Helicobacter pylori and non‐alcoholic fatty liver disease: A new enigma?

Abstract Background and Aim The relationship between Helicobacter pylori ( H. pylori ) and nonalcoholic fatty liver disease ( NAFLD ) is a matter of debate. We achieved this prospective work to study whether H. pylori infection is a risk factor for NAFLD . Methods A cohort multicenter pilot study of 369 adults without NAFLD at baseline was followed up for 2 years. Serum leptin, insulin, tumor necrosis factor‐α, adiponectin, and interleukin‐6 were measured using an enzyme‐linked immunosorbent assay ( ELISA ). Homeostasis model assessment of insulin resistance ( HOMA ‐ IR ) and leptin/adiponectin ratio ( LAR ) were calculated. Fecal H. pylori antigen was measured by ELISA . A total of 127 participants with H. pylori positive were treated and then followed up for 3 months. Results Helicobacter pylori ‐positive patients (46.3%) were associated with an increase in IR , proinflammatory cytokines, C‐reactive protein ( CRP ), LAR , NAFLD ‐liver fat score ( NAFLD ‐ LFS ), and hepatic steatosis index ( HSI ) (all P < 0.01). Multivariate analysis of NAFLD according to HSI and NAFLD ‐ LFS reported that presence of H. pylori, LAR , CRP , IL ‐6, smoking, and age (all P < 0.01) were independent risk factors for the presence of NAFLD . Multiple models adjusted for potential mediators or confounders such as metabolic, inflammatory, and biochemical factors were constructed. After therapy of H. pylori infection, there was a significant reduction in lipogenic profile, IR , leptin, LAR , CRP , proinflammatory cytokines, HSI , and NAFLD ‐ LFS , as well as, increasing HDL . Conclusion Helicobacter pylori infection was related to an increased risk of NAFLD development, through increased markers of IR , inflammatory mediators, and lipid metabolism. Moreover, its eradication can recover these NAFLD risk factors.