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Relapse is a common sequel of antibiotic‐associated colitis due to Clostridium difficile. It has been suggested that Cl. difficile may persist in the stools in spite of the resolution of symptoms after treatment and this may cause the relapse. Our study was designed to define the factors that predispose to relapse and to determine if prolonging treatment to clear Cl. difficile from the stools might prevent relapse. Of 60 consecutive patients, 36 with more severe disease required treatment. Treatment with either vancomycin or bacitracin was continued until the results of the examination of stools for cytotoxin became negative and Cl. difficile could no longer be cultured (sensitivity of culture was 10–100 organisms/mL). This was achieved in 35 patients who were then followed for one month. Symptoms reappeared in 10 (28.6%) of the treated patients while Cl. difficile reappeared in the stools of an additional seven patients (20%) without the recurrence of diarrhoea. On comparing those who relapsed with those who did not, the age (67.3 ± 5.5 years in those who relapsed compared with 51.6 ± 4.4 years; P < 0.025, x¯ ± SE) and a history of recent abdominal surgery (59% of those who relapsed compared with 17%; P < 0.05) were significantly different. Although those who relapsed had received therapy with multiple antibiotic agents more often, this was not statistically significant. Disease was not more severe in patients who relapsed, nor was it more difficult to clear the pathogen from these patients. The 24 untreated patients did not suffer symptomatic relapse. Continuation of treatment until Cl. difficile apparently is absent from the stools is expensive and does not prevent relapse. Elderly patients and those who have recently undergone abdominal sugery are more likely to suffer a relapse.

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In a double‐masked trial, 43 patients with an endoscopically confirmed, symptomatic duodenal ulcer were allocated at random to treatment with either carbenoxolone sodium or placebo, both provided in identical “positioned‐release” capsules. The 40 patients who satisfactorily completed the trial were evenly distributed between the two treatment groups. The groups were well matched with regard to clinical features and initial ulcer size. Endoscopic review of ulcer healing after six weeks' treatment showed that 12 patients (60%) receiving carbenoxolone had healed ulcers, compared with five (25%) receiving placebo (P=0 05). Symptomatic remission occurred by the fourth week in 17 patients (85%) receiving carbenoxolone, compared with six (30%) receiving placebo (P<0.001). The mean (geometric) serum carbenoxolone level in patients with healed ulcers was 31.11 μg/mL compared with 17.75)μg/mL in those with unhealed ulcers (P< 0.005). Side effects of carbenoxolone therapy were observed, but they did not necessitate withdrawal of the drug and were readily controlled in every instance. These results confirm the therapeutic efficacy of carbenoxolone sodium in duodenal ulcer. In addition, a relationship between serum carbenoxolone levels and the occurrence of ulcer healing was observed.