Abstracts of the 2025 Annual Meeting of the ALEH
More infoRecent studies have suggested an association between H. pylori (Hp) active gastric infection and metabolic dysfunction associated steatotic liver disease (MASLD We evaluated whether the H. pylori virulence gene cagA and the host sensor NOD1 (rs2075820) correlate with non-invasive markers of liver injury and fibrosis in patients with MASLD.
Patients / Materials and MethodsIn a prospective study (2021–2024, northeast Argentina), 494 adults with Rome IV functional dyspepsia underwent gastroscopy. Biochemical, clinical parameters, ultrasound, FIB-4 score, liver stiffness measurement (LSM) by vibration-controlled transient elastography, gastric biopsies, and H. pylori cagA and NOD1 single nucleotide polymorphism (rs2075820) were evaluated.Associations were analysed with χ2, ANOVA/Tukey and multivariable logistic regression (*p<0.05).
ResultsParticipants were 60 % women; mean age 49 years; BMI 27.9 kg/m2. MASLD was present in 209 (42 %) and Hp in 252 (51 %). Hp positivity coincided with higher BMI and MASLD prevalence (52 % vs 32 %). Among MASLD subgroup, Hp +/cagA + infection was associated with higher AST (25 ± 11 vs 33 ± 14 U/L), FIB-4 (1.0 ± 0.5 vs 1.5 ± 0.8), and LSM (5.7 ± 2.8 vs 7.8 ± 5.2 kPa) compared with Hp-negative patients (p < 0.05 for all), without significant differences in ALT or GGT.The combined cagA +/NOD1-GG genotype displayed the greatest FIB-4 (1.5) and LSM (8.5 kPa); 41 % of carriers exceeded the ≥8 kPa threshold for advanced fibrosis, yielding an an odds ratio (OR) of 3.99 (95 % CI 1.6–10.0; p = 0.003), which remained significant after adjustment for metabolic comorbidities (adjusted OR 4.98; 95 % CI 1.9–13.5).
ConclusionsIn dyspeptic adults with MASLD, Hp cagA carriage is linked to worse non-invasive liver indices. The cagA +/NOD1-GG genotype independently predicts significant fibrosis, underscoring a bacterial–host genetic synergy that may accelerate MASLD progression.
Conflict of interest: Yes, Fundacion HA Barcelo
