Published 22 September 2009, doi:10.1136/bmj.b3855
Cite this as: BMJ 2009;339:b3855

Letters

Helicobacter pylori and ulcers

Against reductionism

The first 150 words of the full text of this article appear below.

Both positions in the head to head debate "Does Helicobacter pylori really cause duodenal ulcers?" reflect a pathophysiological reductionism that should have long since become obsolete.^{1 2} Just as high cholesterol is not "the cause" of myocardial infarction but one of many risk factors, H pylori is best seen as one among several risk factors for ulcer.

The evidence: most people living with Helicobacter never develop ulcers, some 30% of patients with ulcer do not harbour H pylori infection (with a substantial proportion also lacking exposure to non-steroidal anti-inflammatory drugs), and some patients whose Helicobacter colonisation has been eliminated by antibiotics subsequently develop new ulcers.^{3 4} These facts make it clear that other risk factors, including gastric acid hypersecretion, smoking, psychological stress, and genetic predisposition, play a part in ulcer formation even in the many cases where H pylori is probably directly implicated.

The lateral thinking exemplified by Marshall and Warren should . . . [Full text of this article]

¹ Aventino Medical Group, Rome, Italy 00153

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