Related Experiment Video
Updated: Jun 12, 2025

Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
The interplay between Helicobacter pylori infection and rs738409 PNPLA3 in metabolic dysfunction-associated steatotic
Facundo Maiorana1, Magali Neschuk1, María Virginia Caronia1
1Laboratorio de Biotecnología Molecular (BIOTECMOL), Instituto de Biotecnología de Misiones "Dra. María Ebbe Reca" (InBioMis), Facultad de Ciencias Exactas Químicas y Naturales, Universidad Nacional de Misiones, Misiones, Argentina.
Background:
Recent studies have suggested an association between H. pylori and metabolic-disfunction associated fatty liver disease (MASLD). However, epidemiologic studies have yielded inconsistent results. We aim to evaluate the association of H. pylori and G-allele PNPLA3 in MASLD diagnosis, and markers of severity.
Methods:
A multi-center cross-sectional study was conducted. A total 224 functional dyspepsia (FD) patients cohort who underwent gastroscopy was selected. Biochemical, clinical parameters, ultrasound, FIB-4 score, LSM by VCTE, gastric biopsies, H. pylori status, and rs738409 PNPLA3 were evaluated. A second retrospective cohort of 86 patients with biopsy-proven MASLD who underwent gastroscopy with gastric biopsies was analyzed.
Results:
In the FD cohort MASLD was observed in 52%, and H. pylori-positive in 51%. H. pylori infection was associated with MASLD prevalence, but in multivariate analyses adjusted for G-allele PNPLA3, it became not significant. Then in MASLD-only dyspeptic cohort, H. pylori infection was significantly linked to elevated serum AST levels and increased liver stiffness measurements, suggesting a potential role in liver injury and fibrosis. Histopathological analysis in biopsy-proven MASLD patients further supported these findings, showing a significant association between H. pylori infection and increased NAS score, fibrosis stage, and prevalence of MASH. Notably, the combination of H. pylori infection and G-allele PNPLA3 appeared to exacerbate MASLD severity beyond individual effects.
Conclusions:
Our results suggest that H. pylori infection may play a role in the progression of liver injury and fibrosis in patients with MASLD, especially in those with specific genetic predispositions.
Insights
Helicobacter pylori infection may worsen metabolic dysfunction-associated fatty liver disease (MASLD) progression, particularly in individuals with the PNPLA3 gene variant. This suggests H. pylori contributes to liver injury and fibrosis in MASLD patients.
Area of Science:
- Hepatology
- Gastroenterology
- Genetics
Background:
- Growing evidence suggests a link between H. pylori and metabolic dysfunction-associated fatty liver disease (MASLD).
- Previous epidemiological studies on this association have produced conflicting results.
- This study investigates the roles of H. pylori and the PNPLA3 G-allele in MASLD diagnosis and severity.
Purpose of the Study:
- To evaluate the association between H. pylori infection and MASLD.
- To assess the combined impact of H. pylori and the PNPLA3 G-allele on MASLD severity.
- To explore H. pylori's role in liver injury and fibrosis markers in MASLD patients.
Main Methods:
- A multi-center cross-sectional study involving 224 functional dyspepsia patients.
- Evaluation of clinical, biochemical, and histopathological parameters, including H. pylori status and PNPLA3 rs738409 genotype.
- Analysis of a secondary retrospective cohort of 86 biopsy-proven MASLD patients.
Main Results:
- H. pylori infection was linked to MASLD prevalence in the functional dyspepsia cohort, but this lost significance after adjusting for the PNPLA3 G-allele.
- In MASLD patients, H. pylori correlated with elevated AST, increased liver stiffness, higher NAS scores, and advanced fibrosis.
- The combination of H. pylori and the PNPLA3 G-allele showed a synergistic effect on MASLD severity.
Conclusions:
- H. pylori infection may contribute to liver injury and fibrosis progression in MASLD.
- Genetic predisposition, specifically the PNPLA3 G-allele, may modulate the impact of H. pylori on MASLD.
- These findings highlight the complex interplay between infection, genetics, and liver disease progression.
Related Concept Videos
Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
Gastritis III: Clinical Manifestations and Management
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...

