Relationship between Bile Reflux and the Severity of Gastric Mucosal Damage in Patients with Dyspepsia

Tjokorda Istri Anom Saturti(1), I Ketut Mariadi(2), I Nyoman Triyanayasa(3), Dwijo Anargha Sindhughosa(4), Toshio Kuwai(5),


(1) Division of Allergy and Immunology, Department of Internal Medicine, Udayana University / Prof. Dr. I.G.N.G. Ngoerah Hospital, Denpasar, Bali, Indonesia
(2) Gastroentero-Hepatology Division, Department of Internal Medicine, Faculty of Medicine Udayana University, Bali Indonesia
(3) Department of Internal Medicine, Udayana University / Prof. Dr. I.G.N.G. Ngoerah Hospital, Denpasar, Bali, Indonesia
(4) Division of Gastroenterology-Hepatology, Department of Internal Medicine, Udayana University / Prof. Dr. I.G.N.G. Ngoerah Hospital, Denpasar, Bali, Indonesia
(5) Gastrointestinal Endoscopy and Medicine, Hiroshima University Hospital, Hiroshima, Japan
Corresponding Author

Abstract


Background: Dyspepsia is a complaint of pain in the epigastrium that lasts for at least 1 month and is closely related to upper gastrointestinal complaints such as nausea, vomiting, and a feeling of early fullness. One of the risk factors for dyspepsia is bile acid reflux. The most common endoscopic findings in patients with bile acid reflux include mucosal erythema, the presence of bile acid on the mucosa, erosion, hyperugosity, and gastric mucosal atrophy.

Methods: This study was a cross-sectional study conducted on 99 dyspeptic patients who underwent endoscopy at Prof. Dr. I.G.N.G. Ngoerah Denpasar Hospital. Bile acid examination was performed using the enzymatic calorimetric method, and mucosal damage assessment was based on the Lanza score evaluated by 2 observers. The degree of mucosal damage was classified as mild (score 0-2) and severe (score 3-5).

Results: The age range of the 99 subjects was 19-83 years, with 58 (58.6%) males and 41 (41.4%) females. H. pylori antibodies were detected in 21% of the subjects, and 48% had a pH below 2.77; 48% had a history of NSAID consumption. The mean value of bile acid levels in gastric fluid was 156.07 μmol/L, with a median of 170.09 μmol/L (≥170.09 μmol/L classified as high, <170.09 μmol/L classified as low). During endoscopic observation, mild mucosal damage was found in 61%, and severe damage was found in 39% (kappa 1, P<0.001). According to the Chi-square test, there was a statistically significant relationship between gastric fluid bile acid levels and mucosal damage (P<0.05).

Conclusion: This study concludes that there is a relationship between the level of bile acid in gastric fluid and the degree of mucosal damage.


Keywords


bile acid levels; gastric fluid; gastric mucosal damage degree

References


Jameson JL, Kasper DL, Fauci AS, Hauser SL, Longo DL, Loscalzo J, et al. Harrison's principles of internal MEDICINE, 20E. New York: McGraw-Hill Education; 2018.

Davenport HW. Destruction of the gastric mucosal barrier by detergents and Urea. Gastroenterology. 1968;54(2):175–181.

Di Ciaula A, Wang DQ-H, Molina-Molina E, Lunardi Baccetto R, Calamita G, Palmieri VO, et al. Bile acids and cancer: Direct and environmental-dependent effects. Ann Hepatol. 2017;16.

Martamala RR, Rani AA. The pathogenesis and diagnosis of bile reflux gastropathy. Indones J Gastroenterol Hepatol Dig Endosc. 2001;2(1):14-20.

Matsuhisa T, Arakawa T, Watanabe T, Tokutomi T, Sakurai K, Okamura et al. Relation between bile acid reflux into the stomach and the risk of atrophic gastritis and intestinal metaplasia: A multicenter study of 2283 cases. Dig Endosc. 2013;25(5):519–25.

Li D, Zhang J, Yao WZ, Zhang DL, Feng CC, He Q, Lv HH, et al. The relationship between gastric cancer, its precancerous lesions and bile reflux: A retrospective study. J Dig Dis. 2020;21(4):222–229.

Taha A. Oesophagitis and bile reflux gastritis—clinical and histological assessments. Dig Liver Dis. 2003;35(10):701–705.

Vaezi MF, Richter JE. Contribution of acid and duodenogastrooesophageal reflux to oesophageal mucosal injury and symptoms in partial gastrectomy patients. Gut. 1997;41(3):297–302.

Vere CC, Cazacu S, Comănescu VIOLETA, Mogoantă L, Rogoveanu I, et al. Endoscopical and histological features in bile reflux gastritis. Rom J Morphol Embryol. 2005;46(4):269-74.

Johannesson KÅ, Hammar E, Staël von Holstein C. Mucosal changes in the Gastric Remnant. Eur J Gastroenterol Hepatol. 2003;15(1):35–40.

Dixon MF. Bile reflux gastritis and intestinal metaplasia at the Cardia. Gut. 2002;51(3):351–355.

Chen SL, et al. The influence of bile reflux, gastric acid, and Helicobacter pylori infection on gastric mucosal injury: Severity and localization. Weichang Bingxue. 2002;7:280-285.

Tang C, Zhu Y, Yang X, Xu B, Ye C, Yang Y, et al. Upper gastrointestinal mucosal injury associated with ticagrelor plus aspirin, ticagrelor alone, or aspirin alone at 1‐year after coronary artery bypass grafting. J Gastroenterol Hepatol. 2020;35(10):1720–1730.

Simadibrata M, Makmun D, Abdullah M, Syam AF, Fauzi A, Renaldi K, et al. Konsensus nasional penatalaksanaan dispepsia dan infeksi Helicobacter pylori.

Mariadi IK, Wibawa ID, Wibawa IB. Detection of Helicobacter pylori CagA gene and its association with endoscopic appearance in Balinese dyspepsia patients. Indones J Gastroenterol Hepatol Dig Endosc. 2017;17(2):99–105.

Miftahussurur M, Waskito LA, Fauzia KA, Mahmudah I, Doohan D, Adnyana IK, Khomsan A, Ratnasari N, Rezkitha YA. Overview of Helicobacter pylori infection in Indonesia: What distinguishes it from countries with high gastric cancer incidence? Gut Liver. 2021;15(5):653–665.

Hegyi P, Maléth J, Walters JR, Hofmann AF, Keely SJ. Guts and gall: Bile acids in regulation of intestinal epithelial function in health and disease. Physiol Rev. 2018;98(4):1983–2023.

Bechi P, Cianchi F, Mazzanti R, Fantappiè O, Fiorillo C, et al. Reflux and pH: ‘alkaline’ components are not neutralized by gastric pH variations. Dis Esophagus. 2000;13(1):51–55.


Full Text: PDF

Article Metrics

Abstract View : 85 times
PDF Download : 71 times

DOI: 10.24871/2522024295

Refbacks

  • There are currently no refbacks.