Development and internal validation of a risk prediction model for gastric precancerous lesions integrating Helicobacter pylori serologic typing and host susceptibility polymorphisms

This study aimed to develop and internally validate a clinical risk prediction model for precancerous lesions of gastric cancer (PLGC) in Helicobacter pylori (H. pylori )–positive individuals by integrating H. pylori strain typing, serological gastric function markers, lifestyle factors, and host susceptibility polymorphisms. A total of 82 H. pylori –positive outpatients who underwent gastroscopy with histopathology between July 2020 and December 2021 were enrolled and categorized into a PLGC group (n = 38; chronic atrophic gastritis, intestinal metaplasia, and/or dysplasia) and a non-PLGC control group (n = 44). Demographic, clinical, dietary, and lifestyle information was collected using standardized questionnaires. Fasting blood samples were obtained for pepsinogen I (PG I), pepsinogen II (PG II), pepsinogen I/II ratio (PGR), gastrin-17 (G-17), and serologic H. pylori typing (Type I vs Type II), and 4 gastric cancer susceptibility loci (PSCA rs2976392, PLCE1 rs2274223, PRKAA1 rs59133000, and MUC1 rs4072037) were genotyped using TaqMan assays. Multivariable logistic regression identified older age and Type I H. pylori infection as independent risk factors, whereas higher PG I, higher PGR, and frequent whole-grain intake were protective. Susceptibility loci were not retained in the final model. The derived model showed adequate calibration (Hosmer–Lemeshow P = .426) and strong discrimination (AUC = 0.969), with an optimal cutoff of 0.403 yielding 94.7% sensitivity and 93.2% specificity; bootstrap validation indicated stable performance. This model may support risk stratification and targeted surveillance among H. pylori –positive patients.