To examine the effects of the Capsicum annum L lyophilized fruit extract in experimentally-induced gastric ulcer in rats.
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1. We evaluated injury to the human gastric mucosa caused by low doses of aspirin and its prophylaxis by ranitidine. On two separate occasions, 30 subjects took aspirin 300 mg daily for 12 days either with or without ranitidine 150 mg, 30 min before aspirin. This dose of aspirin caused more than a 5 fold increase in gastric bleeding, from control values of 0.5 microliters 10 min-1 (95% confidence limits 0.3-0.8 microliters 10 min-1) to 2.8 microliters 10 min-1 (1.9-4.1 microliters 10 min-1, P less than 0.01) after 5 days of aspirin. Adaptation did not occur and the gastric bleeding rates remained elevated at 3.4 microliters 10 min-1 (1.9-6.1 microliters 10 min-1) after 12 days of aspirin consumption (P less than 0.01). 2. Coadministration of ranitidine significantly raised intragastric pH and reduced aspirin induced bleeding to 1.5 microliters 10 min-1 (1.0-2.3 microliters 10 min-1) after 5 days and 1.6 (1.0-2.5 microliters 10 min-1) after 12 days (P less than 0.05). 3. Although these values were higher than control levels our results raise the possibility that coadministration of ranitidine may reduce the incidence of peptic ulceration and gastrointestinal haemorrhage which is increasingly reported in some subjects taking low dose aspirin for vascular prophylaxis.
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The objective of this work was to illustrate the suitability of montmorillonite (MMT) as a drug delivery carrier, by developing a new clay-drug composite of ranitidine hydrochloride (RT) intercalated in MMT.
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Since resistance of Helicobacter pylori is developing very fast all over the world, new treatment regimens for eradication are urgently needed.
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In a prospective, double-blinded, single-center study, 42 subjects with chronic urticaria were randomized to high (4,000 IU/d) or low (600 IU/d) vitamin D3 supplementation for 12 weeks. All subjects were provided with a standardized triple-drug therapy (cetirizine, ranitidine, and montelukast) and a written action plan. Data on USS scores, medication use, blood for 25-hydroxyvitamin D, and safety measurements were collected.
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Symptomatic children with HP related gastritis should be treated with triple therapy and HP negative gastritis with H2-receptor antagonist.
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Fifty adult outpatients with endoscopically proven gastric, prepyloric or duodenal ulcers were included in a prospective, randomised double-blind trial of ranitidine (40 mg X 3 daily and 80 mg at bedtime) versus placebo. After 4 weeks the ulcers had healed in 21 of 25 patients receiving ranitidine compared with 7 of 23 in patients receiving placebo (p less than 0.001). The ranitidine treated patients had fewer days of pain (p less than 0.001) and lower consumption of antacids (p less than 0.01) than placebo patients. Patients whose ulcers were not healed after 4 weeks went into an open 4 weeks trial with ranitidine. After the second 4 week period there were still 5 unhealed ulcers, all located in the prepyloric region. No serious side effects or haematological or biochemical abnormalities were observed. It is concluded that ranitidine is a very potent and safe ulcer healing substance. Patients with prepyloric ulcers may need a higher dose or a longer period of treatment.
The kinetics of p. o. (150 mg) and i.v. (50 mg) ranitidine was studied in nine healthy controls and in nine patients with compensated liver cirrhosis. Plasma concentrations and urinary recovery of unchanged drug were determined by high performance liquid chromatography. The pharmacokinetic data observed in the cirrhotic patients did not differ from those of controls after p.o. or i.v. administration. Moreover, oral bioavailability was similar in controls and cirrhotics. In conclusion, the pharmacokinetics of ranitidine is not altered in patients with compensated liver cirrhosis.
This is a double-blind crossover study on 12 normal volunteers. Subjects were studied under conditions of placebo, cimetidine (400 mg b.d.), famotidine (20 mg b.d.), and ranitidine (150 mg b.d.) for one week. Sleep was assessed at the end of each one-week interval via polysomnographic evaluation conducted on nights 6 and 7 of drug administration. On the day between the two nights in the sleep laboratory, a multiple sleep latency test was conducted.
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Acid-related diseases such as gastro-oesophageal reflux disease (GORD) and peptic ulcer are a common cause of morbidity and if inadequately treated can lead to serious complications. The proton-pump inhibitor rabeprazole has been extensively evaluated in well-controlled trials in North America and Europe for the acute treatment of erosive or ulcerative GORD and gastric and duodenal ulcers and for the long-term maintenance of GORD healing. The results show that rabeprazole has a favourable benefit/risk profile for each indication. Rabeprazole 10 and 20 mg given once daily in the morning was highly effective in producing and maintaining healing, providing symptom relief, and improving overall well-being. Healing rates for rabeprazole were equivalent to omeprazole in all indications, and superior (GORD healing and duodenal ulcer healing) or equivalent (gastric ulcer healing) to the histamine 2-receptor antagonist ranitidine. Symptom relief provided by rabeprazole was equivalent or superior to comparator drugs. Rabeprazole was well tolerated in both short- and long-term studies. The incidence of treatment-emergent signs and symptoms related to rabeprazole was low, and these were generally mild or moderate in severity. The overall rate of discontinuations due to adverse events was approximately 3%. There were no deaths related to rabeprazole therapy. These findings indicate a favourable benefit/risk profile for each intended use.