ottawa scale. The quality of evidence for the outcomes of the meta-analysis was assessed using the Grading of Recommendations Assessment, Development and Evaluation approach. Results A total of 14 studies including 1605 patients were identified. Compared with control groups, medication combined with UDCA significantly reduced the number of reflux episodes [mean difference (MD) = − 17.99 times, 95% CI (− 19.84, − 16.14)], shortened the longest duration of reflux [MD = − 9.21 min, 95% CI (− 12.63, − 5.80)], decreased the number of long reflux episodes [MD = − 3.21 times, 95% CI (− 3.76, − 2.66)], increased the clinical response rate [risk ratio = 1.15, 95% CI (1.10, 1.19)], decreased the gastrin content [MD = − 18.03 ng/L, 95% CI (− 33.88, − 2.18)] and alleviated symptoms. Conclusions UDCA demonstrates significant therapeutic efficacy for BRG, particularly with 8-week regimens, supporting its potential as a first-line therapy.

Background: The etiology of nonalcoholic fatty liver disease (NAFLD) involves a complex interaction of genetic and environmental factors. Previous observational studies have revealed that higher leptin levels are related to a lower risk of developing NAFLD, but the causative association remains unknown. We intended to study the causal effect between leptin and NAFLD using the Mendelian randomization (MR) study. Methods: We performed a two-sample Mendelian randomization (TSMR) analysis using summary GWAS data from leptin (up to 50,321 individuals) and NAFLD (8,434 cases and 770,180 controls) in a European population. Instrumental variables (IVs) that satisfied the three core assumptions of Mendelian randomization were selected. The TSMR analysis was conducted using the inverse variance weighted (IVW) method, MR-Egger regression method, and weighted median (WM) method. To ensure the accuracy and stability of the study results, heterogeneity tests, multiple validity tests, and sensitivity analyses were conducted. Results: The findings of the TSMR correlation analysis between NAFLD and leptin were as follows: IVW method (odds ratio (OR) 0.6729; 95% confidence interval (95% CI) 0.4907–0.9235; P = 0.0142), WM method (OR 0.6549; 95% CI 0.4373–0.9806; P = 0.0399), and MR-Egger regression method (P = 0.6920). Additionally, the findings of the TSMR correlation analysis between NAFLD and circulating leptin levels adjusted for body mass index (BMI) were as follows: IVW method (OR 0.5876; 95% CI 0.3781–0.9134; P = 0.0181), WM method (OR 0.6074; 95% CI 0.4231–0.8721; P = 0.0069), and MR-Egger regression method (P = 0.8870). It has also been shown that higher levels of leptin are causally linked to a lower risk of developing NAFLD, suggesting that leptin may serve as a protective factor for NAFLD. Conclusions: Using TSMR analysis and the GWAS database, we investigated the genetic relationship between elevated leptin levels and lowered risk of NAFLD in this study. However, further research is required to understand the underlying mechanisms.