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An immigrant from India presented with a three months history of fever, weight loss, cough and hepatomegaly which were rapidly diagnosed as miliary tuberculosis when gastric lavage revealed acid-fast bacilli. One day after antituberculous therapy was commenced, the patient developed adult respiratory distress syndrome and disseminated intravascular coagulation which were successfully treated by corticosteroids, fresh frozen plasma and mechanical ventilation. Ten other survivors of miliary tuberculosis and adult respiratory distress syndrome were reviewed and the association of adult respiratory distress syndrome with the antimicrobial therapy is discussed.
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To provide effective ranitidine therapy at the lowest possible cost to institutions and patients, the main study objectives were to develop a dosage intervention strategy for intermittent intravenous ranitidine and to document the resultant cost savings through cost-minimization analysis. During a 6-week baseline phase, a pharmacy resident prospectively monitored all patients in the intensive care unit receiving intravenous ranitidine and evaluated appropriateness of dose according to creatinine clearance. Staff pharmacists collected identical data during the 6-week intervention phase but also made recommendations for dosage interval adjustment. In patients with creatinine clearance rates less than 50 mL per minute, the mean number of doses per patient treatment-day was reduced from 2.33 +/- 0.81 during baseline phase to 1.56 +/- 0.70 during intervention phase (P < 0.001). The hospital cost per patient treatment-day was decreased by 33%, from $5.29 +/- 1.83 to $3.54 +/- 1.59 (P < 0.001). Thus a program of prospective monitoring and verbal interventions by pharmacists effectively reduced the number of inappropriate ranitidine doses and hospital cost.
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Pituitary adenylate cyclase activating polypeptide (PACAP) is present in gastric nerves, and PACAP receptors (PAC1) are found on gastric enterochromaffin-like (ECL) cells. Expression of PAC1 splice variants in purified ECL cells was determined by RT-PCR. PACAP effects on ECL cells were analyzed by video imaging of [Ca(2+)](i) and histamine release; its effects on gastric glands were examined by confocal microscopy of [Ca(2+)](i) in ECL and parietal cells. PACAP action on D cells was measured by [Ca(2+)](i) and radioimmunoassay. PACAP effects on acid secretion were determined in fistula rats with or without neutralizing anti-somatostatin antibodies. All splice variants of PAC1 were found, but vasoactive intestinal polypeptide (VIP) receptor (VPAC) products were absent. PACAP-27 and -38 dose-dependently raise [Ca(2+)](i) in ECL cells, and stimulated histamine release. VIP had a much lower affinity, which demonstrates the presence of PAC1 but not VPAC. PACAP elevated [Ca(2+)](i) in ECL and parietal cells of superfused gastric glands, but only the parietal cell signal was inhibited by ranitidine, showing the absence of PAC1 on parietal cells, and demonstrating functional coupling between the cell types. PACAP and VIP stimulated calcium signaling and somatostatin release from D cells with almost equal efficacy. Acid secretion was stimulated after intravenous injection of PACAP into rats treated with somatostatin antibody. PACAP is a candidate as a mediator of neural regulation of acid secretion.
Prolonged fasting and longer time between dosing and sampling reduced the plasma gastrin concentrations after omeprazole (80 mumol/kg x 2 for 14 days) treatment in male rats whereas the amounts of tissue gastrin were essentially unchanged during these initial experiments. After 28 days omeprazole (80 mumol/kg x 2) or ranitidine (375 mumol/kg x 4) that produced corresponding inhibition of acid secretion, increased the tissue gastrin content by 114 and 59%. A low dose of omeprazole (20 mumol/kg x 2) also raised the gastric gastrin content (41%), whereas no change was noted on treatment with a low dose of ranitidine (125 mumol x 4). Following recovery for 28 days no significant increases in gastrin were observed. 1, 3, 7, 14 or 28 days of treatment with omeprazole (80 mumol/kg x 2) gradually increased the gastric gastrin content being significantly raised already after 3 days. We conclude that a) measuring the tissue gastrin content may be the preferable method when changes in gastrin following long-term treatment with acid inhibiting drugs are to be determined, b) the amount of gastrin in the stomach increases rapidly following treatment with omeprazole and is approximately doubled following 28 days of treatment and c) after treatment for 28 days omeprazole was found to cause greater elevations in the tissue gastrin content than ranitidine despite similar degrees of basal acid inhibition.
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One hundred thirty-four patients were enrolled in the second-line study (56 men, 78 women; mean [SD] age, 51.1 [12.4] years; group 1A, 68 patients; group 1B, 66 patients). Subsequently, 41 (30.6%) of these patients were randomized to receive quadruple therapies. Using intent-to-treat (ITT) analysis, the eradication rates did not differ significantly (60.3% and 65.2% in groups 1A and 1B, respectively; 61.9% and 55.0% in groups 2A and 2B, respectively). Perprotocol eradication rates did not differ significantly (66.1% and 68.3% in groups 1A and 1B, respectively); however, the rates were significantly different in group 2A (66.7%) versus group 2B (55.5%) (P = 0.03).
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The alkylating agent cyclophosphamide (CP) is a prodrug requiring cytochrome P-450-mediated bioactivation to form the active 4-hydroxycyclophosphamide (4OHCP). Modifications in the rate of CP bioactivation may have implications for the effectiveness of CP therapy, especially in high-dose regimens. In this study, agents frequently co-administered with CP in high-dose chemotherapy regimens were tested for their possible inhibition of the bioactivation of CP in human liver microsomes. The Km and Vmax values for the conversion of CP to 4OHCP were 93 microM and 4.3 nmol/h.mg, respectively. No inhibition was observed for aciclovir, carboplatin, ciprofloxacine, granisetron, mesna, metoclopramide, ranitidine, roxitromycin and temazepam. Inhibition was observed for amphotericin B, dexamethasone, fluconazole, itraconazole, lorazepam, ondansetron and thiotepa, with IC50 values of 50, >100, >50, 5, 15, >100 and 1.25 microM, respectively. For all but thiotepa, these IC50 values were higher than the therapeutic drug levels and thus considered of no clinical relevance. We conclude that of the tested co-medicated agents, only thiotepa inhibited metabolism of CP to 4OHCP at clinically relevant concentrations, and may thereby influence therapeutic and toxic responses of CP therapy.
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After ethical approval, 90 patients scheduled for elective caesarean delivery were randomly allocated receive either ketorolac 15 mg i.v. bolus 20 min before induction, followed by an infusion of 7.5 mg/h (n=45), or saline placebo (n=45). Anaesthesia was maintained with 50% nitrous oxide in oxygen with 0.5% isoflurane. Haemodynamic variables, plasma cortisol concentrations, uterine relaxation, need for supplementary doses of oxytocin, peri-operative blood loss, haematocrit, Apgar scores at 1 and 5 min, postoperative pain scores at rest and movement, and tramadol consumption were recorded.
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In this experimental study both biological treatability of pharmaceuticals and their potential toxic effect in biological processes were evaluated. The pharmaceuticals were selected among those that are present at higher concentration in the Italian wastewater treatment plant effluents and widely used as antiulcer (ranitidine), beta-blocker (atenolol) and antibiotic (lincomycin). The present paper is the continuation of a work already presented, which used a synthetic wastewater fed to laboratory scale SBR (Sequencing Batch Reactor) operated with different sludge ages (8 and 14 days), different biochemical conditions (aerobic or anoxic-aerobic mode) and several influent drug concentrations (2, 3 and 5 mg/L). In this case a real municipal wastewater was used as influent to the SBR. In parallel, batch tests were conducted to determine the removal kinetics of drugs and nitrogen. Toxicity tests using a titrimetric biosensor to verify possible inhibition on microorganisms were also performed. Finally, the possible adsorption of the pharmaceuticals on activated sludge was evaluated. The drugs under investigation showed different behaviours in terms of both biodegradability and toxicity effect on nitrifiers. Ranitidine showed generally low removal efficiencies (17-26%) and a chronic inhibition on nitrification. Atenolol showed generally higher removal efficiencies than ranitidine, even if the fairly good efficiency obtained in the previous experimentation with synthetic wastewater (up to 90%) was not attained with real wastewater (36%). No inhibition on nitrification was observed on both acclimated and non acclimated microorganisms with a high nitrification activity, whilst it was present with activated sludge characterised by a lower nitrification activity. Consistently with his pharmaceutical properties, lincomycin showed significant inhibition on nitrification activity.
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After randomisation 430 patients with reflux oesophagitis (grade 2 or 3) were assigned to receive omeprazole 20 mg or ranitidine 150 b.i.d. for 8 weeks. Patients were given diary cards to assess their symptoms every day, and record every two weeks a life satisfaction index. Patients were seen after 4 and 8 weeks for symptoms assessment and repeat endoscopy at 8 weeks. The perspective of the analysis was that of the payer. The costs of medical care were based in French drug costs currently advertised, payment for physician and actual mean payment for upper GI endoscopy.
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Twenty-three patients with endoscopically proved recurrences after a primary operation for peptic ulcer disease performed in the course of a 7-year period are reviewed. The time elapsed between the operation and the recurrence ranged from 1 year to 17 years. The patients were mainly males. During the period studied 451 primary operations for peptic ulcer disease were performed in the same department. In 12 out of 23 recurrences the primary operation was also performed in the department of the author. In cases of small duodenal or stomal ulcer with two or more previous laparotomies transthoracic truncal vagotomy is preferred to any kind of abdominal intervention. A useful combination of duodenal exclusion, truncal vagotomy and a reflux-preventing type of GEA for recurrences after B 1 type partial gastrectomies was developed. In cases of late recurrences with mild symptoms the patients have to be first treated with H2-receptor blockers (cimetidine, ranitidine, etc.). The cases resistant to medical management have to be considered for surgery. Their results after a secondary surgical intervention proved to be fairly good, probably due to methods adequately selected for the given patient and to reflux-preventing GEA used in some cases. The consideration of an optimal individual solution for each patient is emphasized.
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Ranitidine produces a blood concentration curve with a pronounced secondary peak when administered orally and parenterally. A pharmacokinetic model is proposed to describe this reabsorption phenomenon. The choice of a discontinuous cyclic transfer was justified on the basis of physiological considerations and the good agreement with data from oral and intravenous administration. It is proposed that ranitidine accumulates mainly from the systemic circulation into a depot from which drug and bioreversible drug are spontaneously released in response to food intake. The evaluation of the extent of the first-pass effect and the evaluation of bioequivalency are complicated by the model-independent AUC approach because the area under the concentration versus time curve (AUC) is dependent on the extent of recycling and thus does not properly reflect the extent of primary absorption. By using intravenous administration as a reference dosage form and the integrated form of the regression equations to calculate the AUC values, the bioavailability of the oral dose was found to be 0.56, which corresponds well with the value of 0.58 obtained by linear-log-linear integration. The least-squares parameter estimate of the primary absorption is 0.43.
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This study is undertaken to evaluate the efficacy and safety of rioprostil, 300 micrograms, compared with ranitidine, 150 mg, when given twice daily for 4-6 weeks to patients with active, uncomplicated duodenal ulcer. The effects of each drug on ulcer healing are evaluated by endoscopy. Of a total of 355 patients who have entered this study, 319 are statistically evaluated for efficacy; 162 receive rioprostil and 157 receive ranitidine. After 4 weeks of treatment, 63% of the patients receiving rioprostil are endoscopically healed, compared with 72% of those receiving ranitidine. After 6 weeks of treatment, the cumulative healing rates are 86% and 93.5% respectively; this difference is statistically significant. Diarrhoea is the main adverse event, but is generally mild and self-limiting. These results indicate that rioprostil, 300 micrograms b.d., is a safe and effective treatment for duodenal ulcer, but is slightly less effective than ranitidine, 150 mg b.d.
Based on these studies, a total of 1540 patients were evaluated for histamine H2-receptor antagonists (verum n = 786, placebo n = 754) and 1235 patients for gastroprokinetics (verum n = 616, placebo n = 619). The probability for treatment success compared to placebo was 0.2026 (0.1261; 0.2791) for histamine H2-receptor antagonists and 0.4029 (0.3042; 0.5069) for gastroprokinetics.
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One hundred and twenty-seven patients with gastric or duodenal ulcer were included in this study. Patients were divided into three groups on the basis of antral H. pylori status and therapeutic modalities. The first group, 58 patients infected by H. pylori, was treated with metronidazole and tripotassium dicitrato bismuthate combined with ranitidine and mylanta. The second group, 40 patients also infected by H. Pylori, was treated with ranitidine and mylanta. The third group, 29 patients, free of H. pylori infection, was designed to evaluate the influence of H2-receptor antagonist on the change of gastrin. When ulcers were completely healed, changes of gastrin concentrations and H. pylori status were re-examined.
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The drug experiences of 1200 patients receiving i.v. histamine H2-receptor antagonists were studied. Forty hospitals in five southeastern states participated in a drug-use evaluation (DUE). In addition to supplying background information, a pharmacist at each hospital used a standardized form to perform a concurrent review of 30 consecutive adult patients who had been started on i.v. cimetidine, ranitidine, or famotidine. In addition to the patient's age and the prescriber's medical specialty, specific DUE criteria included the reason given in the medical record for use; dosage regimen and adjustments made on the basis of the patient's renal function; other GI drugs taken concurrently; pharmacist intervention; simultaneous use of oral medications; occurrence of adverse events; H2-antagonist use with specified drug products known to affect serum drug concentrations of one or both medications; and use of gastric pH monitoring. Therapy with i.v. H2 antagonists was usually started by internal medicine specialists or surgeons, and most of the evaluated patients received such therapy for prevention of stress-related mucosal damage. According to estimated creatinine clearance, 34% of patients were in need of dosage adjustments, but such adjustments were made in only 49% of these. Forty percent of patients began therapy while taking at least one medication orally, and almost one fourth of patients were receiving an additional drug for the treatment of an acid-peptic or related indication. The occurrence of adverse events was similar for the three H2 antagonists studied. The findings identify several problematic areas in the way H2 antagonists are used in clinical practice.
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Upper respiratory tract infections and acid peptic disease were the common illnesses. Generic prescribing and use of essential drugs were low. Some of the drug combinations being used were irrational. Prescriber education may be helpful in encouraging rational prescribing.
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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.
The effect of N-[2-[[[5-[(dimethylamino)methyl]-2-furanyl]methyl]thio]ethyl]-N'-methyl-2-nitro-1,1-ethenediamine hydrochloride ranitidine and NaCl-solution in different dosages on gastric mucosal potential difference during endoscopy was examined in 92 volunteers. After bolus injections of 10-40 mg ranitidine there was a significant maximum increase in potential difference taken from different parts of the stomach and from the gastric juice. No changes were seen in the duodenal mucosal. Following bolus injections of 2.5 and 5 mg ranitidine there was a lower increase in potential difference in the gastric juice. These dosages seem to be insufficient to induce a maximum increase of potential difference in each individual.
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These results suggest that cimetidine increased dofetilide exposure by inhibiting renal tubular dofetilide secretion, whereas ranitidine did not. This effect is not an H2-receptor antagonist class effect but is specific to cimetidine. If therapy with an H2-receptor antagonist is required, it is recommended that cimetidine at all doses be avoided; since ranitidine has no effect on dofetilide pharmacokinetics or prolongation of the QTc interval, it can be seen as a suitable alternative.
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Angiotensin-converting enzyme (ACE) inhibitor-induced angioedema is a rare, albeit serious emergency that can result in airway compromise and potentially death if not treated promptly. Currently, there are no agents approved by the Food and Drug Administration to target ACE inhibitor angioedema and to prevent intubation. C1 inhibitors are approved for hereditary angioedema but may show promise in alleviating inflammation associated with ACE inhibitor angioedema.
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The response of mouse peritoneal macrophages to Escherichia coli lipopolysaccharide (LPS) resulted in induction of histidine decarboxylase (HDC) and, consequently, of histamine production. Concanavalin A had no effect on the reactions. Alpha-fluoromethylhistidine, a suicide inhibitor of HDC, attenuated, in a dose-dependent manner, both spontaneous and LPS-stimulated IL-1 synthesis by macrophages. IL-1 production was significantly blocked by either an H1 anti-histamine, diphenhydramine, or H2 anti-histamine ranitidine, in the absence of any exogenous histamine. Addition of exogenous histamine accentuated the IL-1 production by macrophages as a function of its dose. These results suggest that IL-1 production by mouse peritoneal macrophages is regulated by histamine synthesized in the system per se and that the effect of histamine is dependent on both H1 and H2 histamine receptors located on the surface of the cells.
The sensitivity of histamine H2 receptors of the gastric mucosa after one month treatment with ranitidine, administered daily (5 mg/kg i.m.), was checked in 5 conscious cats provided with gastric fistula. Basal acid secretion as well as the acid response to the H2 agonist dimaprit (60 micrograms/kg/hr) were studied before and at different periods after cessation of ranitidine treatment (1, 3, 7 and 14 days). Control experiments were carried out in 5 gastric fistula cats which received daily physiological saline for one month. Basal acid secretion in treated animals increased significantly (p less than 0.05) from 0.04 +/- 0.002 to 0.24 +/- 0.05 mEq H+/10 min. Also the response to dimaprit increased significantly (p less than 0.05) from 0.49 +/- 0.08 to 0.86 +/- 0.12 mEq H+/10 min. Seven days after cessation of treatment, both basal and stimulated secretion returned to pretreatment levels. In control cats no significant difference was noticed in basal and stimulated secretion at the beginning and at the end of the study.
When antacid medication impairs the gastric digestion, IgE synthesis toward novel dietary proteins is promoted, leading to food allergy.
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These results suggest that clarithromycin plus high-dose ranitidine is a combination which achieves reasonably high H. pylori eradication rates. However, treatment failure inevitably leads to clarithromycin resistance. The improvement of non-ulcer dyspepsia symptoms during acute therapy is independent of H. pylori eradication. Long-term benefit of H. pylori eradication with respect to the symptoms of functional dyspepsia was not observed.
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The effects of thioperamide, an H3 antagonist, and histamine H1 and H2 antagonists (s.c.) on morphine (s.c. or i.c.v.)- and U-50,488H (i.c.v.)-induced antinociception in male ddY mice were examined using the hot-plate (55 degrees C) test. Thioperamide significantly inhibited morphine-induced antinociception, but not U-50,488H-induced antinociception. The suppressive effect of thioperamide on morphine-induced antinociception was reversed by the H1 antagonist pyrilamine, but not by the H2 antagonist zolantidine. On the other hand, pyrilamine significantly potentiated the antinociception induced by morphine, but not that induced by U-50,488H. Zolantidine significantly inhibited morphine-induced antinociception in a dose-dependent manner, but not U-50,488H-induced antinociception. Both astemizole, an H1 antagonist, and ranitidine, an H2 antagonist, which are known to barely cross the blood brain barrier, did not affect morphine-induced antinociception. These results suggest that morphine-induced antinociception may be potentiated by activation of H2 receptors and suppressed by activation of H1 receptors in the brain. Furthermore, neuronal histamine release induced by thioperamide may suppress morphine-induced antinociception through H1 receptors.