Helicobacter pylori Infection and Its Role in the Development of Atrophic Gastritis: A Cross-Sectional Study of 139 Patients

Abstract

Non-autoimmune atrophic gastritis is a known precursor lesion in the gastric cancer pathway and is the main cause of chronic Helicobacter pylori infection. The relationship between infection status and the presence and severity of gastric atrophy was studied in one centre dyspeptic population at one center.

This was a cross-sectional study, and 139 adults were enrolled for diagnostic upper endoscopy. The H. pylori status was determined by histology, rapid urease test, and 13C-urea breath test. Biopsies were performed using the updated Sydney System, and Atrophy was graded, and OLGA was used to stage. Pepsinogen I, II, and gastrin-17 were measured in the serum. Analysis was done in IBM SPSS Statistics 28 using chi-square, t, and Mann-Whitney tests, Spearman correlation, binary logistic regression, and ROC analysis.

1. pylori was detected in 83 (59.7%) and atrophic gastritis in 46 (33.1%) patients. The incidence of atrophy was higher in the infected patients than in the uninfected patients (45.8% vs. 14.3%, p < 0.001). Age (adjusted OR 1.46 per decade) and infection (adjusted OR 4.38, 95% CI 1.78-10.80) were independent associates of atrophy. The pepsinogen I/II ratio correlated negatively with the composite atrophy score (rho = -0.64), and positively with the breath-test values in infected patients (rho = 0.44). A ratio of pepsinogen I/II of 4.1 or lower was used to diagnose atrophy with an AUC of 0.89.

Atrophic gastritis is strongly and independently related to H. pylori infection. Non-invasive serological markers are effective in the detection of atrophy and may be useful in identifying patients for endoscopic surveillance.