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We used multivariate analysis of data from three large similar trials to identify factors associated with endoscopic lesions and healing. We compared the effectiveness of omeprazole 20 mg and 40 mg daily, misoprostol 200 micro g four times daily, and ranitidine 150 mg twice daily in healing ulcers and erosions at different sites and in patients who were Helicobacter pylori positive and negative.
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The optimal strategy for the eradication of Helicobacter pylori has yet to be determined. This paper summarizes some of the latest treatment strategies for eradicating H. pylori infection.
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Postoperative ranitidine plasma concentrations showed only minor differences from preoperative levels, with slightly higher maximum concentrations occurring sooner. The mean area under the curve was on the average 30% higher than preoperatively. All parameters, however, were similar to those in control subjects.
Mongrel pigs (n = 24) were anesthetized with fentanyl, injured by a 10 kg steel bar dropped from a height of 1 m onto the fleshy portion of the posterior thigh, and then 35% of their blood volume was drained through the arterial catheter. All the shed blood plus two times the hemorrhage volume as lactated Ringer's solution was infused after a 1-hour shock period. Either vehicle or ranitidine (1.5 mg/kg) was intravenously administered at the time of resuscitation and every 12 hours thereafter in a blinded fashion. After 72 hours a septic challenge was administered (15 micrograms/kg Escherichia coli lipopolysaccharide [LPS] x 30 min). Serial gastroscopy, gastric pH, hemodynamics, leukocyte counts, cortisol, and tumor necrosis factor were recorded for 180 minutes after LPS.
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Patients with insulin-dependent diabetes mellitus (IDDM) are often affected by chronic infections; antibiotic absorption, however, may be influenced by the disease. H. pylori eradication appears to be reduced in IDDM patients. The aim of the study was to evaluate the efficacy of the most common H. pylori eradication regimens in a population of IDDM-infected patients.
The diverse physiological functions of histamine are mediated through distinct histamine receptors. In this study we investigated the role of H2R and H4R in the effects of histamine on the production of reactive oxygen species by phagocytes in whole blood.
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This study tested the hypothesis that cimetidine and ranitidine, the new H2-antagonist, may influence the pharmacokinetics of theophylline administered i.v. at two different doses (3.4 and 6.5 mg/kg body wt.). Twenty hospitalized patients with chronic obstructive lung disease (COLD) and peptic ulcer were administered cimetidine or ranitidine orally for 8 days at the routine doses of 2 X 400 mg/day and 2 X 150 mg/day, respectively. Blood samples were collected over a 10-h period before and after H2-antagonist therapy. Cimetidine significantly reduced theophylline clearance, but increased its half-life and the area under the curve (AUC) (p less than 0.001). Ranitidine, on the contrary, did not show any interaction with these pharmacokinetic parameters. Neither of the H2-blocking agents modified the volume of distribution. Furthermore, the delay in theophylline elimination due to cimetidine was more evident at the higher dose of the xanthic drug; this effect induced remarkable changes in plasma theophylline concentrations. Consequently, pharmacokinetic interaction between cimetidine and theophylline may produce serious clinical problems in the management of patients treated with both drugs concurrently, problems which do not arise with ranitidine.
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The influence of ranitidine on morphine metabolism, with special emphasise on the ratio between morphine-3-glucuronide and morphine-6-glucuronide was studied in isolated guinea pig hepatocytes. Ranitidine reduced the Kel of morphine dose-dependently with a maximum effect of 50%, and increased the relative concentration of morphine-6-glucuronide to morphine-3-glucuronide. These effects could be due to a direct or indirect effect on the conjugation enzymes involved, or an effect on the transport of morphine or glucuronides across cell membranes. The latter explanation was rejected on the basis of the observation that the ratios between intra- and extracellular concentrations of morphine, morphine-3-glucuronide and morphine-6-glucuronide were not influenced by ranitidine. Increasing concentrations of ranitidine gradually decreased the morphine-3-glucuronide/morphine-6-glucuronide ratio by up to 21%. This could stem from interference of energy or co-substrate supply, or through direct effects on the different UDPGTases involved. The observation that the present effect on morphine glucuronidation was the opposite of that observed when administering a known co-substrate (UDPGA) depletor, indicated that in all probability the effect of ranitidine was a direct inhibition on the uridine 5'-diphosphate glucuronyltransferases involved, with a more pronounced effect for the isoenzymes responsible for the 3'-glucuronidation.
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Using ambulatory ph-metry, intragastric acidity was measured over three separate 24 hour periods in each of 12 healthy volunteers receiving either (a) placebo (1800 h and 2200 h), (b) 300 mg ranitidine (1800 h) and placebo (2200 h), or (c) placebo (1800 h) and 300 mg ranitidine (2200 h). Ranitidine was significantly more effective in decreasing 24 h median intragastric acidity when the drug was administered at 1800 h rather than at 2200 h. Median pH (and interquartile range) was 1.45 (1.4-1.7) on placebo, 2.55 (2.05-3.2) on ranitidine given at 2200 h and 3.35 (2.5-3.85) on ranitidine given at 1800 h (p less than 0.004). The total duration of highly acidic electrode readings (pH less than 1.5) over a 24 h period was reduced significantly by administering the H2-receptor antagonist at 1800 h compared with the later administration. It is suggested that treatment of duodenal ulcers by single administration of ranitidine in the early evening should be evaluated by clinical trial.
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A total of 41 mice were allocated into six groups consisted of 7 mice each. Groups 1 (normal control) and 2 (ulcer control) received distilled water at a dose of 10 ml/kg, groups 3, 4 and 5 were given NAC at doses 100, 300 and 500 mg/kg, respectively, and the 6(th) group received ranitidine (50 mg/kg). All drugs administered orally once daily for 7 days, on the 8(th) day absolute ethanol (7 ml/kg) was administrated orally to all mice to induce the acute ulcer except normal control group. Then 3 h after, all animals were sacrificed then consequently the stomachs were excised for examination.
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A rapid, reliable and sensitive assay for routine determination of ajmaline in plasma by high-performance liquid chromatography with fluorimetric detection is presented. A low limit of detection in plasma (less than 1 ng/ml ajmaline) could be achieved by the extraction of plasma samples and the use of fluorimetric detection. Deproteinization of the plasma sample instead of extraction, or the use of an ultraviolet detector, yielded a higher limit of detection (less than 50 ng/ml). Two different eluents were studied. Eluent 1 allowed clear separation of ajmaline from isoajmaline and sandwicine, but did not separate isoajamaline from sandwicine. With eluent 2, separation of isoajmaline and sandwicine was achieved, but separation of ajmaline from sandwicine was less optimal than with eluent 1. Therefore, eluent 1 was used for further clinical studies. No interference was observed from therapeutic doses of other commonly co-administered drugs, such as acetylsalicylic acid, digoxin, digitoxin, ranitidine, dopamine, dobutamine, furosemide, captopril or glycerol trinitrate. In addition, the chemical stability of ajmaline and a possible rearrangement of ajmaline to its stereoisomers isoajmaline and sandwicine was studied in vivo and in vitro. Ajmaline proved to be unusually stable under both in vivo and in vitro conditions.
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The MediPlus UK database was used to identify all health care resources consumed by patients in the three treatment groups during their first six months of treatment. Patients with more complicated GORD, as indicated by initial referral to a specialist or outpatient hospital visit (< 13%), were excluded from the analysis.
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We have investigated the possibility of measuring acid secretion from human gastric mucosa in vitro as a potential pharmacological preparation. We used open-ended 10 microns-tip, lix-based glass microelectrodes to measure the pH of the mucus layer of gastric biopsies superfused with a HEPES buffered solution in an organ bath. With no drugs added the pH of the mucus layer of biopsies from the body of the stomach stayed constant but the pH of antral biopsies fell slightly by a median of 0.12 pH units over 80 min (P < 0.05). Stimulation of the biopsies with 1-100 microM histamine produced a dose-dependent decrease in pH which was significantly greater in biopsies from the gastric body than from the antrum. 500 pM pentagastrin produced a median fall in pH of 1.20 (P < 0.01) which was prevented by the prior addition of 100 microM omeprazole or 10 microM ranitidine. Omeprazole or ranitidine alone produced slight rises in the median pH of 0.47 (P < 0.05) and 0.26 (P < 0.05) units respectively. Those biopsies which were infected with Helicobacter pylori had a slightly elevated initial pH of about 0.2 of a pH unit (P < 0.05). This novel system provides a means to study human gastric acid secretion in vitro and may be valuable in the testing of new drugs on the stomach.
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The patient is a 22-year-old male with the evaluation of osteosarcoma, T1Gr2NxM0. He received neoadjuvant chemotherapy and later underwent a right above the knee amputation without complication. He was then scheduled to receive adjuvant chemotherapy with high-dose MTX, 12 g/m2 body surface area, followed by leucovorin rescue and ifosfamide. He had an immediate hypersensitivity reaction during the initiation of the MTX infusion with diffuse urticaria, facial swelling, cough, and chest tightness. The infusion was terminated and his symptoms abated. He was later skin tested to confirm allergy to MTX. In order for him to receive the needed chemotherapy, we developed a desensitization protocol that was administered in the intensive care unit. Before the infusion he was pretreated with ranitidine, cetirizine, hydroxyzine, montelukast, and prednisone. He underwent the desensitization without incident on repeated infusions. Serum tryptase levels drawn during the infusions were low, signifying controlled mast cell degranulation.
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Gastroesophageal reflux disease (GERD) is a common condition, and acid-suppressing agents are the mainstays of treatment. For the acute medical management of GERD, two different strategies can be proposed: either the most effective therapy, i.e., proton-pump inhibitors (PPIs), can be given first, or histamine H2-receptor antagonists (H2RAs) can be attempted first (the "step-up" approach).
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To assess the effect of ranitidine on ethanol absorption after ethanol 0.5 g/kg is given in three single doses of 0.167 g/kg to simulate normal social drinking.
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Omeprazole was more effective than ranitidine in healing gastric squamous ulcers in Thoroughbreds in race training. Improvement was detected by 14 days and persisted in most of the group 2 horses for at least 28 days after omeprazole treatment was discontinued.
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Twelve volunteers underwent overnight intragastric pH monitoring after 7 days of treatment with omeprazole, 20 mg twice daily, followed by different treatment supplements at bedtime: placebo; additional omeprazole, 20 mg; ranitidine, 150 mg; and ranitidine, 300 mg.
We obtained data in 186 subjects: 95 healthy controls and 91 GA-inhibitor users (47 on ranitidine and 44 on omeprazole). The 2 groups were comparable for age, gender, weight, length, and incidence of acute gastroenteritis and pneumonia in the 4 months before enrollment. Rate of subjects presenting with acute gastroenteritis and community-acquired pneumonia was significantly increased in patients treated with GA inhibitors compared with healthy controls during the 4-month follow-up period. In the GA inhibitor-treated group, the rate of subjects presenting with acute gastroenteritis and community-acquired pneumonia was increased when comparing the 4 months before and after enrollment. No differences were observed between H2 blocker and PPI users in acute gastroenteritis and pneumonia incidence in the previous 4 months and during the follow-up period. On the contrary, in healthy controls, the incidence of acute gastroenteritis and pneumonia remained stable.
If dyspepsia persists long term, H. pylori eradication treatment may not be the least-cost option for patients with duodenal ulcer.
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We report a case of a prenatal esophagitis and gastritis revealed at 33 weeks of gestation by the presence of bloody amniotic fluid and dilated intestinal loops that was confirmed by endoscopy at birth. Complete recovery occurred after treatment with ranitidine.
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To test the potential of distance running to induce reflux in healthy subjects and the ability of ranitidine to decrease esophageal acid exposure.
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During a controlled, randomized, double blind study, 30 patients of a neurosurgical intensive care unit were treated with ranitidin and placebo (group 1) or ranitidin and pirenzepin (group 2). No significant difference in the effectivity of both methods was established, presumably due to the small number of cases. The pH values of group 2 lay in the median above 3.5, whereby the difference only became statistically significant after a seven-day period of therapy. In how far the increase of the pH value represents the only factor of a stress ulcer prophylaxis requires further investigation, particularly in connection with pulmonary risks caused by this.
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Fifty-eight patients with H. pylori-associated gastritis were treated with a combination regimen of acid inhibitory therapy and antibiotics for 14 days. The levels and isoforms of MMP-2 and MMP-9 were measured by semiquantitative gelatin-zymography, bioactivity assay and enzyme-linked immunosorbent assay in gastric mucosal biopsy homogenates.
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Ranitidine is used to treat symptomatic oesophageal reflux; its effect is probably to a great extent due to reduced gastric secretion. Whether it also affects oesophageal motility is a matter of controversy. In a randomized double-blind study oesophageal motility was recorded in 21 healthy individuals after 3 doses of 150 mg ranitidine or placebo given over 36 h. Ranitidine increased the pressure in the lower oesophageal sphincter from 14 to 18 mmHg (p = 0.05) but otherwise did not influence oesophageal motility.
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Fifteen patients with both nonallergic asthma and symptomatic gastroesophageal reflux were studied before and after an eight-week period of vigorous antireflux therapy, which included ranitidine hydrochloride, 150 mg twice a day. Pulmonary and esophageal symptoms were recorded on daily diary cards. Therapy was associated with prompt amelioration of reflux symptoms and with a less dramatic and more delayed improvement in pulmonary symptoms. Objectively, esophageal erosions healed completely in eight of the ten patients who had them at the beginning of the trial, and pulmonary function measurements improved significantly. Intraesophageal infusions of physiologic saline and 0.1N hydrochloric acid in patients and healthy controls did not significantly alter pulmonary function, as measured by standard spirometry. There is a subset of patients in whom bronchoconstriction is triggered by gastroesophageal reflux. Treatment of reflux in such patients may improve their asthma.
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Both ranitidine and metoclopramide produce neuropsychiatric side effects. Concomitant use of these drugs preoperatively may produce adverse behavioral and emotional changes. Therefore, in 123 unpremedicated patients undergoing tubal occlusion, behavior, cognitive function, and affect were studied before and after a 2-min intravenous injection of placebo (n = 30), ranitidine 50 mg (n = 32), metoclopramide 10 mg (n = 30), or both ranitidine 50 mg and metoclopramide 10 mg (n = 31). Cognitive function was evaluated by the responses to 11 statements devised to assess attitude toward anesthesia and surgery. Affect was assessed by the word chosen out of 11 word-pairs as best describing the feelings at the time. After ranitidine injection, one patient seemed restless and five seemed drowsy. The changes were associated with subjective feelings of agitation (P < 0.05) and restlessness (P < 0.05). After metoclopramide injection, 6 (20%) developed akathisia, 13 (43.3%) seemed restless, and 8 (26.7%) seemed drowsy. The changes were associated with subjective sensation of jumpiness (P < 0.01) and discomfort (P < 0.05). When both ranitidine and metoclopramide were injected, 10 (32.3%) developed akathisia, 4 (12.4%) seemed restless, and 11 (35.5%) seemed drowsy. The changes were associated with subjective feelings of agitation (P < 0.05), jumpiness (P < 0.05), restlessness (P < 0.01), and upset (P < 0.05). Akathisia, a side effect of metoclopramide, seemed to be more prominent when ranitidine was added.
Patients with advanced solid tumors were treated with CBP501 alone (D1/D8/D15, q4w, from 0.9 mg/m(2)), or with cisplatin (both on D1, q3w, from 3.6 mg/m(2) CBP501, 50 mg/m(2) cisplatin). Dose escalation proceeded if dose-limiting toxicity (DLT) was observed in 1 or less of 3 to 6 patients; CBP501 dose increments were implemented according to the incidence of toxicity. MTD was determined from DLTs occurring during the first two cycles.
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Forty-one patients with advanced solid tumors received single-dose LY monotherapy lead-in and 37 patients received LY (10-120 mg) plus pemetrexed/carboplatin (500 mg/m(2) and 5-6 AUC, respectively) across 8 dose levels every 21 days. Primary objective was maximum tolerated dose (MTD) determination; secondary endpoints included safety, antitumor activity, pharmacokinetics, and beta-catenin pharmacodynamics.
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The proportions of patients considered to be in remission (intention to treat) at the end of treatment with placebo, ranitidine 150 mg, omeprazole 10 mg, and omeprazole 20 mg were, respectively, 42%, 50%, 48%, and 59% in the H pylori positive group and 66%, 73%, 64%, and 71% in the H pylori negative group. In H pylori positive patients, the therapeutic gain over placebo was significant for omeprazole 20 mg (17.6%, 95% confidence intervals (CI) 4.2-31.0; p<0.014 using the Bonferroni-adjusted p level of 0.017) but not for omeprazole 10 mg (6.8%, 95% CI -6.7-20.4) or ranitidine 150 mg (8.9%, 95% CI -4.2-21. 9). There was no significant therapeutic gain from active treatment over placebo in H pylori negative patients. Complete disappearance of symptoms and improvement in quality of life also occurred most frequently with omeprazole 20 mg and was significant in both H pylori positive and H pylori negative groups. The six month relapse rate of symptoms requiring treatment was low (<20%) in all groups.