ArticleMedicine2026
Development and internal validation of a risk prediction model for gastric precancerous lesions integrating Helicobacter pylori serologic typing and host susceptibility polymorphisms.
Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.