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Risk Factors for Endoscopic Gastric Mucosal Lesions: Analysis of Lifestyle, Dietary, and Clinical Determinants in 361
Patrick-Lazăr-Dominik Chiciudean1, Ana-Maria Filip2, Sabrina-Nicoleta Munteanu2
1Oncology Department, Mureș County Clinical Hospital, 540140 Târgu Mureș, Romania.
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.
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