S1420 Helicobater pylori Infection and the Risk of Esophagogastric Variceal Bleeding in Patients With Portal Hypertension and Cirrhosis: A Systematic Review and Meta-Analysis

Introduction: Helicobater pylori (H. pylori) is a known cause of non-variceal bleeding in patients with portal hypertension. The role of H. pylori in bleeding from esophagogastric varices in patients with portal hypertension is unclear. We conducted a systematic review and meta-analysis to evaluate the risk of variceal bleeding in patients with portal hypertension and H. pylori infection. Methods: A systematic review of the literature from MEDLINE, EMBASE and Scopus was conducted from inception to May 2025 for studies reporting on the rate of H. pylori infection and variceal bleeding in patients with portal hypertension. Primary outcomes of interest included bleeding from esophageal or gastric varices and H. pylori infection status. Outcomes were expressed as pooled rates and odds ratios with confidence intervals. Standard meta-analysis methods were followed using the random effects model. Heterogeneity was assessed using the I2 statistics. Results: Six single-center studies - 3 prospective and 3 retrospective - involving a total of 810 patients were included. 67.0% patients were man, and H. pylori was positive in 459 (56.7%) patients. H. pylori diagnosis was with biopsy in 3 studies, 13C-urea breath test (13C-UBT) in 2 studies, and was unspecified in the remaining study. Three studies reported on esophageal plus gastric varices, 1 on esophageal varices, 1 on gastric varices, and 1 did not specify variceal location. The etiology of cirrhosis included hepatitis C in 306 (43.1%), hepatitis B in 219 (30.8%), alcohol in 142 (20%) and others/unknown in 43 (6.1%) cases. Patients with cirrhosis were classified per Child-Pugh score as 190 (30.9%) class A, 278 (45.3%) class B and 146 (23.8%) class C. The pooled incidence of combined esophagogastric variceal bleeding in patients with H. pylori was 56.54% (95% CI: 43.93–68.74; I² = 88.1%. The pooled incidence of gastric variceal bleeding in patients with H. pylori was 46.50% (95% CI: 21.10–72.93: I2 = 90.1%). The pooled odds ratio for variceal bleeding in H. pylori–positive vs negative patients was 1.51 (95% CI 0.12–18.49; I2 = 95.7%, P = 0.7484). Conclusion: Our results suggest that H. pylori may not play a significant role in the risk of variceal bleeding in patients with portal hypertension. Larger, prospective studies are needed to better define the role of H. pylori in variceal bleeding and characterize this based on the anatomical location of varices.