Antimicrobial regimens used in eradication are not without risk for cases of antibiotic-associated (pseudomembraneous) colitis have resulted.
A cautionary note. Helicobacter pylori infection is acquired in early childhood, probably by the faecal-oral route. The prevailing wisdom that 'the only good Helicobacter pylori is a dead Helicobacter pylori' is now tempered by the possibility that the organism (or at least certain subtypes) may perform a useful function. This view is based on evidence that gastro-oesophageal reflux symptoms may sometimes be worsened, and response to proton pump inhibitors diminished, after eradication of Helicobacter pylori. More worrying is the increased incidence of carcinoma at the gastro-oesophageal junction which correlates epidemiologically with reduced prevalence of Helicobacter pylori infection.
In summary, Helicobacter pylori eradication therapy
• indicated for gastric and duodenal ulcer not associated with NSAID use, and gastric lymphoma (especially MALT lymphoma),
• not indicated for reflux oesophagitis, and
• equivocal in value for nonulcer dyspepsia, after incidental detection, and for prophylaxis of gastric cancer.
Some 500 million prescriptions for NSAIDs are written each year in the UK, and 10-15% of patients develop dyspepsia whilst taking these drugs. Gastric erosions develop in up to 80%, but these are usually self-limiting. Gastric or duodenal ulcers occur in 1-5%. The incidence increases sharply with age in those over 60, and the risk of ulcers and their complications is doubled in patients over 75 and those with cardiac failure or a history of peptic ulceration or bleeding. Ibuprofen may be less prone to cause these problems than other NSAIDs.
4 The urea breath test measures radiolabelled C02 in expired air after ingestion of labelled urea, exploiting the fact that the organism produces urease and can convert urea to ammonia.
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