Association of hepatobiliary pathology and gastroesophageal reflux disease
DOI: 10.32364/2587-6821-2021-5-6-404-412
A.N. Kazyulin, A.Yu. Goncharenko, I.E. Kalyagin
A.I. Yevdokimov Moscow State University of Medicine and Dentistry, Moscow,
Russian Federation
The problem of comorbidity with a high risk of polypragmasia is relevant in a large group of patients with diseases in the digestive system. Currently, the problem of comorbidity in patients with gastroesophageal reflux disease (GERD) attracts the attention of specialists due to the high disease prevalence and data indicating its association with other digestive system diseases, primarily of the hepatobiliary system. The article presents the results of clinical and experimental studies revealing the pathogenetic connections of GERD and hepatobiliary pathology accompanied by biliary dyskinesia, factors leading to an impairment of the duodenal propulsive activity. It is noted that the most important components of the esophageal mucosa lesion in duodenogastroesophageal reflux are bile acids, lysolecithin and pancreatic enzymes. The relevance of prescribing drugs that can affect the course of pathogenetically related diseases, which can significantly reduce the risk of polypragmasia, is justified. Such drugs include ursodeoxycholic acid, which, in the conditions of the GERD and hepatobiliary pathology association, contributes to the functional state normalization of the liver and biliary tract, reduces biliary dyskinesia, the severity of duodenal hypertension and duodenogastroesophageal reflux. The next example is the rebamipide cytoprotector, which has a multilateral protective effect against the mucous membrane of the GIT, including the esophagus, gastroduodenal zone, small intestine, as well as liver. The expediency of prescribing rebamipide to patients who are refractory to therapy with proton pump inhibitors is justified.
Keywords: comorbidity, hepatobiliary pathology, gast roesophageal reflux disease, ursodeoxycholic acid, rebamipid, proton pump inhibitors.
For citation: Kazyulin A.N., Goncharenko A.Yu., Kalyagin I.E. Association of hepatobiliary pathology and gastroesophageal reflux disease. Russian Medical Inquiry. 2021;5(6):404–412 (in Russ.). DOI: 10.32364/2587-6821-2021-5-6 - 404-412.
Aknowledgement
The authors and the Editorial Board are grateful to Alium JSC for providing the full texts of foreign articles required for the assistance of this publication.
About the authors:
Alexander N. Kazyulin — Dr. Sc. (Med.), Professor of the Department of Propaedeutics of Internal Diseases and Gastroenterology, A.I. Yevdokimov Moscow State University of Medicine and Dentistry; 20/1, Delegatskaya str., Moscow, 127473, Russian Federation; ORCID iD 0000-0002-0327-4280.
Alexandra Yu. Goncharenko — C. Sc. (Med.), Associate Professor of the Department of Propaedeutics of Internal Diseases and Gastroenterology, A.I. Yevdokimov Moscow State University of Medicine and Dentistry; 20/1, Delegatskaya str., Moscow, 127473, Russian Federation; ORCID iD 0000-0002-5483-9325.
Igor E. Kalyagin — C. Sc. (Med.), Assistant of the Department of Propaedeutics of Internal Diseases and Gastroenterology, A.I. Yevdokimov Moscow State University of Medicine and Dentistry; 20/1, Delegatskaya str., Moscow, 127473, Russian Federation; ORCID iD 0000-0002-3407-5372.
Contact information: Alexander N. Kazyulin, e-mail: alexander.kazyulin@yandex.ru.
Financial Disclosure: no authors have a financial or property interest in any material or method mentioned.
There is no conflict of interests.
Received 27.07.2021.
Revised 16.08.2021.
Accepted 30.08.2021.
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15. Kunsch S., Neesse A., Huth J. et al. Increased Duodeno-Gastro-Esophageal Reflux (DGER) in Symptomatic GERD Patients with a History of Cholecystectomy. Z Gastroenterol. 2009;47:744–748. DOI: 10.1055/s-0028-1109176.
16. Fujikawa Y., Tominaga K., Fujii H. et al. High prevalence of gastroesophageal reflux symptoms in patients with non-alcoholic fatty liver disease associated with serum levels of triglyceride and cholesterol but not simple visceral obesity. Digestion. 2012;86(3):228–237. DOI: 10.1159/000341418.
17. Catanzaro R., Calabrese F., Occhipinti S. et al. Nonalcoholic fatty liver disease increases risk for gastroesophageal reflux symptoms. Dig Dis Sci. 2014;59(8):1939–1945. DOI: 10.1007/s10620-014-3113-7.
18. Sun D., Wang X., Gai Z. et al. Bile acids but not acidic acids induce Barrett’s esophagus. Int J Clin Exp Pathol. 2015;8(2):1384–1392. PMID: 25973022.
19. Wijarnpreecha K., Panjawatanan P., Thongprayoon C. et al. Association between gastroesophageal reflux disease and nonalcoholic fatty liver disease: A meta-analysis. Saudi J Gastroenterol. 2017;23(6):311–317. DOI: 10.4103/sjg.SJG_161_17.
20. Hashimoto N. Effects of bile acids on cyclooxygenase-2 expression in a rat model of duodenoesophageal anastomosis. World J Gastroenterol. 2014;20(21):6541–6546. DOI: 10.3748/WJG.V20.I21.6541.
21. Min Y.W., Kim Y., Gwak G.-Y. et al. Non-alcoholic fatty liver disease and the development of reflux esophagitis: A cohort study. J Gastroenterol Hepatol. 2018;33(5):1053–1058. DOI: 10.1111/jgh.14042.
22. Xue J., Xin H., Ren N. et al. Nonalcoholic fatty liver disease increases the risk of gastroesophageal reflux disease: A systematic review and meta-analysis. Eur J Clin Invest. 2019;49:13158. DOI: 10.1111/eci.13158.
23. Tack J. Review article: role of pepsin and bile in gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 2005;22(1):48–54. DOI: 10.1111/j.1365-2036.2005.02609.x.
24. Dixon M.F., Neville P.M., Mapstone N.P. et al. Bile reflux gastritis and Barrett’s oesophagus: further evidence of a role for duodenogastro-oesophageal reflux? Gut. 2001;49:359–363. DOI: 10.1136/gut.49.3.359.
25. Bueverov A.O., Lapina E.L. Duodenogastric reflux as a cause of reflux esophagitis. Farmateca. 2006;1:1–5 (in Russ.).
26. Osadchuk A.M., Davydkin I.L., Palushkina M.G. Refractory form of gastroesophageal reflux disease. Topical and open issues of conservative therapy. Medical almanac. 2012;1:29–34 (in Russ.).
27. Maksimov V.A., Chernyshev A.L., Tarasov K.M., Neronov V.A. Biliary insufficiency. M.: Adamant; 2008 (in Russ.).
28. Gubergrits N.B., Kazyulin A.N. Metabolic pancreatology. Donetsk: LLC "Lebed"; 2011 (in Russ.).
29. Kawabea A., Shimada Y., Soma T. et al. Production of prostaglandin E 2 via bile acid is enhanced by trypsin and acid in normal human esophageal epithelial cells. Life Sciences. 2004;75:21–34. DOI: 10.1016/j.lfs.2003.11.022.
30. Zhang R., Gong J., Wang H., Wang L. Bile salts inhibit growth and induce apoptosis of cultured human normal esophageal mucosal epithelial cells. World J Gastroenterol. 2005;11(41):6466–6471. DOI: 10.3748/wjg.v11.i41.6466.
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