Publications by authors named "Bright-Asare P"

This multicenter randomized, double-blind, 4-wk study compared the new H2-receptor antagonistic roxatidine (R) to placebo (P) for treatment of endoscopically diagnosed active duodenal ulcer disease. Subjects were evaluated after 2 and 4 wk of treatment. Those whose ulcer was unhealed at 2 wk received 2 more weeks of treatment before final evaluation.

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Peptic ulcer develops when offensive factors overwhelm defensive processes in the gastroduodenal mucosa. Offensive factors include NSAIDs, hydrochloric acid-peptic activity, bile reflux, and some products of the lipoxygenase pathway such as leukotriene B4; whereas defensive processes are largely mediated by prostaglandins through poorly understood mechanisms uniformly termed cytoprotection. Cytoprotection, a physiological process working through the products of arachidonic acid metabolism, may result from the net effect of the protective actions of prostaglandins versus the damaging actions of leukotrienes.

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Enprostil is a synthetic prostaglandin E2 analogue with gastric anti-secretory, cytoprotective, and gastrin lowering properties. The current multi-center, double-blind, placebo-controlled study was undertaken to evaluate the efficacy and safety of enprostil (35 micrograms twice daily) for the treatment of duodenal ulcers. The study enrolled 87 patients between the ages of 18 and 85 with an endoscopically proved duodenal ulcer between 0.

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A randomized, multicenter, double-blind, placebo-controlled study was conducted to determine whether ranitidine 150 mg b.i.d.

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Treatment of duodenal ulcer with the histamine H2-receptor antagonist, ranitidine, was assessed in a double-blind, randomized, multicenter trial in which patients were treated for two consecutive 4-week periods with ranitidine 150 mg b.i.d.

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This study was undertaken to evaluate the efficacy of misoprostol taken twice daily for the healing of duodenal ulcer. Three hundred thirty patients with endoscopically proven duodenal ulcer participated in a multicenter, double-blind, controlled trial comparing placebo with misoprostol 200 micrograms and 400 micrograms twice daily for up to four weeks. Patient characteristics were similar in all three treatment groups.

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About 50% of patients receiving intrahepatic infusion of 5-fluorouracil deoxyriboside (5-FUDR) for colorectal cancer with hepatic metastasis develop significant gastroduodenal lesions. This paper reviews two studies on the effect of 16,16 dimethyl prostaglandin E2 (DMPGE2) on 5-fluorouracil-induced mucosal lesions in dogs. DMPGE2 at high doses (2 micrograms X kg-1 X h-1), which reduced histamine-stimulated gastric acid secretion by 65%, reduced gastric mucosal injury.

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Gastric complications occur in 5% to 20% of patients treated with hepatic artery infusion of chemotherapeutic agents for hepatic metastatic lesions. Often these complications are due to catheter dislodgement from the common hepatic artery into the left gastric artery. These studies were designed to answer the following questions: (1) Will chronic infusion of 5-fluorouracil into the left gastric artery produce mucosal injury in dogs; and (2) if so, will 16-16 dimethyl prostaglandin E2 afford protection against such injury? Mongrel dogs, 20 kg, were prepared with a polyethylene catheter in the left gastric artery and a Thomas cannula in the antrum 5 days prior to the study.

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Today, we have effective and potent drugs such as H2-receptor antagonists for the treatment of peptic ulcers. Cimetidine and ranitidine are antisecretory drugs which heal 67-90% of duodenal ulcers in 4 weeks. Certain prostaglandins (PGs) which also heal gastroduodenal ulcers and hemorrhagic gastritis not only diminish gastric acid secretion but also confer unique protective properties on the gastroduodenal mucosa.

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