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Effectiveness of Acid Suppression in Preventing Gastroesophageal Reflux Disease (GERD) After Successful Treatment of Helicobacter pylori Infection

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Abstract

There is evidence that Helicobacter pylori eradication might predispose to gastroesophageal reflux disease (GERD). The aim of this prospective study was to examine the effectiveness of antisecretory treatment, after successful H. pylori eradication, in preventing GERD, since no data exist so far. Eighty initially H. pylori(+) patients, without GERD at the time of H. pylori eradication [50 peptic ulcer (PU) and 30 nonulcer (NU), 55 men, 25 women, median age 38 years, range 19–57], after successful H. pylori eradication were randomized to recieve either omeprazole 20 mg daily (group A) or no treatment (group B) for one year. All patients underwent upper gastrointestinal endoscopy at 0, 6, and 12 months or when GERD symptoms occurred. There were 40 patients in each group, and there were no statistically significant differences between the two groups in terms of sex, age, body weight, ulcer/no ulcer ratio, and other demographic data. Seven patients from group A and five patients from group B were lost to follow-up, and therefore there were 33 and 35 patients in groups A and B, respectively, who completed the study. One of 33 patients in group A (3%) and 10/35 (28.5%) in group B developed GERD symptoms during follow-up (P = 0.0022). The respective values for esophagitis were 0/33(0%) and 6/35(17.1%) (P = 0.0083). In conclusion, antisecretory treatment in H. pylori(+) patients, after successful eradication, is effective in preventing GERD.

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References

  1. Marshall BJ, McGechie DB, Rogers PA, Glancy RJ: Pyloric Campylobacter infection and gastroduodenal disease. Med J Aust 142:439–444, 1985

    Google Scholar 

  2. Rokkas T, Sladen GE: Infection with Campylobacter pylori. J R Coll Physicians London 22:97–100, 1988

    Google Scholar 

  3. Graham D: Campylobacter pylori and peptic ulcer disease. Gastroenterology 96:615–625, 1989

    Google Scholar 

  4. Raws EA, Tytgat GNJ: Cure of duodenal ulcer associated with eradication of Helicobacter pylori. Lancet 335:1233–1235, 1990

    Google Scholar 

  5. Tytgat GNJ, Lee A, Graham DY, Dixon MF, Rokkas T: The role of infectious agents in peptic ulcer disease. Gastroenterol Int 6:76–89, 1993

    Google Scholar 

  6. Graham DY, Lew GM, Klein PD, Evans DG, Evans DJ Jr, Saeed ZA, Malaty HM: Effect of treatment of Helicobacter pylori infection and the long term reccurence of gastric and duodenal ulcer; a randomized, controlled study. Ann Intern Med 116:705–708, 1992

    Google Scholar 

  7. Sentander C, Gravalos RG, Codenilla AG, Pajares JM: Maintenance treatment versus Helicobacter pylori eradication therapy in preventing rebleeding of peptic ulcer disease. A clinical trial and follow up for two years. Gastroenterology 108:A208, 1995

    Google Scholar 

  8. Graham DY, Hepps KS, Ramirez FC, Lew GM, Saeed ZA: Treatment of Helicobacter pylori reduces the rate of rebleeding in peptic ulcer disease. Scand J Gastroenterol 28:939–942, 1993

    Google Scholar 

  9. Jaspersen D, Koerner T, Schorr W, Brennenstuhl M, Raschka C, Hammar CH: Helicobacter pylori eradication reduces the rate of rebleeding in ulcer haemorrhage. Gastrointest Endosc 41:5–7, 1995

    Google Scholar 

  10. Rokkas T, Karameris A, Mavrogeorgis A, Rallis E, Giannikos N: Eradication of Helicobacter pylori reduces the possibility of rebleeding in peptic ulcer disease. Gastrointest Endosc 41:1–4, 1995

    Google Scholar 

  11. Vicary JJ, Peek RM, Falk GW, Goldblum JR, Easley KA, Schnell J, Perez-Perez GI, Halter SA, Rice TW, Blaser MJ, Richter JE: The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology 115:50–57, 1998

    Google Scholar 

  12. O'Connor HJ, Cunnane K: Helicobacter pylori and gastroesophageal reflux disease. Ir J Med Sci 163:369–373, 1994

    Google Scholar 

  13. Vicari JJ, Falk GW, Goldlum JR, Easley K: Helicobacter pylori is not a pathogenetic factor in GERD or its complications. Gastroenterology 112:A322, 1997

    Google Scholar 

  14. Newton M, Bryan R, Burnham WR, Kamm MA: Evaluation of Helicobacter pylori in reflux oesophagitis and Barrett's oesophagus. Gut 40:9–13, 1997

    Google Scholar 

  15. Varanasi RV, Fantry GT, Wilson KT: Decreased prevalence of H. pylori infection in Gastroesophageal reflux disease. Helicobacter 3:188–194, 1998

    Google Scholar 

  16. Labenz J, Blum AI, Bayerdorffer E, Meining A, Stolte M, Borsch G: Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology 112:1442–1447, 1997

    Google Scholar 

  17. Dixon MF, Genta RM, Yardley JH, Correa P: Classification and grading of gastritis. The updated Sydney system. Am J Surg Pathol 20:1161–1181, 1996

    Google Scholar 

  18. Armstrong D, Bennett JR, Blum AL, Dent J, De Dombal FT, Galmiche J-P, Lungell L, Margulies M, Richter JE, Spechler SJ, Tytgat GNJ, Wallin L: The endoscopic assessment of of esophagitis: A progress report on observer agreement. Gastroenterology 111:85–92, 1996

    Google Scholar 

  19. Motalsky H: Intuitive Biostatistics. New York, Oxford University Press, 1995

    Google Scholar 

  20. Locke GR, Talley NJ, Fett SL, Zinsmeister AR, Melton LJ: Prevalence and clinical spectrum of gastroesophageal reflux disease: A population-based study in Olmsted County, Minnesota. Gastroenterology 112:1448–1456, 1997

    Google Scholar 

  21. Collen MJ, Lewis JH, Benjamin SB: Gastric acid secretion in refractory gastroesophageal reflux disease. Gastroenterology 98:654–661, 1990

    Google Scholar 

  22. Miller LS, Vinayek R, Frucht H, Gardner JD, Jensen RT, Maton PN: Reflux esophagitis in patients with Zollinger-Ellison syndrome. Gastroenterology 98:341–346, 1990

    Google Scholar 

  23. Chow WH, Blaser MJ, Blot WJ, Gammon MD, Vaughan TL, Risch HA, Perez-Perez GI, Schoenberg JB, Stanford JL, Rottedam H, West AB, Fraumeni JF Jr: An inverse relation between cagA1 strains of Helicobacterr pylori infection and risk of esophageal and gastric cardia adenocarcinoma. Cancer Res 58:588–590, 1998

    Google Scholar 

  24. Loof L, Gotell P, Elfberg B: The incidence of reflux esophagitis. A study on endoscopy report from a defined catchment area in Sweden. Scand J Gastroenterol 28:113–118, 1993

    Google Scholar 

  25. Petersen H: The prevalence of gastro-esophageal reflux disease. Scand J Gastroenterol 30(suppl 211):5–6, 1995

    Google Scholar 

  26. Goggin PM, Marrero JM, Ahmed H, Jackson PA, Corbishley CM, Northfield TC: Urea hydrolysis in Helicobacter pylori infection. Eur J Gastroenterol Hepatol 3:927–933, 1991

    Google Scholar 

  27. Bersik P, Verdu EF, Armstrong D, Cederberg C, Idstrom J-P, Stolte M, Blum AL: H. pylori related increase in omeprazole (OME) effect is associated with ammonia production. Gastroentereology 110:A64, 1996

    Google Scholar 

  28. Verdu EF, Bercik, P, Armstrong D, Sobovcikova L, Idström J-P, Caderberg C, Blum AL: Production of volatile amines by Helicobacter pylori (Hp) is not relevant in vivo. Gastroenterology 110:A285, 1996

    Google Scholar 

  29. Galmiche JP, Janssens J: The pathophysiology of gastrooesophageal reflux disease: An overview. Scand J Gastroenterol 30(suppl 211):7–18, 1995

    Google Scholar 

  30. Konturek SJ, Konturek PJ, Brzozowski T, Stachnura J, Zombala M: Gastric mucosal damage and adaptive protection by ammonia and ammonium ions in rats. Dig Dis Sci 57:433–445, 1996

    Google Scholar 

  31. El-Omar EM, Penman ID, Ardill JE, Chittajallu RS, Howie C, McColl KE: Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease. Gastroenterology 109:681–691, 1995

    Google Scholar 

  32. El-Omar EM, Penman ID, Dorrian CA, Ardill JE, McColl KE: Eradication of Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer. Gut 34:1060–1065, 1993

    Google Scholar 

  33. Harris AW, Gummett PA, Misiewicz JJ, Baron JH: Eradication of Helicobacter pylori in patients with duodenal ulcer lowers basal and peak acid outputs to gastrin releasing peptide and pentagastrin. Gut 38:663–667, 1996

    Google Scholar 

  34. Gisbert JP, Boixela D, Vila T, de Rafael L, Redondo C, de Argila CM: Basal and stimulated gastrin levels and gastric acid output five months after therapy for Helicobacter pylori eradication in duodenal ulcer patients. J Clin Gastroenterol 22: 90–95, 1996

    Google Scholar 

  35. El-Omar EM, Oien K, El-Nujumi A, Gillen D, Wirz A, Dahill S, Williams C, Ardill JE, McColl KE: Helicobacter pylori infection and chronic gastric acid hypersecretion. Gastroenteerology 113:15–24, 1997

    Google Scholar 

  36. Haruma K, Mihara M, Okamoto E, Kusunoki H, Hananoki M, Tanaka S, Yoshihara M, Sumii K, Kajiyama G: Eradication of Helicobacter pylori increases gastric acidity in patients with atrophic gastritis of the corpus-evaluation of 24–h pH monitoring. Aliment Pharmacol Ther 13:155–162, 1999

    Google Scholar 

  37. Beil W, Birkholz C, Wagner S, Sewing K-F: Interaction of Helicobacter pylori and its fatty acids with parietal cells and gastric H+/K+-ATPase. Gut 25:1176–1180, 1994

    Google Scholar 

  38. Cave DR, Vargas M: Effect of a Campylobacter pylori protein on acid secretion by parietal cells. Lancet 2:187–189, 1989

    Google Scholar 

  39. Feldman M, Cryer B, McArthur KE, Lee E: Relationship between severity of H. pylori (HP) gastritis and gastric acidpepsin secretion in man. Gastroenterology 110:A106, 1996

    Google Scholar 

  40. Yasunaga Y, Shinimura Y, Kanayama S, Yabu M, Nakanishi T, Miyazaki Y, Murayama Y, Bonilla-Palasios JJ, Matsuzawa Y: Improved fold width and increased acid secretion after eradication of the organism in Helicobacter pylori associated enlarged fold gastritis. Gut 35:1571–1574, 1994

    Google Scholar 

  41. Esplugues JV, Barrachina MD, Calatayud S, Pique JM, Whittle BJ: Nitric oxide mediates the inhibition by interleukin-1 beta of pentagastrin-stimulated rat gastric acid secretion. Br J Pharmacol 108:9–10, 1993

    Google Scholar 

  42. McGowan CC, Cover TL, Blaser MJ: Helicobacter pylori and gastric acid: Biological and therapeutic implications. Gastroenterology 110:926–938, 1996

    Google Scholar 

  43. Pfeiffer A, Krömer W, Friemann J, Ruge M, Herawi M, Schätzl M, et al: Muscarinic receptors in gastric mucosa are increased in peptic ulcer disease. Gut 36:813–818, 1995

    Google Scholar 

  44. Robert A, Olafsson AS, Lancaster C, Zhang WR: Interleukin-1 is cytoprotective, antisecretory, stimulates PGE2 synthesis by the stomach, and retards gastric emptying. Life Sci 48:123–134, 1991

    Google Scholar 

  45. Takeuchi K, Ohuchi T, Okabe S: Effects of nitric oxide synthase inhibitor N g-nitro-L-arginine methyl ester on duodenal alkaline secretory and ulcerogenic responses induced by mepirizole in rats. Dig Dis Sci 40:670–677, 1995

    Google Scholar 

  46. Rokkas T, Liatsos C, Karameris A, Petridou E, Papatheodorou G, Kalafatis E: Serologic detection of CagA Helicobacter pylori strains predicts the presence ofpeprtic ulcer in young dyspeptic patients. Gastrointest Endosc 50:511–516, 1999

    Google Scholar 

  47. Yamaoka Y, Kita M, Kodama T, Sawai N, Kashima K, Imanishi J: Induction of various cytokines and development of severe mucosal inflammation by cagA gene positive Helicobacter pylori strains. Gut 41:442–451, 1997

    Google Scholar 

  48. El-Serag HB, Sonnenberg A: Opposing time trends of peptic ulcer and reflux disease. Gut 43:327–333, 1998

    Google Scholar 

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Authors and Affiliations

  1. Gastroenterology Unit, 401 Army General Hospital, Athens, Greece

    T. Rokkas, C. Liatsos & E. Panagou

  2. Gastroenterology Unit, 2nd Department of Internal Medicine, Medical School, University of Athens, Evangelismos Hospital, Athens, Greece

    T. Rokkas, S.D. Ladas & S.A. Raptis

  3. Histopathology Department, 401 Army General Hospital, Athens, Greece

    A. Karameris

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Rokkas, T., Ladas, S., Liatsos, C. et al. Effectiveness of Acid Suppression in Preventing Gastroesophageal Reflux Disease (GERD) After Successful Treatment of Helicobacter pylori Infection. Dig Dis Sci 46, 1567–1572 (2001). https://doi.org/10.1023/A:1010616710501

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