Ranitidine: prophylaxis of duodenal ulcer recurrence.

Ninety-two patients with healed duodenal ulcer received prophylactic treatment with ranitidine, 150 mg at night, to prevent relapse. Patients were reviewed at 4-monthly intervals for clinical assessment and endoscopy. Eighty-two patients completed the trial. After one year sixty-two patients (76%) were in endoscopic remission; ten patients (12%) suffered symptomatic relapse and ten others had asymptomatic ulcers during treatment. There were no clinically significant untoward effects associated with the drug. A single nocturnal dose of 150 mg ranitidine reduces the relapse rate after duodenal ulcer healing.

A double-blind study of trimipramine in the treatment of active duodenal ulceration.

Thirty-six patients with endoscopically proven active duodenal ulcers entered a randomized double-blind trial. Five patients were excluded or lost to follow-up. Fifteen patients received 50 mg trimipramine at night and 16 patients received placebo. Endoscopy at 4 weeks showed ulcer healing in 11 patients (73%) receiving trimipramine and in 6 patients (38%) receiving placebo. Three patients were withdrawn at this stage, and the remainder were followed up for a further 4 weeks while receiving antacids only for symptomatic relief. At final endoscopy after 8 weeks, no further healing had occurred in the trimipramine group, whereas one further patient in the placebo group showed ulcer healing. The frequency and severity of night pain and waking were reduced and antacid consumption was lower int he trimipramine group, but initial drowsiness was greater. Trimipramine appears to be of some value in the treatment of duodenal ulceration.

Early results of surgery in patients considered cimetidine failures.

Fifty-two consecutive unselected duodenal ulcer patients (Group I), who had failed to respond to cimetidine and who subsequently underwent elective vagotomy and drainage, were studied. All patients were symptomatic on cimetidine in full recommended dosage. This group has been compared with another group of 634 duodenal ulcer patients (Group 2) undergoing elective vagotomy and drainage in the 'pre-cimetidine era'. The groups were similar pre-operatively with regard to age, sex, length of history and maximal acid output. Completeness of vagotomy and amount of acid reduction were similar in the two groups. The incidence of recurrent ulceration was 5 per cent in Group I and 5.7 per cent in Group 2. Although, of necessity, follow-up is shorter in the cimetidine failures (mean 2.3 years), there is nothing to suggest that failure to respond to cimetidine precludes a satisfactory surgical result.

The effect of trimipramine (Surmontil) on the gastric secretion of acid and pepsin in patients with duodenal ulceration.

Twenty-three patients with endoscopically proven, symptomatic duodenal ulceration were randomized to receive trimipramine 50 mg daily or placebo. Maximal acid output studies and estimations of pepsin levels were performed before treatment, for 4 weeks while on drug or placebo and for 4 weeks after cessation of treatment. Gastric acid secretion was significantly reduced after 3 weeks treatment with trimipramine and this reduction was maintained for the duration of the study. Gastric pepsin levels were unaffected by the administration of the drug.

Florid granulomatous reaction in a seminoma.

A case of seminoma of the testis complicated by an extensive granulomatous reaction is reported. This reaction was so florid that a benign condition was initially considered until further material for histology was examined and the correct diagnosis made.