A 60 year old woman with chronic duodenal ulcer not responding to Cimetidine, was changed to Ranitidine. She had symptomatic improvement, but had bilateral breast engorgement and tenderness for which treatment was discontinued. A therapeutic trial on a second occasion had the same side effect which came on more rapidly and quickly. This complication in such severe form and recurrence on rechallenge requiring withdrawal of drug was observed for the first time with any H2 receptor antagonist.
A double-blind randomized study in 230 Malaysian patients with duodenal ulcer was conducted to compare the proton-pump inhibitor, omeprazole 20 mg, given once daily in the morning, with ranitidine 300 mg, administered once daily at night. After 2 and 4 weeks of treatment, 222 and 220 patients, respectively, were evaluable according to the study protocol. Omeprazole produced significantly higher healing rates than ranitidine at both 2 weeks (75% versus 46%, respectively, P less than 0.0001) and 4 weeks (97% versus 83%, respectively, P = 0.001). Ulcer symptoms were relieved more rapidly by omeprazole than ranitidine. After 2 weeks, daytime epigastric pain was reported by 30% of ranitidine-treated patients but only by 15% of omeprazole-treated patients, which is a statistically significant difference (P = 0.004). No major clinical or biochemical side effects were recorded for either omeprazole or ranitidine. In conclusion, omeprazole 20 mg was found to be superior to ranitidine 300 mg administered once daily for the treatment of duodenal ulcer as measured by ulcer healing and pain relief.
Twenty-seven patients with peptic ulcer (19 with duodenal ulcer (DU) and eight with gastric ulcer (GU] refractory to H2-antagonists were treated with 40 mg of omeprazole once daily for 4-8 weeks, depending on the rate of ulcer healing. Clinical assessment, endoscopy and laboratory tests were performed at entry, after 2 and after 4 weeks, and if unhealed, also after 8 weeks' treatment. Ten healed patients were given a maintenance therapy of omeprazole 20 mg daily for up to 12 months during which the patients returned for endoscopy, gastric biopsy and laboratory tests at 3-monthly intervals. The initial treatment healed 15 of 19 (79%) DU patients in 2 weeks and all DU patients by 4 weeks. Seven of eight (87%) GU patients healed in 4 weeks and only one required 8 weeks' treatment. Symptom relief was rapid, with most patients being symptom-free within the first day of treatment. Six patients received 12 months' continuous maintenance therapy, one patient 9 months and three patients 6 months' treatment. All patients remained in remission whilst on omeprazole therapy. No adverse events were reported throughout the study. There were no clinically significant changes in haematology or blood chemistry after healing or during the long-term treatment. Biopsy samples revealed no histological changes in the gastric mucosa at any stage. Omeprazole 40 mg therefore was found to produce rapid healing and symptom relief in Asian patients with H2-antagonist-resistant peptic ulcers. Maintenance therapy with omeprazole 20 mg daily was shown to be safe and effective in preventing recurrence of peptic ulceration.
Omeprazole has been shown to have a suppressive effect on Helicobacter pylori. The aim of this study was to determine if prolonged treatment with omeprazole would result in a higher eradication rate than short course treatment. Twenty patients with endoscopy proven duodenal ulcers and unequivocal evidence of Helicobacter pylori (HP) infection based on culture, histology, urease test and Gram's stain of a fresh tissue smear were treated with omeprazole 40 mg om for 2-4 weeks. Following ulcer healing, patients received either maintenance omeprazole 20 mg om or placebo for up to one year. All 20 patients had healed ulcers following a 2-4 week course of omeprazole 40 mg om.. All were negative for HP at the end of treatment. Thirteen patients received short course therapy with omeprazole only, followed by placebo. On follow-up endoscopy at 3 months, only one of 13 (7.7%) had eradicated the bacteria. Seven patients received maintenance treatment with omeprazole 20mg om for one year. Following completion of treatment, patients were followed up at 1, 3 and 6 months. Only one of 7 (14.3%) patients had eradicated the infection on long term follow-up. The eradication rates of HP with both short and long course omeprazole monotherapy were low.
The treatment of perforated duodenal ulcer is controversial. Since the advent of H2 antagonists, the number of ulcer operations has declined tremendously. We wanted to find out if the addition of a H2 antagonist after simple closure of a perforated duodenal ulcer would change the outcome and therefore reviewed 46 patients treated in this fashion. Our results show that this is a safe and effective way of treating patients with perforated duodenal ulcer.
This prospective randomized study investigated the possibility that duodenal ulcer relapse associated with Helicobacter Pylori infection is mediated by oxygen-derived free radicals. To this end, the radical scavengers allopurinol (50 mg 4 times daily) and dimethyl sulphoxide (DMSO, 500 mg 4 times daily) were administered orally. One hundred and forty-six consecutive patients with previous symptomatic endoscopy proven duodenal ulceration, which had been shown endoscopically to have healed in the presence of gastric mucosal infection with Helicobacter Pylori, were randomized to receive for the period of one year either placebo, or cimetidine 400 mg at bedtime, or allopurinol, or DMSO. In one hundred and twenty-six patients evaluable for efficacy, the cumulative relapse at one year was: placebo 47%, cimetidine 24%, allopurinol 6% and DMSO 6%. Cimetidine was significantly effective in preventing the relapse (p < 0.01), however allopurinol and DMSO were superior to cimetidine in this respect (p < 0.05). In the patients who relapsed, ulcer recurrence tended to occur early in those on placebo and cimetidine and to be evenly distributed over the year in those on free radical scavenging therapy. In all groups, ulcer recurrence throughout the maintenance year was more frequently symptomatic than silent. The incidence of infection with Helicobacter Pylori was not influenced by any of the regimens employed and the bacterium was detected with every relapse noted in this study and during the follow-up endoscopy which was carried out at 6 months and at 12 months during the maintenance year. The results suggest that oxygen-derived free radicals are involved in the relapse of duodenal ulceration in patients infected with Helicobacter Pylori.
The aim of the present study was to determine the cost-efficiency of different duodenal ulcer disease treatment practices in Malaysia. Six Malaysian gastroenterologists met to discuss the direct costs related to Helicobacter pylori (HP) eradication treatment. Five treatment strategies were compared: (i) histamine H2 receptor antagonists (H2RA), acid suppression therapy for 6 weeks followed by maintenance therapy as needed; (ii) bismuth triple + proton pump inhibitor (PPI), bismuth (120 mg, q.i.d.), metronidazole (400 mg; t.i.d.), tetracycline (500 mg, q.i.d.) for 7 days and PPI, b.i.d., for 7 days; (iii) OAC, omeprazole (20 mg, b.i.d.), amoxycillin (1000 mg, b.i.d.) and clarithromycin (500 mg, b.i.d.) for 7 days; (iv) OMC, omeprazole (20mg, b.i.d.), metronidazole (400mg, b.i.d.) and clarithromycin (500 mg, b.i.d.) for 7 days; and (v) OAM, omeprazole (20 mg, b.i.d.), amoxycillin (1000 mg, b.i.d.) and metronidazole (400 mg, b.i.d.) for 7 days. A decision tree model was created to determine which therapy would be the most cost-effective. The model considered eradication rates, resistance to anti-microbial agents, compliance and cost implications of treatment regimens, physician visits and ulcer recurrences during a 1 year time period assumption. The H2RA maintenance therapy was the most expensive treatment at Malaysian Ringgit (MR) 2335, followed by bismuth triple therapy (MR 1839), OMC (MR 1786), OAM (MR 1775) and OAC, being the most cost-effective therapy, at MR 1679. In conclusion, HP eradication therapy is superior to H2RA maintenance therapy in the treatment of duodenal ulcer disease. Of the HP eradication regimens, OAC is the most cost-effective.
To determine whether duodenal ulcers continue to heal following successful Helicobacter pylori eradication with short-term eradication therapy without further acid suppression therapy.