Skip to main content
SpringerLink
Log in

Peptic ulcer disease — the transitional zones are important

  • Chapter
Helicobacter pylori

  • 225 Accesses

Abstract

In 1924 Konjetzny declared that ‘an ulcer does not develop in a healthy mucosa’1. Over the next two decades it became increasingly apparent that peptic ulcers were complications of pre-existing chronic inflammation in the gastric and proximal duodenal mucosa. Indeed it emerged that different patterns of gastritis were associated with gastric and duodenal ulcers; the former was found in stomachs with diffuse chronic gastritis with multifocal atrophy whereas duodenal ulcers were associated with a non-atrophic antralpredominant gastritis in which the corpus showed little inflammation2,3. In the 1950s Oi and his colleagues in Tokyo examined large numbers of gastric resections for ulcer disease and made a meticulous study of the location of gastric and duodenal ulcers in relation to the border zones between adjacent mucosal types4,5. The relationship of peptic ulcers to these junctional zones has been a neglected topic which needs re-examination in the light of Helicobacter pylori ecology.

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

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 169.00
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 219.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 219.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Konjetzny GE. Zur chirurgischen Beureilung der chronischen Gastritis. Arch Klin Chirurg. 1924;129:139–171.

    Google Scholar 

  2. Hebbel R. Chronic gastrits: its relation to gastric and duodenal ulcer and to gastric cancer. Am J Pathol. 1943;19:43–71.

    PubMed  CAS  Google Scholar 

  3. Magnus HA. The pathology of simple gastritis. J Pathol Bacteriol. 1946;58:431–439.

    Article  PubMed  CAS  Google Scholar 

  4. Oi M, Oshida K, Sugimura S. The location of gastric ulcer. Gastroenterology. 1959;36:45–59.

    PubMed  CAS  Google Scholar 

  5. Oi M, Sakurai Y. The location of duodenal ulcer. Gastroenterology. 1959;36:60–64.

    PubMed  CAS  Google Scholar 

  6. Kimura K, Takemoto T. Endoscopic recognition of the atrophic border and its significance in chronic gastritis. Endoscopy. 1969;8:87–97.

    Article  Google Scholar 

  7. Kimura K. Chronological transition of the fundic-pyloric border determined by stepwise biopsy of the lesser and greater curvatures of the stomach. Gastroenterology. 1972;63:584–592.

    PubMed  CAS  Google Scholar 

  8. Yoshimura T, Shimoyama T, Fukuda S, Tanaka A, Axon ATR, Munakata A. Most gastric cancer occurs on the distal side of the endoscopic atrophic border. Scand J Gastroenterol. 1999;34:1077–1081.

    Article  PubMed  CAS  Google Scholar 

  9. Ferrero RL, Lee A. The importance of urease in acid protection for the gastric-colonising bacteria H. pylori and H.felis sp. nov. Microbiol Ecol Health Dis. 1991;4:121–134.

    Article  Google Scholar 

  10. Meyer-Rosberg K, Scott DR, Melchers K, Sachs G. The effect of environmental pH on the proton motive force of H. pylori. Gastroenterology. 1996;111:886–900.

    Article  PubMed  CAS  Google Scholar 

  11. McGowan CC, Cover TL, Blasr MJ. Helicobacter pylori and gastric acid: biological and therapeutic implications. Gastroenterology. 1996;110:926–938.

    Article  PubMed  CAS  Google Scholar 

  12. A H+-gated urea channel: the link between Helicobacter pylori urease and gastric colonization. Science. 2000;287:482-485.

    Google Scholar 

  13. Scott DR, Marcus EA, Weeks DL, Lee A, Melchers K, Sachs G. Expression of the Helicobacter pylori urel gene is required for acidic pH activation of cytoplasmic urease. Infect Immun. 2000;68:470–477.

    Article  PubMed  CAS  Google Scholar 

  14. Clyne M, Labigne A, Drumm B. H. pylori requires an acidic environment to survive in the presence of urea. Infect Immun. 1995;63:1669–1673.

    PubMed  CAS  Google Scholar 

  15. Greig MA, Neithercut WD, Hossack M, McColl KEL. Harnessing of urease activity of H. pylori to induce self-destruction of the bacterium. J Clin Pathol. 1991;44:157–159.

    Article  PubMed  CAS  Google Scholar 

  16. Neithercut WD, Williams C, Hossack M, McColl KEL. Ammonium metabolism and protection from urease mediated destruction in H. pylori infection. J Clin Pathol. 1993;46:75–78.

    Article  PubMed  CAS  Google Scholar 

  17. Wiliams C, Neithercut WD, Hossack M, Hair J, McColl KEL. Urease-mediated destruction of bacteria is specific for Helicobacter urease and results in total cellular disruption. FEMS Immunol Med Microbiol. 1994;9:273–280.

    Article  Google Scholar 

  18. Schade C, Flemstrom G, Holm L. Hydrogen ion concentration in the mucus layer on top of acid-stimulated and-inhibited rat gastric mucosa. Gastroenterology. 1994;107:180–188.

    PubMed  CAS  Google Scholar 

  19. Engel E, Peskoff A, Kaufman GL, Grossman MI. Analysis of hydrogen ion concentration in the gastric gel mucus layer. Am J Physiol. 1984;247:G321–38.

    PubMed  CAS  Google Scholar 

  20. Bahari HMM, Ross IN, Turnberg LA. Demonstration of a pH gradient across the mucus layer on the surface of human gastric mucosa in vitro. Gut. 1982;23:513–516.

    Article  PubMed  CAS  Google Scholar 

  21. Roland M, Berstad A, Liavag J. Histological study of gastric mucosa before and after proximal gastric vagotomy in duodenal ulcer patients. Scand J Gastroenterol. 1975;10:181–186.

    PubMed  CAS  Google Scholar 

  22. Watt PCH, Sloan JM, Kennedy TL. Changes in gastric mucosa after vagotomy and gastro-jejunostomy for duodenal ulcer. Br Med J. 1983;287:1407–1410.

    Article  CAS  Google Scholar 

  23. Jonsson KA, Storm M, Bodemar G, Norby K. Histologic changes in the gastroduodenal mucosa after long term medical treatment with cimetidine or parietal cell vagotomy in patients with juxtapyloric ulcer disease. Scand J Gastroenterol. 1988;23:433–441.

    Article  PubMed  CAS  Google Scholar 

  24. Peetsalu A, Maaroos HI, Sipponen P, Peetsalu M. Long-term effect of vagotomy on gastric mucosa and H. pylori in duodenal ulcer patients. Scand J Gastroenterol. 1991;26 (Suppl. 186):77–83.

    Article  Google Scholar 

  25. Logan RP, Walker MM, Misiewicz JJ et al. Changes in the intragastric distribution of H. pylori during treatment with omeprazole. Gut. 1995;36:12–16.

    Article  PubMed  CAS  Google Scholar 

  26. Kuipers EJ, Lee A, Klinkenberg-Knol, Meuwissen SGM. Review article: The development of atrophic gastritis — Helicobacter pylori and the effects of acid suppressive therapy. Aliment Pharmacol Ther. 1995;9:331–340.

    Article  PubMed  CAS  Google Scholar 

  27. Solcia E, Fiocca R, Villani L, Carlsson J, Rudback A, Zeijlon L. Effects of permanent eradication or transient clearance of Helicobacter pylori on histology of gastric mucossa using omeprazole with or without antibiotics. Scand J Gastroenterol. 1996;31(Suppl.215):105–110.

    Article  CAS  Google Scholar 

  28. Kuipers EJ, Lundell L, Klinenberg-Knol EC et al. Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N Engl J Med. 1996;334:1018–1022.

    Article  PubMed  CAS  Google Scholar 

  29. Danon SJ, O’Rouke JL, Moss ND, Lee A. The importance of local acid production in the distribution of Helicobacter felis in the mouse stomach. Gastroenterology. 1995;108:1386–1395.

    Article  PubMed  CAS  Google Scholar 

  30. Graham DY, Alpert LC, Lacey Smith J, Yoshimura HH. Iatrogenic Campylobacter pylori infection is a cause of epidemic hypochlorhydria. Am J Gastroenterol. 1988;83:974–980.

    PubMed  CAS  Google Scholar 

  31. Frommer DJ, Carrick J, Lee A, Hazell SL. Acute presentation of Campylobacter pylori gastritis. Am J Gastroenterol. 1988;83:1168–1171.

    PubMed  CAS  Google Scholar 

  32. Sobala GM, Crabtree JE, Dixon MF et al. Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations. Gut. 1991;32:1415–1418.

    Article  PubMed  CAS  Google Scholar 

  33. Rektorschek M, Weeks D, Sachs G, Melchers K. Influence of pH on metabolism and urease activity of Helicobacter pylori. Gastroenterology. 1998;115:628–641.

    Article  PubMed  CAS  Google Scholar 

  34. Olso ER. Influence of pH on bacterial gene expression. Mol Microbiol. 1993;8:5–14.

    Article  Google Scholar 

  35. Kjelleberg S, editor. Starvation in Bacteria. New York: Plenum Press; 1993.

    Google Scholar 

  36. Goodwin S. Helicobacters shed new light on chaperonins. Lancet. 1995;346:653–655.

    Article  PubMed  CAS  Google Scholar 

  37. Oi M, Ito J, Kumagai F et al. A possible dual control mechanism in the origin of peptic ulcer: a study on ulcer location as affected by mucosa and musculature. Gastroenterology. 1969;57:280–293.

    PubMed  CAS  Google Scholar 

  38. Stadelmann K, Elster K, Stolte M et al. The peptic gastric ulcer — histotopographic and functional investigations. Scand J Gastroenterol. 1971;6:613–623.

    Article  PubMed  CAS  Google Scholar 

  39. Warburton VJ, Everett S, Mapstone NP, Axon ATR, Hawkey P, Dixon MF. Clinical and histological associations of cagA and vacA genotypes in Helicobacter pylori gastritis. J Clin Pathol. 1998;51:55–61.

    Article  PubMed  CAS  Google Scholar 

  40. Dixon MF. Pathophysiology of Helicobacter pylori infection. Scand J Gastroenterol. 1994; 26(Suppl.201):7–10.

    Article  CAS  Google Scholar 

  41. Hanby AM, Poulsom R, Singh S et al. Spasmolytic polypeptide is a major antral peptide: distribution of the trefoil peptides human spasmolytic polypeptide and pS2 in the stomach. Gastroenterology. 1993,105:1110–1116.

    PubMed  CAS  Google Scholar 

  42. Konturek PC, Ernst H, Konturek SJ et al. Mucosal expression and luminal release of epidermal and transforming growth factors in patients with duodenal ulcer before and after eradication of Helicobacter pylori. Gut. 1997;40:463–469.

    PubMed  CAS  Google Scholar 

  43. Terres AM, Pajares JM, OToole D, Ahern S, Kelleher D. H. pylori infection is associated with down-regulation of E-cadherin, a molecule involved in epithelial cell adhesion and proliferation control. J Clin Pathol. 1998;51:410–412.

    Article  PubMed  CAS  Google Scholar 

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

    PubMed  CAS  Google Scholar 

  45. Baron JH. Studies of basal and peak acid output with an augmented histamine test. Gut. 1963;4:136–144.

    Article  PubMed  CAS  Google Scholar 

  46. Baron JH. An assessment of the augmented histamine test in the diagnosis of peptic ulcer: correlations between gastric secretion, age and sex of patients, and site and nature of the ulcer. Gut. 1963;4:243–253.

    Article  PubMed  CAS  Google Scholar 

  47. Card WI, Marks IN. The relationship between the acid output of the stomach following ‘maximal’ histamine stimulation and the parietal cell mass. Clin Sci. 1960;19:147–163.

    PubMed  CAS  Google Scholar 

  48. Graham DY, Genta RM, Malaty H. Which is the most important factor in duodenal ulcer pathogenesis: the strain of H. pylori or the host? In: Hunt RH, Tytgat GNJ, editors. Helicobacter pylori: basic mechanisms to clinical cure. Lancaster: Kluwer; 1996:85–91.

    Google Scholar 

  49. Wormsley KG. Progress report. The pathophysiology of duodenal ulcer. Gut. 1974;15:59–81.

    Article  PubMed  CAS  Google Scholar 

  50. Wormsley KG, Grossman MI. Maximal histalog test in control subjects and patients with peptic ulcer. Gut. 1965;6:427–435.

    Article  PubMed  CAS  Google Scholar 

  51. Wyatt JL, Rathbone BJ, Dixon MF, Heatley RV. Campylobacter pyloridis and acid induced gastric metaplasia in the pathogenesis of duodenitis. J Clin Pathol. 1987;40:841–848.

    Article  PubMed  CAS  Google Scholar 

  52. Schrager J, Spink R, Mitra S. The antrum in patients with duodenal and gastric ulcers. Gut. 1967;8:497–508.

    Article  PubMed  CAS  Google Scholar 

  53. Carrick J, Lee A, Hazell S et al. Campylobacter pylori, duodenal ulcer, and gastric metaplasia: possible role of functional heterotopic tissue in ulcerogenesis. Gut. 1989;30:790–797.

    Article  PubMed  CAS  Google Scholar 

  54. Steer HW. Surface morphology of the gastroduodenal mucosa in duodenal ulceration. Gut. 1984;25:1203–1210.

    Article  PubMed  CAS  Google Scholar 

  55. Barlow TE, Bently FH, Walder DN. Arteries, veins and arteriovenous anastomoses in the human stomach. Surg Gynaecol Obstet. 1951;93:657–671.

    CAS  Google Scholar 

  56. van Zanten SJOV, Dixon MF, Lee A. The gastric transitional zones: neglected links between gastroduodenal pathology and Helicobacter ecology. Gastroenterology. 1999;116:1217–1229.

    Article  PubMed  Google Scholar 

Download references

Authors
  1. M. F. Dixon
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. A. Lee
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. S. J. O. Veldhuyzen Van Zanten
    View author publications

    You can also search for this author in PubMed Google Scholar

Editor information

Editors and Affiliations

  1. Division of Gastroenterology, McMaster University Medical Centre, 1200 Main Street West, Hamilton, Ontario, L8N 3Z5, Canada

    Richard H. Hunt (Professor of Medicine Director) (Professor of Medicine Director)

  2. Department of Gastroenterology and Hepatology, Academic Medical Centre, 9 Meibergdreef, 1105 AZ, Amsterdam, The Netherlands

    Guido N. J. Tytgat (Professor) (Professor)

Rights and permissions

Reprints and permissions

Copyright information

© 2000 Springer Science+Business Media Dordrecht

About this chapter

Cite this chapter

Dixon, M.F., Lee, A., Veldhuyzen Van Zanten, S.J.O. (2000). Peptic ulcer disease — the transitional zones are important. In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3927-4_36

Download citation

  • DOI: https://doi.org/10.1007/978-94-011-3927-4_36

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-5753-0

  • Online ISBN: 978-94-011-3927-4

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics

Search

Navigation