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Editor, – The opening remarks in 'Testing for Helicobacter pylori' (Aust Prescr 1997;20:96-8) are cause for concern in a profession which must essentially be guided by scientific fact.
Drs Lambert and Badov state that 'Helicobacter pylori commonly infects Australians and can cause gastritis, peptic ulcer disease and gastric cancer'.
To the best of my knowledge, there has been no published work which has indicated that H. pylori has actually caused peptic ulcer disease or gastric cancer in humans. Several attempts have been made in experimental animals to induce peptic ulcer by exposing the animals to H. pylori. Thus far, such attempts have failed in all animals except the Mongolian gerbil, and even in this animal it was not possible to induce duodenal ulcer.
There can be no doubting that H. pylori is often found to be present in the upper gastrointestinal tract of patients suffering from peptic ulcer, gastric ulcer, gastric MALT lymphoma or any one of a vast array of other pathologies.
The association with H. pylori does not give scientific basis for authorities, as yet, to state that H. pylori causes peptic ulcer or gastric cancer.
Until proof is available, authorities would be better advised to use more cautious terminology.
John R. Graham
Consultant Physician & Gastroenterologist
Sydney, N.S.W.
Dr David Badov, one of the authors of the article, comments:
The article deals with the diagnostic tests for H. pylori. The opening statement simply reflects a widely accepted view of the causal relationship between H. pylori and peptic ulcer disease and gastric carcinoma. This view is also supported by the Australian Gastroenterology Institute which, in its recent publication 'Helicobacter pylori - Guidelines for healthcare providers' states on page 6:
'H. pylori is now accepted as a cause of: histological gastritis, duodenal ulcer, gastric ulcer and gastric malignancy' (Oct 1995).
This view is based upon the strong and consistent relationship between H. pylori infection and peptic ulcer disease. Infection can be diagnosed worldwide in virtually all patients with duodenal ulcers and in the vast majority of patients with gastric ulcers. There is a definite biological gradient: the risk of peptic ulceration correlates with bacterial load and a known biological mechanism. A final and strong argument in support of the causative role of H. pylori infection in both duodenal and gastric ulcer disease is the effect of bacterial eradication intervention. The risk of recurrent duodenal and gastric ulceration is reduced virtually to zero after eradication therapy.
In regard to gastric carcinogenesis, the World Health Organization has recently classed H. pylori as a definite carcinogen.
