Background: Dual therapy with ranitidine bismuth citrate plus clarithromycin twice daily for 14 days is an effective regimen for eradicating Helicobacter pylori infection. Aim: To determine whether this regimen can be improved by the addition of a second antibiotic, tetracycline hydrochloride, whilst reducing the duration of treatment to 7 days. Methods: Sixty‐one out‐patients were enrolled to this open treatment study. All had H. pylori infection, as determined by 13C‐urea breath test and, for those undergoing endoscopy, by rapid urease test. Patients were treated with ranitidine bismuth citrate 400 mg, clarithromycin 500 mg and tetracycline hydrochloride 500 mg all twice daily for 7 days. Eradication of H.␣pylori was assessed by two separate 13C‐urea breath tests, the first 28–68 days after the completion of treatment, the second 28–162 days later. H. pylori infection was considered cured if both tests were negative. Results: All 61 patients were included in the intention‐to‐treat efficacy analysis. Successful eradication of H.␣pylori was achieved in 55/61 patients (90 %; 95% CI: 82–98%). Fifty‐nine out of sixty‐one patients reported 100% compliance; one patient missed a single dose of medication and the other withdrew at 48 h due to nausea and vomiting. Minor adverse events were reported by 30/61 patients. Conclusion: One‐week triple therapy with ranitidine bismuth citrate, clarithromycin and tetracycline, all twice daily, is a safe and well‐tolerated regimen which eradicates H. pylori in 90% of infected patients.

SUMMARY Gastric acid secretion has a non‐specific bactericidal action which contributes to gastrointestinal defence mechanisms against micro‐organisms. Therapeutic inhibition of acid secretion with histamine H2 receptor antagonists and proton pump inhibitors might therefore be expected to predispose to infection. This article reviews clinical reports of infection occurring during therapeutic gastric acid inhibition, and assesses the risk of infection incurred by such treatment. Non‐typhoid salmonelloses, Campylobacter infections, local candidiasis, and possibly Strongyloides hyperinfections may be more prevalent after acid inhibitory treatment, but concurrent impairment of other gastrointestinal defence mechanisms may be necessary to permit infection.

SUMMARY Simultaneous 24‐hour intragastric acidity and plasma gastrin concentrations were measured in 12 duodenal ulcer patients before and on the twenty‐eighth day of treatment with either ranitidine 150 mg b.d. or omeprazole 20 mg o.m. Median integrated 24‐hour intragastric acidity was decreased significantly from 1148 to 490 and 36 mmol. hour litre−1 during treatment with ranitidine and omeprazole, respectively, whilst median intragastric 24‐hour plasma gastrin was raised significantly from 328 to 799 and 1519 pmol. hour litre−1 respectively. When the results of all 48 experiments were considered together, there was a significant inverse correlation between the 24‐hour integrated values for intragastric acidity and plasma gastrin concentration. Both drugs caused a significant elevation of plasma gastrin throughout the 24 hours, although ranitidine had no effect on intragastric acidity from 1900 to 2200 hours. When compared with similar profiles of acidity and gastrin in pernicious‐anaemia patients, the modest elevations of plasma gastrin observed in this study suggest that neither drug will be associated with clinically relevant enterochromaffin‐like cell proliferation in duodenal ulcer patients.

When compared side-by-side, all the major findings on OGD are seen on Cap-OGD while there is under-reporting of minor findings. Previous experience of ESO-2 capsule reporting improves reading accuracy and indicates the need for training. This pilot study provides a backdrop to explore the possible role of Cap-OGD, especially where patients are reluctant to undergo conventional OGD or where there is risk of prion contamination of the endoscope.