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 19 June 2018

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GastroenterologyHelicobacter pylori

Ulcer pathogenesis

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Frank Tovey and Michael Hobsley Can Helicobacter pylori really be the primary cause of duodenal ulcer? - An update.
Frank Tovey and Michael Hobsley, 05 June 2006

In our Personal View article of 31 July 2000, we pointed out that even after leaving out NSAID-associated ulcer, there were difficulties in accepting the generally-held assumption that Helicobacter pylori is the primary cause of duodenal ulceration.

In summary:

  1. Areas of high prevalence of H. pylori and of duodenal ulcer do not always co-exist [1];
  2. Within areas of high prevalence of H. pylori, geographical variations in the prevalence of duodenal ulceration seem to be related to diet [2];
  3. Despite complete and lasting eradication of H. pylori there is a 20% recurrence rate of ulceration [3];
  4. In patients with a short history of symptoms of the ulcer there is a lesser prevalence of H. pylori than in patients with a longer history [4];
  5. Although we did not refer directly to this fact, the greatest difficulty in accepting H. pylori as the etiological agent is that most patients with the infection do not get ulceration;
  6. Patients without infection may have a duodenal ulcer, and patients with a duodenal ulcer, even if they have the infection in the gastric antrum, may often have no infection in the duodenum.

Today we wish to discuss further points 4 and 5, and raise possibilities in respect of point 6.

The point that early in the disease one is less likely to find H. pylori has been directly confirmed by our own group [5]. Of 137 patients with duodenal ulceration, the 132 with a history of greater than 6 months were all positive for H. pylori. The remaining 5 patients were all negative. Tests for H. pylori included PCR.

With regard to point 5, it has often been suggested that presence or absence of virulence factors in the organism might account for the fact that few of the infected individuals develop ulceration. However, there is abundant evidence that this is not true. Reports from Japan, China, Sudan and Nigeria show no association between the presence of the virulence factors Cag A and Vac A, and the prevalence of duodenal ulcer [6-9].

In the case of point 6, we accept that it is not necessary for H. pylori to be present in the duodenum in all cases of duodenal ulcer. We consider it likely that the patients with the organism in the duodenum are those with duodenogastric metaplasia (DGM), since H. pylori can only live in gastric-type epithelium. DGM is well known to be more frequently present in patients with than in subjects without duodenal ulcer, but whether it should be accepted as an etiological factor depends upon whether it is more frequently present in the population of areas of higher than of lower prevalence of the disease - a problem we are presently studying.


  1. Tovey FI. Peptic ulcer in India and Bangladesh. Gut 1979; 20; 329-47
  2. Join the debate! Click here to post your comments about this Personal View Speech.

  3. Tovey FI. Duodenal ulcer in China. J Gastroenterol Hepatol 1992; 4: 329-42
  4. Laine L, Hopkins RJ, Girardi LSD. Has the impact of Helicobacter pylori therapy on ulcer recurrence in the United States been overstated? Am J Gastroenterol 1998; 93: 1409-15.
  5. Pest P, Zarate J, Varsky C, Man F, Schraier M. Helicobacter pylori in recently diagnosed duodenal ulcer. Acta Gastroenterol Latinoam 1996; 26: 273-6.
  6. Boulos PB, Botha A, Hobsley M, et al. Possible absence of in the early stages of duodenal ulceration. QJM 2002; 95: 749-52.
  7. Maeda S, Kanai F, Ogura K et al. High seropositivity of anti-Cag A antibody in Helicobacter pylori infected patients irrelevant to the presence of peptic ulcers and gastric cancer in Japan. Dig Dis Sci 1997; 42: 1841-7.
  8. Pan ZJ, van der Hulst RWM, Feller M, et al. Equally high prevalence of infection with Cag A+ve Helicobacter pylori in Chinese patients with peptic ulcer disease and those with chronic gastritis-associated dyspepsia. J Clin Microbiol 1997; 35: 1344-7.
  9. El-Madhi AM, Patchett SE, Char S, et al. Does Cag A contribute to ulcer pathogenesis in a developing country, such as Sudan? Eur J Gastroenterol Hepatol 1998; 10: 313-6.
  10. Rocha AM, Rocha GA, Queiroz DM, et al. Anti-Cag A antibodies in Helicobacter pylori-patients and blood donors from Nigeria. Trop Doc 2001; 31: 147-9.

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I agree that the 5 reasons given are valid, but there is a much more powerful argument against H. pylori as a major determinant of duodenal ulcers. This is the ecological argument.

An epidemic of peptic ulcers began in those born in the last quarter of the 19th century (Susser M, Stein, Z. Int J Epidemiology 2001; 30: 13-21). This was earlier for gastric ulcers than for duodenal ulcers, and subsequent generations in Europe, Australia, and elsewhere clearly show it. Successive generations show a falling likelihood of ulcers, so that chronic peptic ulcers in the young (those born in recent decades) have a minimal risk.

An epidemic of H. pylori does not explain this for it fails to explain the asynchrony of duodenal ulcers and gastric ulcers. Where H. pylori, NSAIDs, and heredity - all statistically associated - fit in to the puzzle remains to be determined.


John Duggan, Newcastle, Australia , 30 April 2003

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