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.

Plos One
|September 23, 2024
PubMed
Abstract

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.

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