Skip to main content
Log in

Helicobacter pylori and luminal gastric pH

Relationships in nonulcer dyspepsia

  • Original Article
  • Published:
Digestive Diseases and Sciences Aims and scope Submit manuscript

Abstract

The relationships between gastric pH andHelicobacter pylori infection were studied in 37 consecutive subjects affected with nonclcer dyspepsia. Each underwent esophagogastroduodenoscopy with multiple gastric biopsies for bothH. pylori and histologic assessment, and 24-hr antral pH monitoring.H. pylori was harbored by 59.5% of the subjects with whole gastric spread of infection in all but one patient. Histologic gastritis was shown in 70.3% of the subjects.H. pylori was strongly associated with gastritis, both antral nonatrophic and multifocal atrophic. The ranges of 24-hr pH values were 1.3–6.9 in theH. pylori-positive and 1.2–6.8 in theH. pylori-negative group. Differences in pH values between the two groups were not significant. Moreover, the mean percent time duration of pH above 2, 4, and 6 did not significantly differ between the two groups. Therefore, this study has shown that chronicH. pylori infection is not related to luminal gastric pH.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  1. Warren JR, Marshall BJ: Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet 2:1273–1275, 1983

    Google Scholar 

  2. Marshall BJ, Warren JR: Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1:1311–1314, 1984

    Google Scholar 

  3. Blaser MJ: GastricCampylobacter-like organisms, gastritis and peptic ulcer disease. Gastroenterology 93:371–380, 1987

    Google Scholar 

  4. Rathbone BJ, Wyatt JI, Heatley RV: Possible pathogenetic pathways ofCampylobacter pylori in gastro-duodenal disease. Scand J Gastroenterol 23(suppl 142):40–43, 1988

    Google Scholar 

  5. Ferrero RL, Hazell SL, Lee A: The urease enzymes ofCampylobacter pylori and a related bacterium. J Med Microbiol 27:33–40, 1988

    Google Scholar 

  6. Marshall BJ, Barrett LJ, Prakesh C, McCallum RW, Guerrant RL: Protection ofCampylobacter pyloridis, but notCampylobacter jejuni, against acid susceptibility by urea.In Campylobacter IV: Proceedings of the Fourth International Workshop onCampylobacter Infection. B Kaijsen, E Falsen (eds). Göteborg, University of Göteborg, 1987, pp 402–403

    Google Scholar 

  7. Tompkins DS, West AP:Campylobacter pylori, acid and bile. J Clin Pathol 40:1387, 1987

    Google Scholar 

  8. Giannella RA, Broitman SA, Zamcheck N: Gastric acid barrier to ingested micro-organisms in man: Studiesin vivo andin vitro. Gut 13:251–256, 1972

    Google Scholar 

  9. Brady CE III, Hadfield TL, Hyatt JR, Utts SJ: Acid secretion and serum gastrin levels in individuals withCampylobacter pylori. Gastroenterology 94:923–927, 1988

    Google Scholar 

  10. Murakami M, Yoo JK, Mizuno M, Saita H, Inada M, Miyake T: Effects of ammonia, urea, and urease on the rat gastric mucosa. Gastroenterology 92:A1545, 1987

    Google Scholar 

  11. Hazell SL, Lee A:Campylobacter pyloridis, urease, hydrogen ion back diffusion and gastric ulcers. Lancet 2:15–17, 1986

    Google Scholar 

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

    Google Scholar 

  13. Shallcross TM, Wyatt JY, Millar MR, Heatley RV: Is urease activity a virulence factor forCampylobacter pylori? Klin Wochenschr 67:A63, 1989

    Google Scholar 

  14. O'Connor H, Newbold KM, Alexander-Williams J, Thompson H, Drumm J, Donovan IA: effect of Roux-en-Y biliary diversion onCampylobacter pylori. Gastroenterology 97:958–964, 1989

    Google Scholar 

  15. Offerhaus GJA, Rieu PNMA, Jansen JBMJ, Joosten HJM, Lamers CBHW: Prospective comparative study of the influence of postoperative bile reflux on gastric histology andCampylobacter pylori infection. Gut 30:1552–1557, 1989

    Google Scholar 

  16. Mobley HLT, Cortesia MJ, Rosenthal LE, Jones BD: Characterization of urease fromCampylobacter pylori. J Clin Microbiol 26:831–836, 1988

    Google Scholar 

  17. Slomiany BL, Bilski J, Murty VLN, Sarosiek J, Dworkin B, Van Horn K, Zielenski J, Slomiany A:Campylobacter pyloridis degrades mucin and undermines gastric mucosal integrity. Biochem Biophys Res Commun 144:307–314, 1987

    Google Scholar 

  18. Gledhile T, Leicester RS, Addis B, Lightfoot N, Barnard J, Viney N, Darkin D, Hunt RH: Epidemic hypochlorhydria. Br Med J 289:1383–1386, 1985

    Google Scholar 

  19. Graham DY, Alpert LC, Smith JL, Yoshimura HH: IatrogenicCampylobacter pylori infection is a cause of epidemic achlorhydria. Am J Gastroenterol 83:974–980, 1988

    Google Scholar 

  20. Talley NJ, Fung LH, Gilligan IJ, McNeil D, Piper DW: Association of anxiety, neuroticism, and depression with dyspepsia of unknown cause. A case-control study. Gastroenterology 90:886–892, 1986

    Google Scholar 

  21. Talley NJ, Piper DW: A prospective study of social factors and major life event stress in patients with dyspepsia of unknown cause. Scand J Gastroenterol 22:268–272, 1987

    Google Scholar 

  22. Gad A, Dobrilla G:Campylobacter pylori and non-ulcer dyspepsia. 1. The final results of a double-blind multicentre trial for treatment with pirenzepine in Italy. Scand J Gastroenterol 24(suppl 167):39–43, 1989

    Google Scholar 

  23. Manning AP, Thompson WG, Heaton KW, Morris AF: Towards positive diagnosis of irritable bowel. Br Med J 2:653–654, 1978

    Google Scholar 

  24. Gad A: Erosion: A correlative endoscopic histopathologic multicenter study. Endoscopy 18:76–79, 1986

    Google Scholar 

  25. Maratka Z: Terminology definitions and diagnostic criteria in digestive endoscopy. Scand J Gastroenterol 19(suppl 103):8–65, 1984

    Google Scholar 

  26. Gray SF, Wyatt JI, Rathbone BJ: Simplified modified Giemsa technique for identifyingCampylobacter pyloridis. J Clin Pathol 39:1279–1280, 1986

    Google Scholar 

  27. Correa P: Chronic gastritis: A clinico-pathological classification. Am J Gastroenterol 83:504–509, 1988

    Google Scholar 

  28. Rauws EAJ, Tytgat GNJ: IV Diagnosis ofCampylobacter pylori infection.In Campylobacter pylori. EAJ Rauws, GNJ Tytgat (eds). Amsterdam, WC den Ouden BV, 1989, pp 23–43

    Google Scholar 

  29. Mela GS, Savarino V, Moretti M, Bonifacino G, Sumberaz A, Zentilin P: Clinical relevance of sampling rate in the characterization and analysis of 24-hour gastric acidity. A report on 413 cases. Scand J Gastroenterol 24:683–687, 1989

    Google Scholar 

  30. Mela GS, Savarino V: Processing gastric pH measurements. Gut 30:1438–1439, 1989

    Google Scholar 

  31. Savarino V, Mela GS: Comparison of gastric body and antral pH. Gut 30:1434–1435, 1989

    Google Scholar 

  32. Savarino V, Mela GS, Zentilin P, Scolabrini P, Bonifacino G, Gambaro P, Celle G: Comparison of the effects of placebo, ranitidine, famotidine and nizatidine on intragastric acidity by means of continous pH recording. Digestion 42:1–6, 1989

    Google Scholar 

  33. McNulty CAM: Detection ofCampylobacter pylori by the biopsy urease test.In Campylobacter pylori and Gastroduodenal Disease. BJ Rathbone, RV Heathley (eds). Oxford, Blackwell Scientific Publications, 1989, pp 69–73

    Google Scholar 

  34. Zar JH: Biostatistical Analysis, 2nd ed. Englewood Cliffs, New Jersey, Prentice-Hall, Inc, 1984

    Google Scholar 

  35. Dixon MF, O'Connor HJ, Axon ATR, King RFJK, Johnston D: Reflux gastritis: Distinct histopathological entity? J Clin Pathol 39:524–530, 1986

    Google Scholar 

  36. Bechi P, Amorosi A, Mazzanti R, Romagnoli P, Tonelli L: Gastric histology and fasting bile reflux after partial gastrectomy. Gastroenterology 93:335–343, 1987

    Google Scholar 

  37. Bechi P, Amorosi A, Mazzanti R, Buccarelli A, Pantalone D, Cortesini C: Short-term effects of bile diversion on postgastrectomy gastric histology. Dig Dis Sci 33:1288–1296, 1988

    Google Scholar 

  38. Dixon MF: Progress in the pathology of gastritis and duodenitis.In Current Topics in Pathology. Gastrointestinal Pathology. GT Williams (ed). Berlin, Springer-Verlag, 1990, pp 1–40

    Google Scholar 

  39. Karttunen T, Niemelä S, Lethola J, Heikkilä J, Mäentausta J, Räsänen O:Campylobacter-like organisms and gastritis: Histopathology, bile reflux and gastric fluid composition. Scand J Gastroenterol 22:478–486, 1987

    Google Scholar 

  40. Borody T, Hennessy W, Daskalopoulos G, Carrick J, Hazell SL: Double blind trial of De-Nol in non-ulcer dyspepsia associated withCampylobacter pyloridis gastritis. Gastroenterology 92:A1324, 1987

    Google Scholar 

  41. Loffeld RJLF, Potters HVJP, Stobberingh E, Flendrig JA, Van Spreenwel JP, Arends JW:Campylobacter associated gastritis in patients with non-ulcer dyspepsia: A double blind placebo associated controlled trial with colloidal bismuth subcitrate. Gut 30:1206–1212, 1989

    Google Scholar 

  42. Rauws EAJ, Tytgat GNJ: III Epidemiology ofCampylobacter pylori infection.In Campylobacter pylori. EAJ Rauws, GNJ Tytgat (eds). Amsterdam, WC den Ouden BV, 1989, pp 13–21

    Google Scholar 

  43. Lambert JR, Dunn K, Borromeo M, Korman MG, Hansky J:Campylobacter pylori. A role in non-ulcer dyspepsia. Scand J Gastroenterol 24(suppl 160):7–13, 1989

    Google Scholar 

  44. Morris A, Maher K, Thomsen L, Miller M, Nicholson G, Tasman Jones C: Distribution ofCampylobacter pylori in the human stomach obtained at post-mortem. Scand J Gastroenterol 23:257–264, 1988

    Google Scholar 

  45. Jones DM, Eldridge J, Fox AJ, Sethi P, Whorwell PJ: Antibody to the gastricCampylobacter-like organism (“Campylobacter pyloridis”): Clinncal correlations and distribution in the normal population. J Med Microbiol 22:57–68, 1986

    Google Scholar 

  46. Dixon MF:Campylobacter pylori and chronic gastritis.In Campylobacter pylori and Gastroduodenal Disease. BJ Rathbone, RV Heathley (eds). Oxford, Blackwell Scientific Publications, 1989, pp 106–116

    Google Scholar 

  47. Fox JG, Correa P, Taylor NS, Zavala D, Fontham E, Janney F, Rodriguez E, Hunter F, Diavolitsis S:Campylobacter pylori-associated gastritis and immune response in a population at increased risk of gastric carcinoma. Am J Gastroenterol 84:775–781, 1989

    Google Scholar 

  48. Fimmel CJ, Etienne A, Ciluffo T, von Ritter C, Gasser T, Rey JP, Caradonna-Moscatelli P, Sabbatini F, Pace F, Bühler HW, Bauerfeind P, Blum AL: Long-term ambulatory gastric pH monitoring: validation of a new method and effect of H2-antagonists. Gastroenterology 88:1842–1851, 1985

    Google Scholar 

  49. Savarino V, Mela GS, Scalabrini P, Sumberaz A, Fera G, Celle G: 24-Hour study of intragastric acidity in duodenal ulcer patients and normal subjects using continuous intraluminal pH-metry. Dig Dis Sci 33:1977–1980, 1988

    Google Scholar 

  50. McLauchlan G, Fullarton GM, Grean GP, McColl KEL: Comparison of gastric body and antral pH: a 24 hour ambulatory study in healthy volunteers. Gut 30:573–578, 1989

    Google Scholar 

  51. Chiverton SG, Burget DW, Hunt RH: Do H2 receptor antagonists have to be given at night? A study of the antisecretory profile of SKF 94482, a new H2 receptor antagonist which has a profound effect on daytime acidity. Gut 30:594–599, 1989

    Google Scholar 

  52. O'Connor HJ, Axon ATR: Campylobacter pylori, gastric ulceration and the post-operative stomach.In Campylobacter pylori and Gastroduodenal Disease. BJ Rathbone, RV Heathley (eds). Oxford, Blackwell Scientific Publications, 1989, pp 125–138

    Google Scholar 

  53. Smith JTL, Pounder RE, Nwokolo CU, Lanzon-Miller S, Evans DG, Graham DY, Evans DJ Jr: Inappropriate hypergastrinaemia in asymptomatic healthy subjects infected withHelicobacter pylori. Gut 31:522–525, 1990

    Google Scholar 

  54. Goldie J, Jalali S, Hunt RH, Richardson H: Study of media and pH requirements for the growth ofCampylobacter pylori. Gastroenterology 94:A150, 1988

    Google Scholar 

  55. Steer HW: Duodenal epithelium in peptic ulceration. J Pathol 146:355–362, 1985

    Google Scholar 

  56. Marshall BJ, Armstrong JA, McGechie DB, Glancy RJ: Attempt to fulfill Koch's postulates for pyloricCampylobacter. Med J Aust 142:436–439, 1985

    Google Scholar 

  57. Megraud F:Campylobacter pylori: Enzymes.In Campylobacter pylori and Gastroduodenal Disease. BJ Rathbone, RV Heathley (eds). Oxford, Blackwell Scientific Publications, 1989, pp 39–47

    Google Scholar 

  58. Morris A, Nicholson G: Ingestion ofCampylobacter pyloridis causes gastritis and raised fasting gastric pH. Am J Gastroenterol 82:192–199, 1987

    Google Scholar 

  59. Sidebotham RL, Batten JJ, Karim QN, Spencer J, Baron JH: Breakdown of gastric mucus in presence ofHelicobacter pylori. J Clin Pathol 44:52–57, 1991

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Additional information

This work was supported in part by grants from ministero Pubblica Istruzione and from Regione Toscana.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Bechi, P., Del, R., Amorosi, A. et al. Helicobacter pylori and luminal gastric pH. Digest Dis Sci 37, 378–384 (1992). https://doi.org/10.1007/BF01307731

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF01307731

Key Words

Navigation