Ahmed Abdel-Razik1, Nasser Mousa1, Walaa Shabana1, Mohamed Refaey2, Rania Elhelaly3, Rasha Elzehery3, Mostafa Abdelsalam4, Ayman Elgamal5, Mervat R Nassar5, Atef Abu El-Soud5, Ahmed S Seif6, Ahmed M Tawfik7, Niveen El-Wakeel8, Waleed Eldars8. 1. Tropical Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt. 2. Tropical Medicine Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt. 3. Clinical Pathology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt. 4. Nephrology and Dialysis Unit, Internal Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt. 5. Department of Tropical Medicine, Menoufia University, Menoufia, Egypt. 6. Hepatology and Gastroenterology Department, Shebin Elkom Teaching Hospital, Menoufia, Egypt. 7. Diagnostic & Interventional Radiology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt. 8. Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
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.
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 pyloriinfection 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.
Authors: Christian S Alvarez; Andrea A Florio; Julia Butt; Alvaro Rivera-Andrade; María F Kroker-Lobos; Tim Waterboer; Maria Constanza Camargo; Neal D Freedman; Barry I Graubard; Mariana Lazo; Eliseo Guallar; John D Groopman; Manuel Ramírez-Zea; Katherine A McGlynn Journal: Helicobacter Date: 2020-10-02 Impact factor: 5.182
Authors: Ahmed Abdel-Razik; Nasser Mousa; Rania Elhelaly; Rasha Elzehery; Ahmad S Hasan; Mostafa Abdelsalam; Ahmed Salah Seif; Ahmed M Tawfik; Niveen El-Wakeel; Waleed Eldars Journal: Front Med (Lausanne) Date: 2020-03-24
Authors: Basit Siddiqui; Muhammad Kamran; Shiyam Sunder Tikmani; Rabeea Azmat; Zain Mushtaq; Saad Bin Zafar; Muhammad Tahir Khan; Javed Yakoob; Zaigham Abbas Journal: SAGE Open Med Date: 2021-06-18