J Anal Toxicol. 1991 Mar-Apr;15(2):101-3.
Ranitidine interference with the monoclonal EMIT d.a.u. amphetamine/methamphetamine immunoassay.

Poklis A, Hall KV, Still J, Binder SR.

Medical College of Virginia Hospital, Department of Pathology, Virginia Commonwealth University, Richmond 23298-0597.

The interference of ranitidine with the monoclonal EMIT d.a.u. amphetamine/methamphetamine immunoassay (ME) was investigated. Urine specimens collected from 23 patients receiving 150-300 mg of ranitidine daily were found to contain 7-271 mg/L of the drug when analyzed by Remedi automated high pressure liquid chromatography. Only patient specimens and urine samples with ranitidine added at concentrations greater than 91 mg/L gave false positive ME results. Of the 63 patient urine samples analyzed by ME, 12 gave false positive results. All false positive results occurred in the first or second void after ingestion. No false positive results occurred with the polyclonal EMIT d.a.u. amphetamine or TDx amphetamine/methamphetamine II assays.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2051743&dopt=Abstract ranitidine






Mol Pharmacol. 1992 Aug;42(2):373-81.
Theoretical studies on the histamine H2 receptor: molecular mechanism of action of antagonists.

Giraldo J, Martin M, Campillo M, Pardo L.

Department of Biostatistics, Faculty of Medicine, Universidad Autonoma de Barcelona, Spain.

The previously defined sites in the histamine H2 receptor model [Mol. Pharmacol. 40:980-987 (1991)] were used to elucidate the pharmacological mechanism of action of compounds that act as antagonists at the receptor. In this model, a formate anion is used both as the negative site at which the histamine cation is anchored to the receptor and as a proton acceptor site. An ammonium cation is used as a proton donor site. The proposed model of recognition of cimetidine, tiotidine, and ranitidine suggests that the monocationic form of the antagonists is the most favorable species to bind the receptor. Moreover, the mode of recognition follows the same trends obtained for compounds that act as agonists; the protonated site of the molecule, i.e., imidazolium in cimetidine, guanidinium in tiotidine, or substituted ammonium in ranitidine, anchors at the negative site of the receptor, whereas the nonbasic part, i.e., cyanoguanidine in cimetidine and tiotidine and nitrodiaminoethene in ranitidine, is located between the proton donor and acceptor sites. An energetic analysis of the interaction between the antagonists and the receptor model, including the energies of ligand desolvation, shows that histamine cannot compete effectively with cimetidine, tiotidine, or ranitidine for binding to the H2 receptor. The predicted order of antagonist potencies, based on differences of formation enthalpies (delta delta H1), reproduces qualitatively the experimental rank order.

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Endokrynol Pol. 1991;42(3):415-20.
[Behavior of thyrotropic, triiodothyronine, thyroxine and cortisol hormone levels in blood serum of patients with duodenal ulcer treated with ranitidine]

[Article in Polish]

Przybylowski J, Kowalski D, Widlak H, Kowalska K, Garmulewicz M.

Klinika Chorob Wewnetrznych Instytutu Medycyny Klinicznej w Kielcach AM w Krakowie.

Blood serum concentrations of thyrotropic hormone (TSH), triiodothyronine (T3), thyroxine (T4) and cortisol have been measured in 50 patients with duodenal ulcer. The determinations were repeated after a specific time of treatment with ranitidine: in 45 patients after 3 weeks and in 37 after additional 30 days of treatment. During the first period of treatment ranitidine was administered at a dose of 300 mg divided into two daily doses and during the second period of treatment at a single daily dose of 150 mg. A small but statistically significant changes, an increase in T3 and a decrease in TSH concentration, were observed before the treatment. No changes concerning these two parameters were found as an effect of the treatment. A decrease in the concentration of T4 was found, on the other hand, after three weeks of ranitidine administration. This decrease persisted after further 30 days of chronic treatment with ranitidine. No significant changes concerning blood serum cortisol concentration were found in any of the studied groups.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1364490&dopt=Abstract ranitidine






Aliment Pharmacol Ther. 1990;4 Suppl 1:29-45.
Tolerance during 29 days of conventional dosing with cimetidine, nizatidine, famotidine or ranitidine.

Nwokolo CU, Smith JT, Gavey C, Sawyerr A, Pounder RE.

Academic Department of Medicine, Royal Free Hospital School of Medicine, London, UK.

Twenty-four-hour intragastric acidity and 24-h plasma gastrin concentration were measured on four occasions in six groups of eight healthy male subjects. Each group was studied before dosing, and on days 1, 15 and 29 of dosing with a standard regimen of an H2-receptor antagonist (cimetidine 800 mg nocte, nizatidine 300 mg nocte, famotidine 40 mg nocte, ranitidine 150 mg nocte, ranitidine 150 mg b.d., or ranitidine 300 mg nocte). On the first day of dosing, each regimen using an H2-antagonist caused a significant decrease of intragastric acidity and a significant rise of plasma gastrin concentration. Continued dosing with each H2-antagonist resulted in a significant attenuation of the effect on intragastric acidity, which was most noticeable overnight, but no significant change of plasma gastrin concentration. When grouped together, median integrated nocturnal acidity for the 48 subjects was 485, 35, 67 and 117 mmol.h/L for days 0, 1, 15 and 29, respectively, associated with a median nocturnal integrated plasma gastrin concentration of 46, 72, 79 and 73 pmol.h/L. The study demonstrates that a degree of tolerance develops during continued dosing with all available H2-receptor antagonists, and that this phenomenon occurs during sustained elevation of plasma gastrin concentration.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1983345&dopt=Abstract ranitidine






Methods Find Exp Clin Pharmacol. 1990 Nov;12(9):631-6.
Ranitidine alters antipyrine metabolism in control and phenobarbital-treated mice.

Espiritu-Quiza MF, Skinner MH, Blaschke TF.

Department of Medicine, Stanford University Medical Center, CA.

The effect of ranitidine on both induced (phenobarbital) and uninduced cytochrome P450 enzymes was investigated in mice using the [14C]-labeled antipyrine breath test. Ranitidine administration resulted in a decrease in the fraction of the administered dose of antipyrine exhaled as radiolabeled CO2 (CERAUC0-infinity) indicating inhibition in the demethylase pathway (Kdm), and resulted in induction of enzymes in the non-demethylase pathways (Kndm) as well. No change in antipyrine total elimination rate constant (Kel) was seen after ranitidine administration alone. Concurrent administration of ranitidine and phenobarbital resulted in an increase in the (Kel) but the change was less than that seen after phenobarbital alone. A reduction in CERAUC0-infinity was seen after the combination treatment while phenobarbital alone resulted in an increase in this parameter. Ranitidine, therefore, alters the pattern of antipyrine metabolism by inhibition of demethylase enzymes and induction of non-demethylase enzymes, the former activity being more pronounced in induced forms. Because of the simultaneous occurrence of both effects, no change in antipyrine half-life was noted with uninduced P450 isozymes.

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Rev Esp Enferm Dig. 1990 Dec;78(6):335-40.
[Effects of ranitidine on regenerating parietal cells. A stereologic study]

[Article in Spanish]

Torreblanca Lopez J, Ibanez Delgado F, Lopez-Campos JL, Moreno Onorato FJ.

Facultad de Biologia, Departamento de Biologia Celular, Hospital Infanta Elena, Sevilla, Universidad de Sevilla.

In this work, we have carried out a stereological and morphological study in order to verify the effects of Ranitidine on regenerating parietal cells. We have used a control group and operated or non-operated groups treated with 2, 10 and 50 mg/kg/day Ranitidine. In operated groups an ulcer was provoked by cauterization with a metallic plate in the gastric fundus. Groups treated with high doses of Ranitidine showed an increase in the connective tissue of the gastric mucosa. The stereological study in treated groups shows a decrease in the parietal volume density, and an increase in the cellular profile. Changes detected in the parietal volume density would originate a decrease in the production of CIH.

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Digestion. 1990;47 Suppl 1:64-8; discussion 76.
Efficacy and safety of omeprazole in the long-term treatment of peptic ulcer and reflux oesophagitis resistant to ranitidine.

Brunner GH, Lamberts R, Creutzfeldt W.

Department of Gastroenterology and Hepatology, Medical School, Hannover, FRG.

A total of 143 patients with peptic ulceration of the duodenum, stomach and oesophagus who did not respond to 3 or more months of high-dose treatment with ranitidine, 450 mg or more daily, were treated with oral omeprazole, 40 mg daily. In 94% of the patients, ulcers healed within 2-8 weeks. After healing, 133 patients underwent long-term maintenance treatment with omeprazole, 40 mg daily, for 1-5 years (continuing). During maintenance therapy with omeprazole, no endoscopically verified relapses occurred, and no drug-related adverse effects were seen. There were no significant changes in routine laboratory tests in any patient, including 27 with concomitant liver cirrhosis. Basal serum gastrin levels, which were already elevated by the previous high-dose ranitidine treatment, rose to 4 times normal levels after 4 months of treatment with omeprazole. Thereafter, no further increases in basal serum gastrin levels were observed, even after 5 years of administration. The volume density of argyrophilic cells in the oxyntic mucosa increased during omeprazole treatment, but no dysplasia of the gastric enterochromaffin-like cells was seen. In conclusion, omeprazole was highly effective in healing ranitidine-resistant peptic ulcers, and subsequent maintenance therapy with omeprazole, 40 mg daily, was found to be effective and safe over the period observed.

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Am J Hosp Pharm. 1990 Jul;47(7):1547-51.
Implementing therapeutic interchange of intravenous famotidine for cimetidine and ranitidine.

Oh T, Franko TG.

Department of Pharmacy, Mercy Hospital, Miami, FL 33133.

The steps taken to implement a therapeutic interchange program for i.v. histamine H2-receptor antagonists and to determine the potential cost savings are described. A literature review conducted by pharmacists at a 273-bed nonteaching community hospital showed that i.v. famotidine was as safe and effective as i.v. cimetidine or ranitidine and that it was feasible to add famotidine to total parenteral nutrition (TPN) solutions. Because of famotidine's cost advantage, it was proposed that i.v. famotidine be used in place of specific dosage regimens of i.v. ranitidine or cimetidine and in TPN solutions ordered for patients receiving concurrent H2-antagonist therapy. The approval of the hospital attorney and hospital gastroenterologists was secured, and a formal proposal was submitted. The pharmacy department distributed a memorandum describing the advantages of famotidine, conducted inservice education sessions, and sought the compliance of physicians by placing reminders on order forms and patient charts and by contacting physicians directly. The program was implemented in May 1989. During the first three months, only one physician insisted that patients receive i.v. ranitidine rather than famotidine. It was projected that the interchange of i.v. famotidine for cimetidine or ranitidine would result in a total savings of $37,565 during the first year due to reductions in the cost of drugs, supplies, and nursing labor. The acceptance of a therapeutic interchange program for H2 antagonists was excellent, and the projected savings are substantial.

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Am J Hosp Pharm. 1990 Jul;47(7):1574-9.
In vitro evaluation of the stability of ranitidine hydrochloride in total parenteral nutrient mixtures.

Williams MF, Hak LJ, Dukes G.

School of Pharmacy, University of North Carolina, Chapel Hill 27599-7360.

The stability of ranitidine hydrochloride in various total parenteral nutrient (TPN) solutions was studied, as well as the effect of ranitidine on the stability of lipid emulsion and amino acids in these solutions. Ranitidine hydrochloride 25 mg/mL was added to each of the following mixtures to make final concentrations of approximately 50 and 100 mg/L: (1) TPN solution containing 4.5% amino acids, 22.7% dextrose, and electrolytes; (2) 10% lipid emulsion; (3) TPN solution containing 3.7% amino acids, 18.5% dextrose, 3.7% lipid emulsion, and electrolytes (all-in-one mixture); and (4) 0.9% sodium chloride injection. Mixtures were tested at room temperature and at 4 degrees C and were either protected from or exposed to fluorescent light. Sampling was done at 0, 12, 24, 36, and 48 hours, and the ranitidine concentration was determined by high-performance liquid chromatography. Samples were also analyzed for lipid particle size distribution and for amino acid content. At 48 hours, the all-in-one mixtures retained 86.0% to 91.4% of the initial ranitidine concentration. With one exception (ranitidine 50 mg/L in 0.9% sodium chloride injection, stored at room temperature and not protected from light), all other solutions retained at least 90% of the initial concentration at 48 hours. No visible changes in color and minimal changes in pH values were noted. There were no important changes in lipid particle-size distribution; 96% of all particles counted from any mixture were smaller than 1.44 microns in diameter at 48 hours. Ranitidine did not have an effect on amino acid concentrations in these mixtures.(ABSTRACT TRUNCATED AT 250 WORDS)

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