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This study aimed to evaluate the diagnostic utility of serum pepsinogen (PG) and gastrin-17 (G-17) in assessing the severity of gastric mucosal atrophy in patients with chronic atrophic gastritis (CAG). We analyzed 157 patients with histologically confirmed CAG (82 mild, 75 moderate-to-severe) and 157 patients with chronic non-atrophic gastritis, treated between December 2023 and October 2025. Serum levels of PGI, PGII and Gastrin-17 were measured. Two prespecified logistic regression models were used: Model 1 (Clinical Association Model) to identify factors independently associated with atrophy severity, and Model 2 (Serum-Only Diagnostic Model) to evaluate diagnostic performance. Receiver operating characteristic (ROC) curves were used to assess Model 2. The prevalence of gastric cancer family history and positive Helicobacter pylori (Hp) infection, and the levels of PGII, were higher in the CAG group than in the non-CAG group, while the levels of PGI, PGI/PGII, and G-17 were lower in the CAG group ( P < 0.05). The moderate-to-severe group had a higher prevalence of gastric cancer family history and positive Hp infection, a higher proportion of OLGA stage III-IV, and higher PGII levels than the mild group. The levels of PGI, PGI/PGII, and G-17 were lower in the moderate-to-severe group ( P < 0.05). In Model 1, family history of gastric cancer, Hp infection, PGI/PGII ratio and Gastrin-17 levels were independently associated with moderate-to-severe atrophy in CAG patients ( P < 0.05). PGI, PGI/PGII, and G-17 showed a significant negative correlation with atrophy severity, whereas PGII showed a significant positive correlation ( P < 0.05). In the derivation cohort, the serum-only Model 2 (PGI/PGII + G-17) showed higher apparent discrimination than any single marker, with an internally derived sensitivity of 94.67% and specificity of 76.83% ( P < 0.05). These estimates require independent external validation. The serum-only model combining PGI/PGII and Gastrin-17 showed promising internal discrimination in this derivation cohort. However, these estimates require independent external validation, and the model is not yet ready for routine clinical decision-making or primary screening. Not applicable.
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Dong et al. (2026) studied this question.
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