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Education And Debate

Controversies in Management: Eradication largely prevents relapse

BMJ 1994; 309 doi: (Published 10 December 1994) Cite this as: BMJ 1994;309:1570
  1. C J Hawkey, professora
  1. a Division of Gastroenterology, University Hospital, Nottingham NG7 2UH

    Eradication of Helicobacter pylori should be pivotal in managing peptic ulceration

    Like tuberculosis, peptic ulcer was once a disease of unknown cause. Both were managed by empirical or symptomatic treatments which included (for tuberculosis) the wearing of gold, being touched by King Charles II, and use of cough suppressants,1 and (for peptic ulcer) venesection, rhubarb infusions, nutrient enemas, and drugs which suppress acid.2 With recognition of their infectious aetiology and the use of effective antibiotics, both can now be cured.3 4 Not all patients are cured (often because of poor compliance), but those who are cured rarely experience recurrence.

    Reasons for eradicating H pylori

    Deliberate ingestion of H pylori leads to a persistent active antral gastritis,4 which longitudinal studies have shown to increase the risk of duodenal ulcer about 30 times and the risk of gastric ulcer eight times.5 The prevalence of H pylori in patients with symptomatic duodenal ulcer (about 95%) and in patients with gastric ulcer (70-80%) is much higher than in the general population,4 and 37% of asymptomatic Italian blood donors who were positive for H pylori had duodenal ulceration, erosive duodenitis, or active gastric ulcers.6

    Eradication of H pylori with one week antibiotic regimens heals duodenal ulcers as rapidly as reported for omeprazole.7 More importantly, many controlled trials have established that relapse of gastric and duodenal ulcer after eradication is rare, with annual relapse rates of 0-3%8 9 compared with 60-90% untreated or 10-30% with continued treatment with H2 receptor antagonists.10 11 This is because eradicating H pylori eliminates the cause of the ulcer diathesis. The associated antral active gastritis resolves rapidly and chronic gastritis over several months.10 The complications of ulcer are prevented.11 Such considerations have persuaded the United States National Institutes of Health to recommend that treatment to eradicate H pylori is offered to all patients who have a duodenal ulcer.

    Invalid reasons for not eradicating

    Reliability—H pylori is eradicated more effectively than Mycobacterium tuberculosis. A recent meta-analysis found an average 87% eradication with standard tetracycline based triple therapy.9 For the numerically challenged prescriber who advances the number of tablets to be taken as a reason not to eradicate, equally effective one week regimens are now emerging.9 Imperfections of existing regimens and the prospect of future improvement have not prevented prescribers from treating tuberculosis with antibiotics, nor should they stop treatment of H pylori.

    Toxicity—Up to one third of patients have experienced antibiotic related side effects, but these are usually mild. However, data are accumulating that H2 antagonists and proton pump inhibitors used for maintenance treatment are less benign than once thought, with increased enteric infections12 and accelerated gastric atrophy13 among the side effects.

    Cost—The cost of a single course of two week standard triple therapy is about pounds sterling 15.00. The addition of two weeks of amoxycillin to omeprazole costs pounds sterling 4.67. Compared with life long treatment with H2 receptor antagonists or proton pump inhibitors these costs are minimal.

    Validity of treatment—In the Nottingham catchment area (about 630 000 people) roughly a quarter of a million courses of antibiotics are prescribed annually, many for conditions such as sore throats or urinary tract infections. In this context, using antibiotics for peptic ulcer, which has been estimated to have a 4% annual incidence of complications and from which over 4000 patients a year die in the United Kingdom, does not seem unjustified.

    Too soon to change—Conservatism in medical practice can be defensible, and there are legitimate concerns—for example, the hazards of indiscriminate use are considerable; benefits may be obtained at the price of other unwanted and hazardous actions; in the old and unfit it may be better to use existing treatments; the relapse (recrudescence) rate is not fully determined. All of these are sentiments uttered, not about treatment for H pylori, but about cimetidine at an analogous stage of its development.14 15 For H pylori such conservatism is less defensible than it was in the 1970s for cimetidine since the drugs used for eradication are well known and established.

    It took Koch eight months to establish the tubercule bacillus as the cause of tuberculosis, 3 and by all accounts his colleagues and rivals were rapidly convinced of his case. It is difficult to explain why, faced with a far greater body of data, today's doctors show greater resistance to the evidence for, and therapeutic implications of, the infectious aetiology of peptic ulceration. True, Koch was able to transmit tuberculosis to guinea pigs whereas a satisfactory animal model for H pylori is still lacking. Conversely, the case for eradicating H pylori rests directly on many therapeutic trials, a compelling line of evidence to which Koch was not able to turn. The reason for the resistance is surely that prescribers have got used to the comfort of being able to suppress but not cure peptic ulceration with acid suppressing drugs. However, if history had been reversed so that H pylori and its associated diseases had already been treated with antibiotics, alongside streptococcal sore throats, tuberculous pneumonia, or urinary infections, we would rightly have greeted the advent of acid suppressing drugs as no more than a useful symptomatic adjunct to curative treatment, alongside gargles, cough suppressants, and potassium citrate.


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