Helicobacter pylori infection represents a well-established risk factor for the development of gastric carcinogenesis, yet reliable clinical or endoscopic predictors of infection remain poorly defined. Identifying non-invasive or endoscopic markers of this infection could improve early detection, which is crucial for effective prevention and clinical management. This single-center study included 737 patients who underwent upper gastrointestinal endoscopy. We compared clinical, laboratory, and endoscopic features between H. pylori-positive and H. pylori-negative individuals. A total of 263 with H. pylori-positive gastric biopsies and 474 with H. pylori-negative biopsies were enrolled in our study. Cerebrovascular disease (9.51% vs. 5.51%, p = 0.04, OR = 1.80), type 2 diabetes mellitus (T2DM—22.05% vs. 15.86%, p = 0.04, OR 1.5), and alcohol consumption (18.96% vs. 9.3%, p = 0.00, OR = 2.28) were significantly more prevalent among H. pylori-positive patients. Heartburn was more commonly reported in H. pylori-negative individuals (23.77% vs. 15.38%, p = 0.01, OR = 0.58). Laboratory parameters showed no significant differences between groups. Regarding endoscopic findings, corporal erythema (26.92% vs. 16.17%, p = 0.00, OR = 1.91), corporal erosions (11.54% vs. 5.32%, p = 0.00, OR = 2.32), and submucosal hemorrhages (20.91% vs. 11.6%, p = 0.00, OR = 2.01) were associated with H. pylori infection. In the multivariate logistic regression models, alcohol consumption and corporal lesions remained independent predictors of H. pylori-associated gastritis, even after adjusting for age, sex, and PPI use. This study identifies alcohol consumption and specific corporal mucosal changes as novel, independent predictors of H. pylori infection. Heartburn was negatively associated with active H. pylori infection, while the rest of the symptoms did not predict infection or mucosal lesions. The laboratory parameters did not differ significantly between groups. These findings underscore the potential of targeted endoscopic evaluation and risk-based screening (particularly among T2DM and alcohol-consuming populations) to enhance early detection and management of H. pylori-associated disease.

Background/Objectives: Gastric mucosal lesions represent a significant health burden, with Helicobacter pylori infection being the primary cause of chronic gastritis worldwide. However, the role of modifiable lifestyle factors in modulating the severity of gastric lesions remains incompletely characterized, particularly in Eastern European populations. This study aimed to analyze the relationship between dietary behaviors, smoking, alcohol consumption, and the severity of endoscopic gastric lesions in Romanian patients. Methods: We conducted a cross-sectional study including 361 patients who underwent upper gastrointestinal endoscopy at Târgu Mureș County Clinical Emergency Hospital between 2019 and 2025. Endoscopic lesion severity was classified on an ordinal scale (0 = normal; 1 = edema/erythema; 2 = erosions; 3 = ulcer/bleeding). Dietary intake was assessed using a validated food frequency questionnaire, with foods classified as pro-inflammatory or protective. Ordinal logistic regression models were used to examine associations between lifestyle factors and the severity of gastric lesions, adjusted for age, sex, and H. pylori status. Results: Among participants (median age 65 years, 46.5% male), 45.2% had clinically significant lesions (≥2). H. pylori infection was present in 31.6% of participants. Current smoking (15.2% of participants) showed a trend toward increased severity of gastric lesions (fully adjusted OR 1.59, 95% CI 0.93–2.71, p = 0.092), though not statistically significant. Among current smokers, 52.7% had clinically significant lesions versus 43.8% among non/former smokers. The smoking–alcohol interaction was not statistically significant (interaction OR = 1.19, 95% CI: 0.34–4.17, p = 0.780). Dietary balance score showed no association with the severity of gastric lesions (OR = 1.061 per 10-unit increase, p = 0.355). NSAID use emerged as the strongest predictor (OR = 1.68, 95% CI 1.01–2.78, p = 0.044). The number of cumulative risk factors correlated significantly with clinically significant lesions (Spearman r = 0.107, p = 0.042), with prevalence increasing from 34.5% in patients with 0–1 factors to 83.3% with 6+ factors. Conclusions: Current smoking showed a trend toward increased severity of gastric lesions in this Romanian cohort, though not reaching statistical significance. NSAID use was the only significant independent predictor. The dose–response relationship between cumulative risk factors and the severity of lesions emphasizes the importance of comprehensive risk assessment and multi-factorial interventions in gastric disease prevention. However, as a cross-sectional study, these associations cannot establish causality and should be confirmed in prospective cohorts.

Background: Autoimmune gastritis (AIG) and Helicobacter pylori gastritis are distinct etiologies of chronic gastritis, yet comparative data on their long-term progression remain limited. Objectives: We compared the evolution of precancerous gastric lesions in patients with AIG and H. pylori-associated gastritis. Methods: This retrospective single-center cohort included 116 patients (52 histologically defined AIG, 64 H. pylori-associated gastritis) who underwent two upper endoscopies with Sydney-protocol biopsies at least 12 months apart between 2013 and 2024 (median follow-up 60 and 49 months). The primary outcome was the development of glandular atrophy or intestinal metaplasia (IM) not present at baseline. Results: New atrophy or IM developed in 61.5% (32/52) of AIG and 34.4% (22/64) of H. pylori patients (adjusted odds ratio [OR] 3.81, 95% confidence interval [CI] 1.53–9.49). Incident atrophy was more frequent in AIG (65.1% vs. 31.5%), including in comparison with baseline H. pylori-positive patients only (adjusted OR 3.02, 95% CI 1.08–8.46), whereas differences in IM were less consistent. Progression occurred in 42.9% of patients who were H. pylori-negative after treatment and 55.6% of persistently infected patients (p = 0.70). Proton pump inhibitor (PPI) use, an exploratory clinical risk score, and symptom changes were not associated with progression. Conclusions: In this selected cohort with repeat endoscopy, histologically defined AIG was associated with more frequent histological progression, particularly glandular atrophy, than H. pylori-associated gastritis. Prospective studies with serologically confirmed AIG and neoplastic endpoints are needed to inform risk stratification.