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PubMed1985

A comparative trial of ranitidine 300 mg at night with ranitidine 150 mg twice daily in the treatment of duodenal and gastric ulcer.

A multicenter double-blind comparative trial of oral ranitidine, 300 mg hs versus 150 mg bid, was conducted in 89 patients with duodenal ulcer (DU) and 54 with gastric ulcer (GU). Antacid tablets were prescribed prn. After 4 wk of treatment there were no statistically significant differences in the ulcer healing rates associated with the once daily (DU 86.4%, GU 62.5%) and the twice daily (DU 84.4%, GU 73.3%) regimens. Antacid consumption, by both DU and GU patients, was higher in the 150 mg bid group, but the differences did not achieve statistical significance. Further improvement in cumulative healing rates in response to both treatment regimens was observed following a second 4-wk treatment for those patients whose ulcers had failed to heal during the 1st month. Smoking adversely affected the rate of ulcer healing in DU patients, but had no significant effect on GU healing. No serious adverse effects or biochemical abnormalities were observed. Ranitidine 300 mg hs appears to be equally safe and effective as the standard regimen of 150 mg bid in the short-term treatment of uncomplicated gastroduodenal ulcer.

Adult↗
PubMed1985

Comparison of ranitidine, domperidone maleate and ranitidine + domperidone maleate in the short-term treatment of reflux oesophagitis.

In the treatment of reflux oesophagitis, either drugs preventing regurgitation of gastric juice in the lower oesophagus or pharmacological agents increasing the pH of the refluxing material are employed. In the present study 45 outpatients with reflux oesophagitis were randomly treated with either ranitidine (150 mg b.i.d.) or domperidone maleate (20 mg t.i.d.) or both drugs for six weeks. Before and after treatment the severity of dyspeptic symptoms and the grade of endoscopic and histological changes were assessed. The three therapeutic regimens were significantly and equally effective in inducing symptomatic relief and promoting endoscopic and histological disappearance or improvement of oesophagitis. The combined use of ranitidine and domperidone maleate failed to show any additional benefit compared with treatment with either drug alone.

Clinical Trials as Topic↗
PubMed1998

One-week triple therapy with ranitidine bismuth citrate, clarithromycin and metronidazole versus two-week dual therapy with ranitidine bismuth citrate and clarithromycin for Helicobacter pylori infection: a randomized, clinical trial.

OBJECTIVE: The aim of this study was to compare the efficacy and side effects of 1-wk triple therapy with ranitidine bismuth citrate (RBC) 400 mg b.i.d., clarithromycin 500 mg b.i.d., and metronidazole 500 mg b.i.d., to 2-wk dual therapy with RBC 400 mg b.i.d. and clarithromycin 500 mg b.i.d. for H. pylori infection in a randomized, clinical trial. METHODS: Patients (18-80 yr) with a culture proven H. pylori infection were randomized to one of these regimens. Side effects were scored on a semiquantitative scale. Endoscopy was performed > or = 4 wk after treatment. Antral biopsy samples were taken for hematoxylin-eosin stain (HE), rapid urease test, and culture and corpus samples for culture and HE. Two weeks after the endoscopy, a 13C-urea breath test was performed. Eradication failure was defined as detection of H. pylori by culture or by at least two other tests. RESULTS: A total of 104 patients, 54 men, age 54+/-14 yr, (36 duodenal ulcer, 16 gastric ulcer, and 52 functional dyspepsia) were included. Gender, age, and diagnosis were comparable in both groups. Fourteen of 52 patients in both triple and dual therapy, respectively, had significant side effects, but all patients completed the course. Eradication results were 49 of 52 (94%; 95% CI: 84-99%) and 50 of 52 (96%; 95% CI: 87-100%) on intention to treat analysis and 44 of 46 (96%; 95% CI: 85-99%) and 48 of 49 (98%; 95% CI: 89-100%) on per protocol analysis for triple and dual therapy respectively. CONCLUSION: Both regimens are very effective and well tolerated in the treatment of H. pylori infection. The triple regimen has the advantage of being shorter.

Adolescent↗
PubMedDate not supplied

Interactions and non-interactions with ranitidine.

At present, there are two H2-receptor antagonists available for the treatment of peptic ulcer disease - cimetidine and ranitidine. Cimetidine is well known to interact with a number of concurrently administered drugs. Like cimetidine, ranitidine binds to cytochrome P-450 in the liver where it appears to exert an inhibitory effect, but to a lesser extent than cimetidine. Both H2-receptor antagonists may also reduce hepatic blood flow. Several drugs which are known to interact with cimetidine have been found not to interact significantly with ranitidine, including propranolol, lignocaine, phenytoin and diazepam. However, significant pharmacokinetic interactions between ranitidine and several other drugs have been established. These interactions may be attributed variously to an effect of ranitidine on hepatic metabolism or to an effect on the absorption of concomitantly administered drugs. For example, the bioavailability of midazolam is significantly increased due to the influence of ranitidine on gastric pH and thus on absorption of midazolam, leading to an increased soporific effect of this benzodiazepine; an effect of ranitidine on oxidative liver metabolism also appears to be a contributory factor in this interaction. Conversely, ranitidine distinctly reduced protein-bound cobalamin absorption from a mean of 7.66% prior to ranitidine administration to 0.84% during treatment with ranitidine 300 mg daily. A significant pharmacokinetic interaction has also been demonstrated between ranitidine and procainamide: the AUC of procainamide increased and the renal clearance fell significantly from a mean of 378 to 309 ml/min with ranitidine co-administration. However, this interaction is due to a different mechanism. In this case, ranitidine appears to compete with procainamide for the common renal proximal tubular secretion site. The reported interactions of ranitidine with warfarin, metoprolol, nifedipine, theophylline and fentanyl appear to be due to inhibition of cytochrome P-450. In a clinical study, warfarin clearance was significantly reduced from 66.7 to 48.7 ml/min by ranitidine, and by cimetidine to 42.9 ml/min. Similarly, the elimination half-lives of metoprolol and nifedipine were distinctly prolonged and the AUCs significantly increased by ranitidine. However, the latter pharmacokinetic interactions appear unlikely to be of clinical significance since the clinical effects of metoprolol and nifedipine were unaffected by ranitidine treatment. In therapeutic concentrations, ranitidine inhibited the disappearance of fentanyl from an in vitro microsomal preparation, indicating that it inhibits microsomal drug metabolism.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMed1993

Gastric anti-secretory, mucosal protective, anti-pepsin and anti-Helicobacter properties of ranitidine bismuth citrate.

Ranitidine bismuth citrate is a novel compound formed from ranitidine and a bismuth citrate complex. In conscious dogs, ranitidine bismuth citrate had similar activity to ranitidine hydrochloride as an inhibitor of histamine-induced gastric acid secretion when oral doses containing equivalent amounts of ranitidine base (0.1 or 0.3 mg/kg) were compared. In the rat, ranitidine bismuth citrate (3-30 mg/kg p.o.) prevented gastric mucosal damage induced by ethanol (fundic damage) and indomethacin (antral damage). Ranitidine hydrochloride and tripotassium dicitrato bismuthate were also effective against indomethacin-induced damage, but were both significantly less potent than ranitidine bismuth citrate in this model. Ranitidine hydrochloride was inactive against ethanol-induced damage. In vitro, ranitidine bismuth citrate (1 mmol/L) inhibited human pepsin isoenzymes 1, 2, 3 and 5. Pepsin 1 was inhibited to a similar extent by ranitidine bismuth citrate, bismuth citrate and tripotassium dicitrato bismuthate at concentrations equivalent to 1 mmol/L bismuth, but ranitidine (1 mmol/L) was inactive. Ranitidine bismuth citrate was more potent than tripotassium dicitrato bismuthate as an inhibitor of pepsins 2, 3 and 5. Ranitidine bismuth citrate inhibited both Helicobacter pylori (effective concentration 4-32 micrograms bismuth/ml) and H. mustelae (1-4 micrograms bismuth/ml); similar results were obtained with tripotassium dicitrato bismuthate. Bismuth citrate was slightly less effective, and ranitidine hydrochloride was inactive (> 125 micrograms/ml). In ferrets naturally colonized with H. mustelae, oral treatment with ranitidine bismuth citrate, 12 or 24 mg/kg twice daily for 4 weeks, caused a dose related clearance of H. mustelae. Qualitatively similar results were obtained in a small study with tripotassium dicitrato bismuthate and bismuth citrate.

Animals↗
PubMed1995

Gastrointestinal transit and distribution of ranitidine in the rat.

PURPOSE: Ranitidine gastrointestinal distribution was examined in the rat small intestine after oral administration to determine whether intestinal transit or secretion (exsorption) may influence the appearance of secondary peaks in ranitidine serum concentration-time profiles. METHODS: Male Sprague-Dawley rats received ranitidine (50 mg/kg) by oral gavage, and the mass of ranitidine recovered in all small intestinal segments (approximately 12 cm each) was determined 30, 60, 90, or 120 min after administration. In a separate group of anesthetized rats, the small intestine was divided into two segments of equal length that were perfused with normal saline in a single-pass manner. Rats received an escalating, zero-order IV infusion of ranitidine for 30 min, and venous blood and intestinal effluent were collected over 90 min to quantitate ranitidine exsorption. RESULTS: Thirty min after oral administration, > 50% of the recovered ranitidine mass resided in the lower half of the small intestine in all rats. Ranitidine mass in 5 of 16 rats displayed a bimodal distribution with significant amounts of ranitidine recovered from the stomach 60 to 90 min after dosing. Ranitidine exsorption was more efficient from the lower jejunum and ileum than from the duodenum and upper jejunum. However, intestinal secretion of ranitidine was minor (5% of the IV dose). CONCLUSIONS: Ranitidine absorption from the lower ileum contributes significantly to systemic ranitidine concentrations before and during the time of the first concentration maximum. Separation of the drug mass into multiple boluses may contribute to secondary peaks in ranitidine concentration-time profiles. Exsorption did not contribute significantly to ranitidine distribution in the gastrointestinal tract.

Animals↗
PubMed1985

Stability of ranitidine hydrochloride and amino acids in parenteral nutrient solutions.

The stability of ranitidine hydrochloride in parenteral nutrient (PN) solutions and the effect of ranitidine hydrochloride on the amino acids in the PN solutions were studied. Six PN solutions (three each with amino acid contents of 2.125 and 4.25%) were prepared. Each PN solution also contained dextrose 25%, electrolytes, trace elements, vitamins, and heparin sodium. Ranitidine hydrochloride injection was added to four of the PN samples. Of the final samples, two contained no ranitidine, two contained ranitidine hydrochloride 50 micrograms/mL, and two contained ranitidine hydrochloride 100 micrograms/mL. Admixtures of ranitidine hydrochloride at the two concentrations in 0.9% sodium chloride injection were also prepared. Samples were observed for color change and tested for pH during storage at room temperature. Concentrations of amino acids were measured after 24 hours in samples without ranitidine and in samples containing ranitidine hydrochloride 100 micrograms/mL. Ranitidine hydrochloride content was determined by high-performance liquid chromatography at 12, 24, and 48 hours. No visual changes or pH changes occurred by 24 hours. All PN solutions became darker by 48 hours. The presence of ranitidine hydrochloride did not substantially affect amino acid concentrations. At 24 hours, at least 90% of the initial ranitidine concentrations remained in all samples. In three of the four PN samples at 48 hours, less than 90% of initial ranitidine concentrations remained. Ranitidine hydrochloride in concentrations of 50 and 100 micrograms/mL in parenteral nutrient solutions containing 4.25 and 2.125% crystalline amino acids is stable for 24 hours at room temperature. Under these conditions, concentrations of the amino acids contained in the PN solutions were not affected by the addition of ranitidine hydrochloride.

Amino Acids↗
PubMed1990

Double blind comparative study of omeprazole and ranitidine in patients with duodenal or gastric ulcer: a multicentre trial. Cooperative study group.

We studied omeprazole and ranitidine in promoting duodenal ulcer healing in a multicentre trial by comparing the proportion of healed ulcers after two, four, and eight weeks of treatment. Altogether, 194 patients (143 men) were randomly allocated according to a prearranged treatment schedule to either drug and were treated double blind. Each received 40 mg omeprazole in the morning and a ranitidine placebo morning and evening or 150 mg ranitidine morning and evening with an omeprazole placebo in the morning. A total of 188 patients (94 taking omeprazole, 94 taking ranitidine) completed the trial. Sixty four (68%) omeprazole treated and 45 (48%) ranitidine treated patients had healed ulcers at two weeks, 91 (99%) omeprazole treated and 79 (88%) ranitidine treated had healed ulcers by four weeks, and 91 (100%) omeprazole treated and 86 (97%) ranitidine treated patients had healed ulcers by eight weeks. The overall difference in healing rates was significant (p = 0.0008, Mantel-Haenszel test). The differences were significant also at two weeks (20%, 95% confidence interval 5.6 to 34.4, p less than 0.01) and at four weeks (11%, 95% CI 3.7 to 17.3, p less than 0.01), but not at eight weeks (3%, 95% CI -0.5 to + 7.3, p = 0.25), using the chi 2 statistic, the study having a power to detect a 20% difference on 90% of occasions. After two weeks of treatment complete symptom relief was observed in 70 (74%) patients receiving omeprazole and in 58 (62%) receiving ranitidine. Diary cards showed a significantly lower percentage of days with pain in the omeprazole treated group (7.4% v 21.4%, p < 0.02) when assessed over either the first two weeks or over weeks three and four treatment. A total of 144 patients with healed duodenal ulcer were followed up, with no treatment, for six months. At the end of this period 19 (26%) of 74 patients healed with omeprazole and 17 (24%) of 70 patients healed with ranitidine were still in remission. A similar protocol was used for 46 patients (25 men) with gastric ulcer who were randomly allocated to treatment with omeprazole or ranitidine as described above. Forty patients (16 omeprazole, 24 ranitidine) completed trial. Thirteen (81%) omeprazole treated and 14 (58%) ranitidine treated patients had healed ulcers at four weeks; at eight weeks 14 (93%) omeprazole treated and 20 (87%) ranitidine treated patients had healed ulcers. These differences were not significant at four weeks (p = 0.25) or eight weeks (p = 0.96). Twenty seven gastric ulcer patients were followed up for six months and seven (58%) of the 12 omeprazole healed and five (33%) of the 15 ranitidine healed patients were in remission at six months. Unwanted adverse events were trivial except for one fatality in a 67 year old women, who died from bronchopneumonia and myocardial ischaemia while receiving treatment with omeprazole, which was judged to be unrelated to her death.

Aged↗
PubMed1995

Kinetics of ranitidine metabolism in dog and rat isolated hepatocytes.

1. Freshly isolated hepatocytes from rat and dog have been evaluated as a model for the metabolism of ranitidine in vivo. 2. Isolated hepatocytes from the male and female dog and male Wistar and random hooded rat metabolized ranitidine to ranitidine N-oxide, ranitidine S-oxide, desmethylranitidine and two unidentified minor metabolites. The furoic acid metabolite of ranitidine, previously reported to be a minor metabolite in vivo in rat and dog, was not detected in hepatocytes from either species. 3. The kinetics for ranitidine metabolism in hepatocytes were monophasic for the formation of the three major metabolites in dog and Wistar rat and for N-demethylation of ranitidine in the random hooded rat, but biphasic in this latter strain for the N- and S-oxidation of ranitidine. 4. Ranitidine N-oxide was reduced to ranitidine by Wistar rat hepatocytes but not by hepatocytes from the random hooded rat or dog. Ranitidine S-oxide was metabolized by hepatocytes from both species to one of the unidentified metabolites but was not reduced to ranitidine in either species. Desmethylranitidine was not a substrate for metabolism in hepatocytes from either species. 5. The relative quantitative importance of ranitidine N-oxide, ranitidine S-oxide and desmethylranitidine produced by the hepatocytes was consistent with the profiles of these three metabolites in vivo in rat and dog. The results confirm the value of isolated hepatocytes as a predictive model for in vivo drug metabolism.

Animals↗
PubMedDate not supplied

The effect of three different ranitidine dosage regimens on reducing gastric acidity and volume in ambulatory surgical patients.

STUDY OBJECTIVE: To evaluate three different preoperative oral dosing regimens of ranitidine in ambulatory patients who had significant risk of aspiration pneumonitis (gastric pH < or = 2.5 or volume > or = 25 ml at intubation or extubation). DESIGN: Double-blind, placebo-controlled, randomized trial. SETTING: St. Francis Hospital of Buffalo, New York. PATIENTS: Two hundred seventy-one ambulatory patients about to undergo a surgical procedure under general anesthesia, of whom 241 (89%) completed the trial and were considered evaluable. INTERVENTIONS: Patients were randomly assigned to receive one of four regimens administered orally before surgery: placebo at bedtime the night before and in the morning on the day of surgery; ranitidine 150 mg at bedtime and in the morning; ranitidine 150 mg at bedtime and placebo in the morning; or ranitidine 300 mg at bedtime and placebo in the morning. MEASUREMENTS AND MAIN RESULTS: Patients who received ranitidine 150 mg twice/day, ranitidine 150 mg at bedtime, or ranitidine 300 mg at bedtime had a significantly (p < 0.05) lower frequency of a gastric pH 2.5 or below at intubation or extubation than those taking placebo twice/day (3%, 45%, and 31%, respectively, vs 86%). In addition, gastric volume at intubation or extubation was 25 ml or above in significantly fewer patients receiving ranitidine 150 mg at bedtime than placebo (37% vs 13%, p < 0.05). Overall, the number of patients with risk factors for aspiration pneumonitis was significantly lower with ranitidine 150 mg twice/day (20%), ranitidine 150 mg at bedtime (48%), and ranitidine 300 mg at bedtime (35%) than placebo (86%) (p < 0.001), and significantly lower with ranitidine 150 mg twice/day than ranitidine 150 mg at bedtime (p < 0.05). CONCLUSIONS: Ranitidine 150 mg twice/day preoperatively reduced to the greatest degree the percentage of patients who developed significant risk factors for aspiration pneumonitis after surgery under general anesthesia.

Ambulatory Surgical Procedures↗
PubMed1996

Effects of ranitidine bismuth citrate on gastric acid secretion and gastrin release in subjects with and without Helicobacter pylori infection.

BACKGROUND: Ranitidine bismuth citrate is a novel antiulcerant that provides the antisecretory activity of ranitidine and the gastric mucosal protection and antibacterial properties of bismuth. METHODS: This randomized, double-blind, placebo-controlled study evaluated the effects of single doses of ranitidine bismuth citrate 200 mg, 400 mg and 800 mg and ranitidine hydrochloride 150 mg on gastrin release and suppression of gastric acid secretion, and compared acid secretory profiles and gastrin release between Helicobacter pylori-negative and -positive patients. Plasma gastrin concentrations were determined by radioimmunoassay under basal conditions and in response to peptone meal stimulation. Acid secretion was measured under basal conditions and in response to peptone meal stimulation. Presence of H. pylori was determined by both 14C-urea breath test and ELISA serology. RESULTS: Inhibition of gastric acid output by ranitidine bismuth citrate was both time- and dose-dependent over the 9-h post-dose study period. Doses of ranitidine bismuth citrate 400 mg and ranitidine hydrochloride 150 mg, which are equimolar, produced similar suppression of acid output regardless of H. pylori status. Ranitidine bismuth citrate had no effect on plasma gastrin concentrations regardless of H. pylori status. All doses of ranitidine bismuth citrate were well tolerated. CONCLUSIONS: Ranitidine bismuth citrate caused time- and dose-dependent reductions in meal-stimulated and between-meal gastric acid output regardless of H. pylori status. The magnitude of decreased acid secretion was similar with ranitidine bismuth citrate 400 mg and ranitidine hydrochloride 150 mg. Ranitidine bismuth citrate had no effect on plasma gastrin concentrations.

Administration, Oral↗
PubMed1996

Ranitidine 300 mg twice daily and 150 mg four-times daily are effective in healing erosive oesophagitis.

BACKGROUND: Ranitidine 150 mg q.d.s. is the currently recommended dosage in the United States for the treatment of erosive oesophagitis. To determine whether a higher dose of ranitidine administered less frequently would also be effective in healing erosive oesophagitis, we compared ranitidine 300 mg b.d. with ranitidine 150 mg q.d.s. in the treatment of erosive oesophagitis. METHODS: This multicentre, double-blind, randomized, placebo-controlled study conducted in the United States compared two dosages of ranitidine in 772 patients with endoscopically diagnosed erosive oesophagitis. Patients were treated with ranitidine 300 mg b.d., ranitidine 150 mg q.d.s. or placebo for up to 12 weeks. Endoscopies were repeated after 4, 8 and 12 weeks of treatment. RESULTS: Ranitidine 300 mg b.d. was significantly more effective than placebo in healing erosive oesophagitis at weeks 8 and 12 (51 vs. 36% and 66 vs. 52%, respectively; P < or = 0.004). Significantly higher healing rates were also achieved with ranitidine 150 mg q.d.s. compared with placebo at 4, 8 and 12 weeks (37 vs. 21%, 62 vs. 36% and 77 vs. 52%, respectively; P < 0.001). Healing rates were significantly higher with ranitidine 150 mg q.d.s. than with ranitidine 300 mg b.d. at all scheduled endoscopies (P < or = 0.041). CONCLUSIONS: Ranitidine 300 mg b.d. is effective in healing erosive oesophagitis and may be appropriate as an alternative dosage regimen to ranitidine 150 mg q.d.s. in some patients with erosive oesophagitis.

Adult↗