O-14 NON-ALCOHOLIC FATTY LIVER DISEASE IS INFLUENCED BY THE INTERACTION OF HELICOBACTER PYLORI INFECTION AND G-ALLELE OF PNPLA3

Introduction and Objectives

The pathophysiology of NAFLD is only partially unrevealed; it is considered as a multifactorial disorder, attributed to multiple, parallel “hits,” both genetic and environmental. It has been described that the single nucleotide polymorphism at rs738409 in the PNPLA3 gene is strongly associated with hepatic steatosis and its progression. Conversely, H. pylori infection has been related to metabolic syndrome, type-2 diabetes mellitus, and dyslipidemia, which are known risk factors for NAFLD. However, the evaluation of Infection and the rs738409 polymorphism in the PNPLA3 gene has not been explored.

Materials and Methods

this is a preliminary report of a prospective multicenter study from December 2020 to June 2021 in northeastern Argentina. 76 dyspeptic adult patients who fulfilled the ROME-IV criteria and underwent gastroscopy, of which 69 were included. The presence of H. pylori was determined by gastric histology. Biochemical and clinical parameters were recorded. NAFLD was defined by liver ultrasonography. The PNPLA3 gene was analyzed by PCR-RFLP in rs738409.

Results

The prevalence of NAFLD was 45% (31/69), with Hpyl+ 48% (17/36) and Hpyl- 42% (14/33) (p: ns). The variables significantly associated with NAFLD were BMI, dyslipidemia, Diabetes/prediabetes, presence of the G allele of PNPLA3, and the GG genotype. In the multivariate analysis, BMI (OR 1.63 95%CI 1.22-2.19) and the G-allele of PNPLA3 (OR 7.35 95%CI 1.34-40) were independently associated with NAFLD. When subjects with NAFLD were analyzed, the interaction between Hpyl and PNPLA3 allele-G was significantly associated with NAFLD (65%) and increased risk of liver fibrosis (FIB-4 > 1.3 41%).

Conclusions

the presence of NAFLD was associated with BMI and G-allele of PNPLA3. The combination of Hpyl infection and the G-allele of PNPLA3 were associated with NAFLD and risk of fibrosis (FIB-4)