Eradication of Helicobacter pylori in management of peptic ulceration

BMJ 1995; 310 doi: https://doi.org/10.1136/bmj.310.6978.531 (Published 25 February 1995) Cite this as: BMJ 1995;310:531

Evidence supports eradication only in patients who have helicobacter and peptic ulceration

  1. J P Miller,
  2. S G W Jones
  1. Consultant gastroenterologist Registrar in gastroenterology Department of Medicine, Withington Hospital, Manchester M20 2LR

    EDITOR,—C O Record emphasises the prevalence of Helicobacter pylori infection in patients without peptic ulcer disease,1 but this in no way diminishes the possibility that the bacterium is an important causal factor in ulcer disease. Secretion of acid is also common in patients without peptic ulceration, but we doubt if that has prevented Record from successfully using drugs that suppress such secretion. Neither acid nor helicobacter infection are the sole cause of peptic ulceration, but both are likely to be important causal factors in a multifactorial disorder. Most ulcers can be healed and kept healed by the suppression of either helicobacter or acid.

    Record uses hypochlohydria in the early stages of helicobacter infection as an argument against a role for the bacterium in the genesis of duodenal ulcer disease, which occurs in patients with normal or increased production of acid. In chronic helicobacter infection, however, evidence suggests that the bacterium promotes secretion of both gastrin and acid.2

    We agree that there is no ideal regimen for eradicating helicobacter, but Record's assumption that four weeks' treatment is required is unnecessarily pessimistic. Standard triple treatment is recommended to be given for two weeks,3 as is the licensed dual treatment of omeprazole and amoxycillin. Promising one week regimens have also been reported.4

    Record's discussion of whether eradication cures the disease is superficial. Record cites a single study, published only as a letter.5 Since 94 of the patients were positive for helicobacter at the time of relapse the study is irrelevant to the efficacy of eradication of helicobacter in preventing relapse. Record neglects the substantial body of trial data showing that eradication of the organism is followed by a major reduction in, or even absence of, relapse in patients with both duodenal and gastric ulceration.4

    Record implies that all 20 million carriers of helicobacter would have to be treated for the burden of gastroduodenal disease in the community to be altered. The evidence, however, supports eradication only in patients positive for the bacterium who have peptic ulceration. Results in non-ulcer dyspepsia are unpredictable and often disappointing, and the efficacy of eradicating the bacterium as prophylaxis against gastric cancer remains to be established. We believe that Peter C Rubin's commentary is correct: “If a person with peptic ulcer disease is shown to have H pylori then eradication is indicated.”1


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