Burns Incl Therm Inj. 1988 Dec;14(6):504-7.
Preventive measures for stress ulcers in burn patients.

Rath T, Walzer LR, Meissl G.

Department of Plastic and Reconstructive Surgery, Ludwig Boltzmann Institute of Experimental Plastic Surgery, Vienna, Austria.

Between January 1981 and December 1985 336 patients with deep partial and full skin thickness burn injuries covering more than 20 per cent of the body surface area (BSA) were treated in our burn unit. During the first 3.5 years prophylactic therapy for stress ulcers consisted of cimetidine or ranitidine whereas during the last 18 months a combination of ranitidine and sucralfate was used. Over the whole period a protein-rich enteral feeding was instituted as early as possible after injury. Six times 200 mg/day cimetidine were administered intravenously during the first 4-6 days after injury, followed by a reduction to 4 x 200 mg/day usually until the end of the third week. Subsequently cimetidine was given orally in doses of 5 x 200 mg/day. Ranitidine (3 x 112 mg) was given intravenously until enteral feeding started, usually for the first 4 days, after oral nutrition had started the dosage was reduced to 3 x 56 mg/day. Over the past 18 months 4 x 1 g/day granular powdered sucralfate in combination with 3 x 56 mg/day ranitidine were given. The incidence of gastrointestinal bleeding was 2.5 per cent and no patient required surgical therapy. With respect to prophylaxis of bleeding and perforation of stress ulcers the triple regimen using sucralfate, ranitidine in low dosages and protein-rich enteral feeding appeared to be as effective as the earlier use of cimetidine or ranitidine. Side-effects of H2-blockade treatment, especially the high incidence of pneumonias caused by ascending infection from the gastrointestinal tract, were not seen. The high incidence of diarrhoea during H2-blockade treatment in combination with high protein enteral feeding remains to be solved.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2907978&dopt=Abstract ranitidine






Gut. 1988 Jul;29(7):890-3.
Alteration of H2 receptor sensitivity in duodenal ulcer patients after maintenance treatment with an H2 receptor antagonist.

Jones DB, Howden CW, Burget DW, Silletti C, Hunt RH.

Division of Gastroenterology, McMaster University Medical Centre, Hamilton, Ontario, Canada.

The effects of a specific H2 receptor agonist impromidine, on gastric acid secretion were measured in six patients with duodenal ulcer in clinical remission before and after three months treatment with ranitidine 150 mg nocte. After treatment basal acid output increased from 1.2 to 2.8 mmol/h and after maximal impromidine stimulation from 36.9 (4.7) to 44.2 (6.2) mmol/h (p less than 0.02). Intravenous ranitidine 50 mg was given at the end of the impromidine infusion on each study day; the antisecretory effect of intravenous ranitidine was accentuated after the treatment with ranitidine from a trough acid output of 8.5 (1.2) mmol/h before, to 3.8 (1.5) mmol/h (p less than 0.05) after, treatment. The increased response to the H2 agonist impromidine and the H2 antagonist ranitidine after treatment with ranitidine suggests an enhanced sensitivity of the H2 receptor. This might be explained on the basis of an increase in the number of H2 receptors ('up-regulation').

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2969357&dopt=Abstract ranitidine






Aliment Pharmacol Ther. 1988 Jun;2(3):245-52.
Prophylaxis of aspirin-induced gastric mucosal bleeding with ranitidine.

Hawkey CJ, Somerville KW, Marshall S.

Department of Therapeutics, University Hospital, Nottingham, UK.

The ability of ranitidine to protect the human gastric mucosa against aspirin-induced damage was investigated by timed measurements of blood loss collected by gastric washing. Ranitidine (150 mg) 1 h or 5 h before 900 mg aspirin (5 doses of each) over 48 h reduced subsequent mean bleeding from 7.7 microliters/10 min to 2.6 microliters/10 min or 3.4 microliters/10 min, respectively. Both regimens were antisecretory at the time of aspirin administration, as judged by a rise in the pH of the aspirated washings. The prolonged protection against aspirin-induced bleeding achieved with twice daily dosing with ranitidine has clinical potential in the management of patients taking anti-inflammatory drugs.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2979248&dopt=Abstract ranitidine






J Pharmacol Exp Ther. 1988 Jun;245(3):887-94.
Inhibition by ranitidine of acetaminophen conjugation and its possible role in ranitidine potentiation of acetaminophen-induced hepatotoxicity.

Rogers SA, Gale KC, Newton JF, Dent JG, Leonard TB.

Department of Drug Metabolism, Smith Kline & French Laboratories, Philadelphia, Pennsylvania.

Pretreatment with ranitidine (RA) potentiates the hepatotoxicity of acetaminophen (APAP) in male Fischer 344 rats. The present studies were undertaken to investigate the role of APAP metabolism in this potentiation. Administration of RA (50 mg/kg p.o.) to male Fischer 344 rats 30 min before [3H]APAP (750 mg/kg p.o.) increased the plasma concentrations of acetaminophen at 2 hr (193%) and 4 hr (277%) after APAP. Covalent binding of [3H]APAP-related material to hepatic macromolecules in RA-pretreated animals was similar to APAP alone values up to 12 hr after treatment; however, 24 hr after APAP, binding in the RA-pretreated animals was twice that observed in animals given [3H]APAP alone. Urinary excretion (0-24 hr) of APAP and APAP glucuronide were reduced in ranitidine-pretreated animals to 64 and 66% of control, respectively, indicating that in vivo RA altered APAP conjugation with glucuronic acid. APAP uridine diphosphoglucuronyltransferase activity in rat hepatic microsomes was competitively inhibited by RA (0.1-2 mM). The Ki apparent for RA inhibition of APAP uridine diphosphoglucuronyltransferase was 0.04 mM. In contrast, neither APAP nor 4-nitrophenol sulfotransferase activity in rat hepatic cytosol was inhibited by RA at concentrations up to 5 mM. Together, these results support the suggestion that RA-mediated alterations of APAP conjugation may explain the potentiation of APAP-induced hepatotoxicity by RA in rats.

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Am J Hosp Pharm. 1988 May;45(5):1100-2.
Stability of ranitidine hydrochloride in total nutrient admixtures.

Cano SM, Montoro JB, Pastor C, Pou L, Sabin P.

Department of Pharmacy, Hospital Valle de Hebron, Barcelona, Spain.

The stability of ranitidine hydrochloride in total nutrient admixtures (TNAs) containing 5% intravenous fat emulsion was studied. A TNA containing lipids and glucose was prepared aseptically in three ethylene-vinyl acetate bags. Ranitidine hydrochloride 100 mg and 200 mg was added to two of the bags to yield concentrations of 50 micrograms/mL and 100 micrograms/mL, respectively. The third bag served as a control. At 0, 12, 24, 48, and 72 hours, the ranitidine content was measured by high-performance liquid chromatography, the pH of the admixtures was determined, and the bags were visually inspected for signs of color changes, creaming, or precipitates. Particle-size distribution was measured at 72 hours and compared with that in the control bag at time zero. No appreciable changes in pH occurred over 72 hours, and no visual changes were observed. At concentrations of 50 and 100 micrograms/mL of admixture, ranitidine hydrochloride activity declined approximately 80% during the study period. Approximately 10% of the initial concentration was lost in 12 hours. In both cases, there was no variation in particle-size distribution compared with that in the control bag at time zero. Ranitidine hydrochloride appears to be stable for up to 12 hours at room temperature in the admixtures studied, and the lipid emulsion apparently was not altered during this period by ranitidine.

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Am J Med. 1988 Oct;85(4):525-7.
Induction of theophylline toxicity and inhibition of clearance rates by ranitidine.

Roy AK, Cuda MP, Levine RA.

Department of Medicine, State University of New York, SUNY-Health Science Center, Syracuse 13210.

PURPOSE: Theophylline is metabolized by the hepatic microsomal oxidase system, as is ranitidine, although the latter has a much lower affinity for the system. The incidence of theophylline toxicity is rare when the two drugs are administered simultaneously. We observed the development of clinical and chemical toxicity in three elderly patients receiving oral theophylline therapy for chronic obstructive pulmonary disease after the administration of ranitidine therapy for peptic ulcer disease. PATIENTS AND METHODS: Three patients with chronic obstructive pulmonary disease who had been receiving theophylline for prolonged periods of time were studied. Two patients presented with complaints of epigastric pain, which was attributed to acid-peptic disease; the other patient presented with hematemesis, which was shown to be due to gastric and duodenal ulcers. Ranitidine was administered for treatment of acid-peptic disease. Theophylline clearance rates were determined before, during, and after ranitidine treatment. When symptoms of theophylline toxicity developed, the dose of theophylline was either stopped or reduced. Subsequently, patients were readministered their usual dose of theophylline. RESULTS: The effect of simultaneous administration of both drugs resulted in similar reductions in theophylline clearance rates. Serum theophylline levels returned to pretreatment values after cessation of ranitidine treatment. In one patient, rechallenge with ranitidine during steady-state theophylline treatment resulted in recurrence of clinical and chemical theophylline toxicity. CONCLUSION: These observations suggest that treatment with ranitidine may cause clinically apparent interactions with theophylline since both drugs are metabolized by the same cytoch




J Pediatr Gastroenterol Nutr. 1988 Sep-Oct;7(5):645-50.
Prognostic value of serum pepsinogen I in children with peptic ulcer.

Oderda G, Altare F, Dell'Olio D, Ansaldi N.

Sezione di Gastroenterologia, Universita di Torino, Italia.

Serum pepsinogen I (PG I) levels were determined by radioimmunoassay in 23 children with peptic ulcer disease (PUD) before and after treatment with ranitidine and in 44 children who were being investigated for recurrent abdominal pain. Upper gastrointestinal endoscopy was performed in all. No lesions were detected in controls, while 18 patients showed a duodenal ulcer, 4 had an antral ulcer, and 1 had both. An 8-week course of ranitidine healed PUD in 93.5% of them, while long-term (1-5 years) endoscopic follow-up showed a 41.9% ulcer relapse rate after stopping treatment. Gastric acid secretion after pentagastrin stimulation [maximal acid output (MAO)] was tested in all controls and in 22 PUD patients: While controls had normal MAO values for their age, 65% of patients had a secretion above the normal range. No significant correlation was detected between serum PG I and MAO either in controls or in patients. Mean serum PG I concentrations were not significantly higher in the whole patient group than in controls, but PUD patients who relapsed after discontinuing ranitidine treatment had shown on admission significantly higher PG I levels when compared both with those who did not relapse and with controls. All patients who relapsed, but only 42.8% of those who did not, had a serum PG I concentration above the normal upper limit for a pediatric population (56.7 ng/ml). None of the PUD patients who had serum PG I levels under this limit relapsed. Our results suggest that pretreatment serum PG I levels in children with PUD may predict fairly accurately which will not relapse after attaining ulcer healing by a short-term ranitidine course.

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Res Vet Sci. 1988 Nov;45(3):291-5.
Effects of cimetidine and ranitidine on basal gastric pH, free and total acid contents in horses.

Sangiah S, McAllister CC, Amouzadeh HR.

Department of Physiological Sciences, College of Veterinary Medicine, Oklahoma State University, Stillwater 74078.

The basal gastric pH, free and total acid contents from five adult horses were determined at two-hour intervals for six- to eight-hour periods. The basal gastric pH, free and total acid contents varied from 2.14 +/- 0.08 to 2.41 +/- 0.14, 28.63 +/- 8.27 to 17.89 +/- 2.86 mmol litre-1 and 41.38 +/- 9.72 to 37.38 +/- 3.70 mmol litre-1, respectively. Cimetidine (8.8 mg kg-1 orally) and ranitidine (2.2 mg kg-1 orally) increased the basal gastric pH to above 3.6 (P less than 0.05) with a concomitant reduction of 75 per cent and 75 to 100 per cent in the basal gastric free acid content, respectively, for an eight-hour period. Cimetidine (4.4 mg kg-1, intramuscularly) and ranitidine (1.4 mg kg-1, intramuscularly) increased the basal gastric pH to above 3.6 with a concomitant reduction of 54 to 93 per cent and 69 to 100 per cent in the basal gastric free acid content, respectively, for an eight-hour period. This study shows that the horse is a basal acid secretor, and that cimetidine and ranitidine, two widely used histaminergic-H2 type antagonists in human clinical practice are effective in horses with ranitidine being approximately four times more potent than cimetidine.

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Acta Pathol Jpn. 1988 Oct;38(10):1285-96.
The effects of ranitidine and cysteamine on intestinal metaplasia induced by X-irradiation in rats.

Watanabe H, Kamikawa M, Nakagawa Y, Takahashi T, Ito A.

Department of Cancer Research, Hiroshima University, Japan.

The influence of ranitidine and cysteamine on intestinal metaplasia was examined in 7-month-old male Crj: CD (SD) rats. At the age of 5 weeks, the animals were treated with 10 Gy doses of X-rays at 3-day intervals up to a total of 20 Gy in the gastric region, and 6 months after irradiation, the rats received either ranitidine (0.02% in diet) or cysteamine (0.1% in drinking water) for 2 months. The incidence and number of intestinal metaplasia with alkaline phosphatase-positive foci in rats given X-rays and cysteamine (group 4) were significantly low compared with those in rats given X-rays and ranitidine (group 3) (p less than 0.01). In both the pyloric and the fundic gland mucosae, the average numbers of type C metaplasia (intestinal crypts with Paneth cells) and total numbers of metaplastic foci in rats of group 3 were much higher than those in group 4 (P less than 0.05). The present results showed that the occurrence of intestinal metaplasia was significantly increased after administration of ranitidine and decreased by cysteamine.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3218508&dopt=Abstract ranitidine