Helicobacter pylori infection prevents erosive reflux oesophagitis by decreasing gastric acid secretion (original) (raw)

Abstract

BACKGROUND_—_Helicobacter pylori infection is less prevalent and atrophic gastritis is less extensive in patients with reflux oesophagitis than those without it, but few studies have examined this relationship directly. _AIMS_—We investigated the relationship between H pylori infection, acid secretion, and reflux oesophagitis in Japanese subjects. _SUBJECTS_—A total of 105 patients with erosive reflux oesophagitis were compared with 105 sex and age matched patients without reflux oesophagitis. _METHODS_—The diagnosis of H pylori infection was made by histological examination of gastric mucosal biopsy specimens, rapid urease test, and detection of serum IgG antibodies. Acid secretion was assessed by the endoscopic gastrin test. RESULTS_—_H pylori infection was present in 36 patients with erosive reflux oesophagitis (34.3%) and in 80 control subjects (76.2%) (odds ratio 0.163, 95% confidence interval 0.09-0.29). Overall acid secretion was significantly greater in patients with reflux oesophagitis. Among H pylori positive patients, acid secretion was greater in patients with reflux oesophagitis than those without oesophagitis. _CONCLUSION_—In Japan, erosive reflux oesophagitis occurs most often in the absence of H pylori infection and gastric hyposecretion. Even in the presence of H pylori infection, reflux oesophagitis is more likely to develop in patients without gastric hyposecretion. H pylori infection may inhibit reflux oesophagitis by inducing hypoacidity. Keywords: Helicobacter pylori; gastro-oesophageal reflux disease; reflux oesophagitis; acid secretion

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Figure 1 .

Figure 1  

(A) Atrophy scores in the antrum (left) and body (right) assessed by the updated Sydney system were significantly lower in patients with reflux oesophagitis than in control subjects (antrum 0.52 (0.86) v 1.20 (0.98), p<0.01; body 0.09 (0.29) v 0.54 (0.89), p<0.01 by Mann-Whitney U test). (B) Atrophy scores of both the antrum (left) and body (right) were not different between the reflux oesophagitis and control groups among the Helicobacter pylori (HP) negative subjects while they were significantly lower in the former than the latter when compared in HP positive individuals (antrum 0.97 (0.90) v 1.59 (0.81), p<0.01; body 0.21 (0.41) v 0.72 (0.96), p<0.01 by Mann-Whitney U test).

Figure 2 .

Figure 2  

(A) Gastritis scores in the antrum (left) and the body (right) assessed by the updated Sydney system were significantly lower in patients with reflux oesophagitis than in control subjects (antrum 1.16 (1.73) v 2.20 (1.70), p<0.01; body 0.57 (1.01) v 1.98 (1.56), p<0.01 by Mann-Whitney U test). (B) Gastritis scores in the antrum (left) and body (right) were not different between the reflux oesophagitis group and control group in the Helicobacter pylori (HP) negative subjects. However, gastritis score of the corpus was significantly lower in patients with oesophagitis than in controls in HP positive subjects (1.47 (1.13) v 2.63 (1.23), p<0.01 by Mann-Whitney U test) although the difference in the antrum was not significant in the HP positive subjects.

Figure 3 .

Figure 3  

(A) The endoscopic gastrin test (EGT) value was significantly higher in patients with reflux oesophagitis than in control subjects (3.65 (2.17) mEq/10 minutes v 1.86 (1.77); p<0.01 by Mann-Whitney U test). (B) The EGT value was not different between patients with and without reflux oesophagitis among the Helicobacter pylori (HP) negative individuals but it was significantly higher in patients with reflux oesophagitis than in controls in HP positive subjects (3.08 (2.18) mEq/10 minutes v 1.44 (1.70); p<0.01 by Mann-Whitney U test).

Selected References

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  1. ALLISON P. R. Reflux esophagitis, sliding hiatal hernia, and the anatomy of repair. Surg Gynecol Obstet. 1951 Apr;92(4):419–431. [PubMed] [Google Scholar]
  2. Ahtaridis G., Snape W. J., Jr, Cohen S. Clinical and manometric findings in benign peptic strictures of the esophagus. Dig Dis Sci. 1979 Nov;24(11):858–861. doi: 10.1007/BF01324902. [DOI] [PubMed] [Google Scholar]
  3. Armstrong D., Bennett J. R., Blum A. L., Dent J., De Dombal F. T., Galmiche J. P., Lundell L., Margulies M., Richter J. E., Spechler S. J. The endoscopic assessment of esophagitis: a progress report on observer agreement. Gastroenterology. 1996 Jul;111(1):85–92. doi: 10.1053/gast.1996.v111.pm8698230. [DOI] [PubMed] [Google Scholar]
  4. Asaka M., Kimura T., Kudo M., Takeda H., Mitani S., Miyazaki T., Miki K., Graham D. Y. Relationship of Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population. Gastroenterology. 1992 Mar;102(3):760–766. doi: 10.1016/0016-5085(92)90156-s. [DOI] [PubMed] [Google Scholar]
  5. Azuma T., Konishi J., Tanaka Y., Hirai M., Ito S., Kato T., Kohli Y. Contribution of HLA-DQA gene to host's response against Helicobacter pylori. Lancet. 1994 Feb 26;343(8896):542–543. doi: 10.1016/s0140-6736(94)91496-6. [DOI] [PubMed] [Google Scholar]
  6. Bock O. A., Richards W. C., Witts L. J. The relationship between acid secretion after augmented histamine stimulation and the histology of the gastric mucosa. Gut. 1963 Jun;4(2):112–114. doi: 10.1136/gut.4.2.112. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Borén T., Falk P., Roth K. A., Larson G., Normark S. Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens. Science. 1993 Dec 17;262(5141):1892–1895. doi: 10.1126/science.8018146. [DOI] [PubMed] [Google Scholar]
  8. Dent J., Holloway R. H., Toouli J., Dodds W. J. Mechanisms of lower oesophageal sphincter incompetence in patients with symptomatic gastrooesophageal reflux. Gut. 1988 Aug;29(8):1020–1028. doi: 10.1136/gut.29.8.1020. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Dodds W. J., Dent J., Hogan W. J., Helm J. F., Hauser R., Patel G. K., Egide M. S. Mechanisms of gastroesophageal reflux in patients with reflux esophagitis. N Engl J Med. 1982 Dec 16;307(25):1547–1552. doi: 10.1056/NEJM198212163072503. [DOI] [PubMed] [Google Scholar]
  10. Furukawa N., Iwakiri R., Koyama T., Okamoto K., Yoshida T., Kashiwagi Y., Ohyama T., Noda T., Sakata H., Fujimoto K. Proportion of reflux esophagitis in 6010 Japanese adults: prospective evaluation by endoscopy. J Gastroenterol. 1999 Aug;34(4):441–444. doi: 10.1007/s005350050293. [DOI] [PubMed] [Google Scholar]
  11. Hackelsberger A., Schultze V., Günther T., von Arnim U., Manes G., Malfertheiner P. The prevalence of Helicobacter pylori gastritis in patients with reflux oesophagitis: a case-control study. Eur J Gastroenterol Hepatol. 1998 Jun;10(6):465–468. doi: 10.1097/00042737-199806000-00005. [DOI] [PubMed] [Google Scholar]
  12. Hetzel D. J., Dent J., Reed W. D., Narielvala F. M., Mackinnon M., McCarthy J. H., Mitchell B., Beveridge B. R., Laurence B. H., Gibson G. G. Healing and relapse of severe peptic esophagitis after treatment with omeprazole. Gastroenterology. 1988 Oct;95(4):903–912. doi: 10.1016/0016-5085(88)90162-x. [DOI] [PubMed] [Google Scholar]
  13. Hirschowitz B. I. A critical analysis, with appropriate controls, of gastric acid and pepsin secretion in clinical esophagitis. Gastroenterology. 1991 Nov;101(5):1149–1158. doi: 10.1016/0016-5085(91)90062-p. [DOI] [PubMed] [Google Scholar]
  14. Iijima K., Ohara S., Sekine H., Koike T., Kubota Y., Kato K., Asaki S., Toyota T. A new endoscopic method of gastric acid secretory testing. Am J Gastroenterol. 1998 Nov;93(11):2113–2118. doi: 10.1111/j.1572-0241.1998.00603.x. [DOI] [PubMed] [Google Scholar]
  15. Kahrilas P. J., Dodds W. J., Hogan W. J., Kern M., Arndorfer R. C., Reece A. Esophageal peristaltic dysfunction in peptic esophagitis. Gastroenterology. 1986 Oct;91(4):897–904. doi: 10.1016/0016-5085(86)90692-x. [DOI] [PubMed] [Google Scholar]
  16. Klinkenberg-Knol E. C., Jansen J. M., Festen H. P., Meuwissen S. G., Lamers C. B. Double-blind multicentre comparison of omeprazole and ranitidine in the treatment of reflux oesophagitis. Lancet. 1987 Feb 14;1(8529):349–351. doi: 10.1016/s0140-6736(87)91726-0. [DOI] [PubMed] [Google Scholar]
  17. Koike T., Ohara S., Sekine H., Iijima K., Kato K., Shimosegawa T., Toyota T. Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis. Am J Gastroenterol. 1999 Dec;94(12):3468–3472. doi: 10.1111/j.1572-0241.1999.01593.x. [DOI] [PubMed] [Google Scholar]
  18. Newton M., Bryan R., Burnham W. R., Kamm M. A. Evaluation of Helicobacter pylori in reflux oesophagitis and Barrett's oesophagus. Gut. 1997 Jan;40(1):9–13. doi: 10.1136/gut.40.1.9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Peek R. M., Jr, Miller G. G., Tham K. T., Perez-Perez G. I., Zhao X., Atherton J. C., Blaser M. J. Heightened inflammatory response and cytokine expression in vivo to cagA+ Helicobacter pylori strains. Lab Invest. 1995 Dec;73(6):760–770. [PubMed] [Google Scholar]
  20. Rider J. H. Sanitary Features of Irrigation. Am J Public Health Nations Health. 1930 Nov;20(11):1187–1191. doi: 10.2105/ajph.20.11.1187. [DOI] [PMC free article] [PubMed] [Google Scholar]
  21. Shirota T., Kusano M., Kawamura O., Horikoshi T., Mori M., Sekiguchi T. Helicobacter pylori infection correlates with severity of reflux esophagitis: with manometry findings. J Gastroenterol. 1999 Oct;34(5):553–559. doi: 10.1007/s005350050372. [DOI] [PubMed] [Google Scholar]
  22. Stanciu C., Bennett J. R. Oesophageal acid clearing: one factor in the production of reflux oesophagitis. Gut. 1974 Nov;15(11):852–857. doi: 10.1136/gut.15.11.852. [DOI] [PMC free article] [PubMed] [Google Scholar]
  23. Vantrappen G., Rutgeerts L., Schurmans P., Coenegrachts J. L. Omeprazole (40 mg) is superior to ranitidine in short-term treatment of ulcerative reflux esophagitis. Dig Dis Sci. 1988 May;33(5):523–529. doi: 10.1007/BF01798351. [DOI] [PubMed] [Google Scholar]
  24. Varanasi R. V., Fantry G. T., Wilson K. T. Decreased prevalence of Helicobacter pylori infection in gastroesophageal reflux disease. Helicobacter. 1998 Sep;3(3):188–194. doi: 10.1046/j.1523-5378.1998.08001.x. [DOI] [PubMed] [Google Scholar]
  25. Vicari J. J., Peek R. M., Falk G. W., Goldblum J. R., Easley K. A., Schnell J., Perez-Perez G. I., Halter S. A., Rice T. W., Blaser M. J. The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology. 1998 Jul;115(1):50–57. doi: 10.1016/s0016-5085(98)70364-6. [DOI] [PubMed] [Google Scholar]
  26. Werdmuller B. F., Loffeld R. J. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci. 1997 Jan;42(1):103–105. doi: 10.1023/a:1018841222856. [DOI] [PubMed] [Google Scholar]