Transactions of the Royal Society of Tropical Medicine and Hygiene
Volume 102, Issue 12 , Pages 1171-1175, December 2008

Controversies in the Helicobacter pylori/duodenal ulcer story

  • Michael Hobsley

      Affiliations

    • Department of Surgery, Royal Free and University College London Medical School, University College London, London, UK
    • Corresponding Author InformationCorresponding author. Present address: Fieldside, Barnet Lane, Totteridge, London N20 8AS, UK. Tel.: +44 20 8445 6507.
  • ,
  • Frank I. Tovey

      Affiliations

    • Department of Surgery, Royal Free and University College London Medical School, University College London, London, UK
  • ,
  • John Holton

      Affiliations

    • Centre for Infectious Diseases and International Health, Royal Free and University College London Medical School, University College London, London, UK

Received 21 April 2008; received in revised form 24 April 2008; accepted 24 April 2008.

Summary 

In patients with Helicobacter pylori-positive duodenal ulcer (DU), the organism must be eradicated to achieve rapid, stable healing. However, evidence is against much else that is commonly accepted. (1) Does H. pylori cause the ulcer? Evidence against includes archaeopathology, geographical prevalence, temporal relationships and H. pylori-negative DU patients. DU can recur after eradication of H. pylori infection, and DUs may remain healed after reduction of acid secretion despite persistent infection. The faster healing of ulcers when H. pylori has been eradicated is due to the organism's interference with neoangiogenesis and the healing of wounded epithelial cells. (2) Does H. pylori infection persist until pharmacologically eradicated? Studies based on current infection show that H. pylori infection is a labile state that can change in 3 months. High rates of gastric acid secretion result in spontaneous cure, whereas low rates permit re-infection. Hydrochloric acid, necessary for producing a DU, is strongly associated with the likelihood of an ulcer. At the start, patients owe their ulcer to gastric hypersecretion of hydrochloric acid; approximately 60% may be H. pylori-negative. If acid is suppressed, the less acid milieu encourages invasion by H. pylori, especially if the strain is virulent.

Keywords: Helicobacter pylori, Duodenal ulcer, Aetiology, Diet, Gastric acid secretion, Antibodies

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S0035-9203(08)00206-X

doi:10.1016/j.trstmh.2008.04.035

Transactions of the Royal Society of Tropical Medicine and Hygiene
Volume 102, Issue 12 , Pages 1171-1175, December 2008