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 12 December 2017

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Personal View

GastroenterologyStomach & duodenum

Peptic ulcer

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Frank Tovey and Michael Hobsley Can Helicobacter pylori really be the primary cause of duodenal ulcer?
Frank Tovey and Michael Hobsley, 31 July 2000
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If non-steroidal anti-inflammatory drugs are excluded, there remain several problems with regard to Helicobacter pylori infection being the primary cause of duodenal ulceration.

Reports in the literature of H. pylori-negative duodenal ulceration varying between 30% and 75% [1], particularly in areas where the overall prevalence of H. pylori infection is low, seem to be appearing with increasing frequency.

In areas of Africa, China and India, where the prevalence of H. pylori infection approaches 90%, only relatively few subjects develop duodenal ulceration. The higher prevalence of duodenal ulceration in southern areas of India and China compared with northern areas [2,3], despite similar prevalence of H. pylori infection, suggest that some other factor such as dietary differences is the primary cause.

Evidence suggests that infection with H. pylori was almost ubiquitous in the 19th century when duodenal ulceration was rare yet, despite the rising incidence of duodenal ulceration during the last century, the prevalence of H. pylori infection has fallen steadily [4].

The prevalence of H. pylori infection in patients with only a short history of duodenal ulceration has been reported to be lower than in patients with a longer history [5]. It is difficult to conceive of an aetiological agent that is absent at the start of the condition that it is supposed to produce.

Most writers on H. pylori as the cause of duodenal ulceration assume that the mechanism is via colonization of the duodenum. However, there is evidence that many patients with duodenal ulcer have no colonization of the duodenum even if there is colonization of the antrum [5-7].

A meta-analysis [8] has shown a 20% recurrence rate of duodenal ulceration following complete eradication of H. pylori.

To summarize:

  • Duodenal ulceration can occur without H. pylori infection of the antrum or of the duodenum.
  • The prevalence of H. pylori is in many circumstances very different to the prevalence of duodenal ulceration, and the respective prevalences can change in opposite directions.
  • H. pylori is often absent early in the history of duodenal ulceration compared with later in the history.

Join the debate! Click here to post your comments about this Personal View Speech.

Frank Tovey and Michael Hobsley
Department of Surgery, Royal Free and University College Medical School, London, England.

This article originally appeared on 31 July 2000.

References

  1. Tovey FI, Hobsley M. Is Helicobacter pylori the primary cause of duodenal ulceration? J Gastroenterol Hepatol 1999; 14:1053-6.
  2. Tovey FI. Peptic ulcer in India and Bangladesh. Gut 1979; 20: 329-42.
  3. Tovey FI. Duodenal ulcer in China. J Gastroenterol Hepatol 1992; 4: 329-42.
  4. Blaser MJ. Helicobacters are indigenous to the human stomach: duodenal ulceration is due to changes in gastric microecology in the modern era. Gut 1998; 43: 721-7.
  5. Dres Pest P, Zarate J, Vassky C, Man F, Schraier M. Helicobacter pylori in recently diagnosed duodenal ulcer. Acta Gastroenterol Latinoamer 1996; 26: 273-6.
  6. Kim N, Lim SH, Lee KM, Choi SE. Long term effect of Helicobacter pylori eradication on gastric metaplasia in patients with duodenal ulcer. J Clin Gastroenterol 1998; 27: 246-52.
  7. Pospai D. Is Helicobacter pylori colonisation of gastric metaplasia determining either duodenal ulcer development or relapse? Gut 1997; 41 (Suppl.2): A108.
  8. Laine L, Hopkins RJ, Girardi LS. Has the impact of Helicobacter pylori therapy on ulcer recurrence in the United States been overstated? Am J Gastroenterol 1998; 93: 1409-15.

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YourComments

 

H. pylori may not be directly related to the development of duodenal ulcer, rather it may be an associated condition. It is a fact that there is an increased association between gastritis and H. pylori positivity, but may not be the same with respect to duodenal ulcer. Duodenal ulcer per se may be as a result of increased secretion of acid by the acid secreting cells. This increased secretion may be related to any situation where there is increased inflammation of the gastric mucosa. This could be the reason why a significant number of duodenal ulcers respond to eradication of H. pylori.

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Kim Vaiphei, Chandigarh, India, 18 January 2001

 

For the past few years, I have been receiving reports from my Pathology Department documenting coccobacillary organisms that are definitely not H. pylori on antral biopsies. Giemsa stains and urease testing fails to reveal H. pylori, and for the most part, the patients in question do not have ulcer disease.

I am in the process of trying to convince my Pathology and Microbiology Departments to take a closer look at these organisms, since they say that they are very common. Isn't That how H. pylori was discovered initially?

I would like the biopsy specimens to be cultured, and only then can we discover the true nature of these bugs.

Do you have any insight into my finding? Would anyone like to collaborate in research on this topic?

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Perry J. Milman, Lake Success, USA, 16 October 2000

 

I was most interested in Frank Tovey and Michael Hobsley's 'Persoanl View' article in which they voice doubt for a primary role for H. pylori in benign pepticulcer disease.

I too, have reservations for such a primary role. Let me firstly remind you that a fundamental anatomical feature of gastric peptic ulcers is a propensity for them to occur along the lesser curve of the antrum. I just cannot see how H. pylori (a luminal organism) would selectively pick off that site and leave other areas unaffected.

I am one who has an interest in the role of the vasculature in inflammatory disorders of the gut and would remind the readers of some interesting work done by Dr Chris Piasecki (Royal Free Hospital) a couple of decades ago. He showed that gastric peptic ulcers occurred where they did because the arteries supplying the lesser curvature were small end arteries (Review: J Physiol Pharmacol 1992; 43: 99-112). He argued that during times of stress, when sympathetic vasoconstriction and muscle spasm might cause reduced blood flow to dependent mucosa, ischemia would lead to mucodsal necrosis (ulceration). In this situation H. pylori would be considered to be a secondary aggressor factor (together with acid) preventing healing.

I'm not a betting man but I'd put few bob on stress-induced mucosal ischemia being a recognised cause of peptic ulcer disease in the near future. It certainly goes a long way in explaining the anatomy of peptic ulcer disease.

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Dr Andrew Anthony, London, UK, 19 September 2000

 

I would like to make the following comments:
1) Colonisation of the duodenum is not mandatory for H. pylori-related ulcer disease; changes in gastric physiology via colonisation in the antrum may be the mechanism of ulceration.
2) I am still not sure whether duodenal ulcer disease was "rare" in 19th century.
3) Although H. pylori-negative duodenal ulceration is high in western countries, the incidence of peptic ulcer disease is very low as compared to developing countries - in parallel with prevalence of H. pylori.

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Dr Etham Tankhurt, Izmir, Turkey, 19 September 2000

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