Differential impacts of Helicobacter pylori antibody typing on gastric secretory function: a cross-sectional study based on serum biomarkers.

[OBJECTIVE] Although gastric secretory dysfunction is common in H.pylori-associated gastropathy, the precise mechanisms underlying these functional alterations across different H.pylori antibody subtypes remain incompletely elucidated. This cross-sectional clinical observational study aimed to systematically investigate the associations between specific H.pylori antibody subtype infection status and multiple gastric functional parameters, thereby elucidating potential differences in their impact on gastric secretory function.

[METHODS] A total of 2,618 patients were included in this analysis. Serum levels of pepsinogen I (PGI), pepsinogen II (PGII), the PGI/PGII ratio (PGR), gastrin-17 (G-17), and H.pylori antibody subtypes were measured. A cross-sectional study design was employed to analyze baseline characteristics and serological data.

[RESULTS] Compared to the H.pylori-positive group, the H.pylori-negative group demonstrated significantly higher PGI (P = 0.020) and PGR (P < 0.001) levels, while PGII levels were markedly lower (P < 0.001). In the H.pylori subtype analysis, both H.pylori(I) and H.pylori(II) groups exhibited elevated PGII levels compared to the negative group, whereas PGR showed a progressive decreasing trend: H.pylori(I) < H.pylori(II) < H.pylori(-) (P < 0.001). Furthermore, both infected groups had significantly higher G-17 levels than the H.pylori(-) group (all P < 0.001). Males showed higher PGI levels in the infected groups, while in the H.pylori(-) group, multiple parameters (PGII, PGI, G-17) were elevated in males compared to females (P < 0.05). Patients aged ≤ 60 years had lower PGI and PGII levels but higher PGR (P < 0.05). Correlation analysis further indicated that G-17 was positively correlated with PGII and negatively correlated with PGR (P < 0.05).

[CONCLUSIONS] H.pylori infection characteristically alters gastric functional serum markers in a virulence-dependent manner. These patterns biologically reflect the continuous pathological process from gastric mucosal inflammation to atrophy. Our findings underscore the clinical relevance of integrating H.pylori subtyping with gastric function assessment in gastric cancer risk screening, providing a novel perspective for the precise identification of high-risk individuals.