Assessment of gastric atrophy has long relied exclusively on histological evaluation of systematic biopsies according to the Sydney protocol. A paradigm shift is currently underway: endoscopy is emerging as a standalone diagnostic tool. The validated Kimura Takemoto classification allows real-time diagnosis of gastric atrophy, mapping of its extent, and targeted biopsy sampling. Current recommendations advocate an integrated endoscopy–histology approach with dual risk stratification. In cases of discordance, the higher associated risk dictates surveillance.

The aim of our study was to evaluate the prevalence and predictive factors of gastric atrophy.

This was a single-center, cross-sectional study conducted over six months. Included patients were naïve to Helicobacter pylori eradication therapy and had not received recent antibiotics or proton pump inhibitors (PPIs). After excluding cases of isolated fundic atrophy on histology, 289 patients were analyzed. Endoscopic evaluation of atrophy was performed using the Kimura–Takemoto classification. Biopsies were obtained according to the Sydney protocol. H. pylori infection was diagnosed by histology.

The mean age was 46 ± 10 years, with a male-to-female ratio of 1.2 and a mean BMI of 25.4 ± 3.7 kg/m². H. pylori infection was detected in 73.3% of cases. Endoscopic atrophy was present in 35.6% of patients, compared with 5.2% for histological atrophy. No significant association was found between atrophy and H. pylori status (p = 0.79 for endoscopy; p = 0.76 for histology). In multivariate analysis, age was the only independent factor associated with gastric atrophy. Each additional year of age increased the probability of endoscopic atrophy by 3% (OR = 1.03; 95% CI [1.01–1.05]) and histological atrophy by 6% (OR = 1.06; 95% CI [1.02–1.11]). Cohen’s kappa coefficient measuring agreement between endoscopy and histology was low (κ = 0.15; 95% CI [–0.03; 0.33]), indicating no significant correlation between both methods.

Age is the main determinant of gastric atrophy, potentially reflecting the cumulative mucosal damage over time. The low prevalence of histological atrophy compared with published data from regions with similar H. pylori prevalence may be explained by intrinsic limitations of histology: under-sampling inherent to the Sydney protocol, subjective interpretation, and low sensitivity for early atrophy. The absence of association with H. pylori was unexpected and warrants further investigation. Our findings support the relevance of a combined endoscopy–histology approach with dual stratification to optimize gastric cancer risk assessment.