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Helicobacter pylori and non-alcoholic fatty liver disease: A new enigma?
Helicobacter. 2018 Dec; 23(6):e12537.H

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.

Authors+Show Affiliations

Tropical Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.Tropical Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.Tropical Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.Tropical Medicine Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.Clinical Pathology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.Clinical Pathology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.Nephrology and Dialysis Unit, Internal Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.Department of Tropical Medicine, Menoufia University, Menoufia, Egypt.Department of Tropical Medicine, Menoufia University, Menoufia, Egypt.Department of Tropical Medicine, Menoufia University, Menoufia, Egypt.Hepatology and Gastroenterology Department, Shebin Elkom Teaching Hospital, Menoufia, Egypt.Diagnostic & Interventional Radiology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30246507

Citation

Abdel-Razik, Ahmed, et al. "Helicobacter Pylori and Non-alcoholic Fatty Liver Disease: a New Enigma?" Helicobacter, vol. 23, no. 6, 2018, pp. e12537.
Abdel-Razik A, Mousa N, Shabana W, et al. Helicobacter pylori and non-alcoholic fatty liver disease: A new enigma? Helicobacter. 2018;23(6):e12537.
Abdel-Razik, A., Mousa, N., Shabana, W., Refaey, M., Elhelaly, R., Elzehery, R., Abdelsalam, M., Elgamal, A., Nassar, M. R., Abu El-Soud, A., Seif, A. S., Tawfik, A. M., El-Wakeel, N., & Eldars, W. (2018). Helicobacter pylori and non-alcoholic fatty liver disease: A new enigma? Helicobacter, 23(6), e12537. https://doi.org/10.1111/hel.12537
Abdel-Razik A, et al. Helicobacter Pylori and Non-alcoholic Fatty Liver Disease: a New Enigma. Helicobacter. 2018;23(6):e12537. PubMed PMID: 30246507.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Helicobacter pylori and non-alcoholic fatty liver disease: A new enigma? AU - Abdel-Razik,Ahmed, AU - Mousa,Nasser, AU - Shabana,Walaa, AU - Refaey,Mohamed, AU - Elhelaly,Rania, AU - Elzehery,Rasha, AU - Abdelsalam,Mostafa, AU - Elgamal,Ayman, AU - Nassar,Mervat R, AU - Abu El-Soud,Atef, AU - Seif,Ahmed S, AU - Tawfik,Ahmed M, AU - El-Wakeel,Niveen, AU - Eldars,Waleed, Y1 - 2018/09/23/ PY - 2018/06/11/received PY - 2018/08/18/revised PY - 2018/08/18/accepted PY - 2018/9/25/pubmed PY - 2019/2/12/medline PY - 2018/9/25/entrez KW - Helicobacter pylori KW - hepatic steatosis KW - insulin resistance KW - nonalcoholic fatty liver disease SP - e12537 EP - e12537 JF - Helicobacter JO - Helicobacter VL - 23 IS - 6 N2 - 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. SN - 1523-5378 UR - https://www.unboundmedicine.com/medline/citation/30246507/Helicobacter_pylori_and_non_alcoholic_fatty_liver_disease:_A_new_enigma L2 - https://doi.org/10.1111/hel.12537 DB - PRIME DP - Unbound Medicine ER -