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Comparison of the total effective rate on gastroscopic figure in the treated group and the control group (86.7% vs 80.0%) showed insignificant difference, but the cure rate and markedly effective rate in the former (50.0% and 20.0%) was higher than that in the latter (40.0% and 15.0%) respectively. Comparison of the total effective rate on TCM syndrome in the treated group and in the control group (96.7% vs 70.0%) showed insignificant difference, but the cure rate and markedly effective rate in the former (63.3% and 23.3%) was higher than that in the latter (50.0% and 20.0%) respectively. Serum levels of CD3+, CD4+, CD8+ got restored to normal range in the treated group after treatment but it was not so in the control group. IL-8 level in gastric mucosa was improved in both groups but the improvement in the treated group was better.
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One hundred sixty rats were randomly divided into 4 groups (n = 10) as follows: the model group (MP group), the control group (CP group), the ranitidine group (RP group) and the XTTF granule group (XP group). Rats in the MP group received no drugs, rats in the CP group received 0.2 mL of a 0.9% sodium chloride solution via oral gavage, and rats in the RP and XP groups received the same volume of ranitidine (50 mg/kg) or XTTF granule (4.9 g/kg). The cold-restraint stress model was applied to induce stress ulcers after 7 consecutive days of drug administration. Afterwards, rats were sacrificed at 0, 3, 6 and 24 h. Gastric pH was measured by a precise pH meter; gastric emptying rate (GER) was measured by using a methylcellulose test meal; myeloperoxidase activity (MPO), macrophage migration inhibitory factor (MIF), proliferating cell nuclear antigen (PCNA), and heat shock protein 70 (HSP70) were measured by immunohistochemical staining; and mucosal cell apoptosis was measured by transferase dUTP nick end labeling.
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Evidence documenting the safety of acid-suppressing drugs in pregnancy is very limited. The authors assessed the prevalence of congenital malformations in first trimester-exposed pregnancies to cimetidine, omeprazole, and ranitidine and compared it with nonexposed pregnancies between 1991 and 1996. Two different sources were used, the United Kingdom General Practice Research Database and the Italian Friuli-Venezia Giulia Health Database. The final study cohort included 1,179 pregnancies from the United Kingdom and 1,057 from Italy. Abortions or ectopic pregnancies were not included. There were 20 stillbirths and 2,261 live-born babies in both cohorts combined, with 100 offspring identified with a malformation. The overall malformation rate was 4.4%. The relative risks for nongenetic congenital malformations associated with the use of cimetidine, omeprazole, and ranitidine were 1.2 (95% confidence interval (CI): 0.6, 2.3), 0.9 (95% CI: 0.3, 2.2), and 1.4 (95% CI: 0.8, 2.4), respectively, compared with the nonexposed. No specific grouping in the distribution of malformations was observed in any of the three exposed groups. Moreover, no relation was found between drug exposure and preterm delivery or growth retardation. These findings suggest that the use of acid-suppressing drugs during the first trimester of pregnancy is not associated with a major teratogenic risk.
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The inducible isoform of nitric oxide synthase (iNOS) may be involved in the mucosal injury associated with inflammatory bowel disease (IBD). In contrast with iNOS, the inducible heme oxygenase 1 (HO-1) is considered to act as a protective antioxidant system.
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A novel pituitary peptide, designated 7B2, was shown to be present in the adrenal gland. 7B2-like immunoreactivity was mainly localized in the adrenal medulla, similarly to NPY and VIP. In order to elucidate the neural and humoral regulation of adrenal 7B2, NPY and VIP content, Wister rats were treated with reserpine (RES), ranitidine (RANT) or chlorpheniramine maleate (CPhM) for 7-10 days. The thyroid hormone excess and deficient states were experimentally produced with thyroxine (T4) treatment for 2 weeks, methylmercaptoimidazole (MMI) for 4 weeks, or a thyroidectomized state (Tx) for 4 weeks. Orchiectomy or neonatal monosodium glutamate (MSG) treatment was also done. 7B2, NPY and VIP contents were measured by specific radioimmunoassays. RES and RANT treatments caused significant 7B2 reduction (p less than 0.01) and adrenal NPY was significantly decreased by RES (p less than 0.05), while CPhM induced a VIP decreased (p less than 0.05). Orchiectomy did not affect the peptides concentrations, though MSG treatment did cause a reverse change in VIP and NPY. Although T4 administration did not cause any significant change, MMI treatment and Tx induced significant increase (p less than 0.05 or p less than 0.01) in these peptides. Gel or high performance liquid chromatographic analysis revealed the majority of each immunoreactivity coeluted with each standard. These results suggested that adrenal NPY seemed to be coregulated with catecholamine, while VIP was mainly affected by histaminergic control. Furthermore 7B2 might be modulated by both catecholaminergic and histaminergic nervous control. Thyroid hormone deficiency may also affect the amount of these peptides.
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To verify if cimetidine, ranitidine, and famotidine, when inoculated by ip route in mice, do enhance macrophage activation and whether or not such activation is altered with prior use of sodium thioglycolate. KIND OF STUDY: Experimental.
A significant percentage of patients taking nonsteroidal anti-inflammatory drugs (NSAIDs) experience some type of adverse gastrointestinal symptoms, lesions of the gastroduodenal tract being clinically the most relevant. NSAIDs cause gastrointestinal damage by 2 independent mechanisms: a topical effect, which is pH and pKa related, and a systemic effect mediated by cyclooxygenase (COX) inhibition with a reduction in prostaglandin synthesis. Using endoscopy, gastroduodenal lesions identified include subepithelial haemorrhages, erosions and ulcers. The prevalence of ulceration in NSAID users has been reported as being between 14 and 31% with a 2-fold higher frequency of gastric ulcers compared with duodenal ulcers. Among the strategies used to decrease the risk of ulcer development are: (i) the use of analgesics other than NSAIDs; (ii) use of the lowest possible dosage of NSAID; (iii) the use of a COX-2 selective NSAID; (iv) the use of low doses of corticosteroids instead of NSAIDs; (v) avoidance of concomitant use of NSAIDs and corticosteroids; and (vi) use of preventive therapy. In an attempt to reduce the incidence of NSAID-induced gastrointestinal lesions, the following approaches have been proposed: (i) use of the prostaglandin analogue misoprostol, which is an antiulcer drug which has been proven to be as effective in the prevention of NSAID-induced gastric and duodenal ulcers as in the reduction of serious upper gastrointestinal complications; (ii) histamine H2 receptor antagonists (H2 antagonists), e.g. ranitidine, cimetidine and famotidine, which are useful in the prevention of NSAID-induced duodenal ulcers during long term treatment, but not in the prevention of NSAID-induced gastric ulcers; (iii) proton pump inhibitors, e.g omeprazole, and pantoprazole, whose efficacy in preventing NSAID-associated ulcers has been recently demonstrated; and (iv) barrier agents, e.g. sucralfate, which cannot be recommended as prophylactic agents to prevent NSAID-induced gastropathy. The first step in the treatment of NSAID-associated ulcers lies in a reduction in the dosage of the NSAID or discontinuation of the drug. If NSAID treatment cannot be withdrawn, a proton pump inhibitor appears to be the most effective treatment in healing ulcers, accelerating the slow healing observed with H2 antagonists.
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The OMNIUM and ASTRONAUT trials may have provided an unrealistic sense of security regarding the effectiveness of omeprazole for protection against ulcer recurrence in chronic NSAID users.
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The stability of ranitidine hydrochloride after being mixed with commonly used i.v. beta-lactam antibiotics and administered by simulated Y-site injection was studied. Solutions of ranitidine 1 mg/mL (as the hydrochloride salt), aztreonam 16.7 mg/mL, ceftazidime 20 mg/mL (with sodium carbonate), and piperacillin 30 mg/mL (as the sodium salt) were prepared by reconstitution in i.v. mini-bags. To simulate Y-site injection, 2 mL of ranitidine hydrochloride was mixed with 2 mL of each antibiotic in glass test tubes. These admixtures were prepared in triplicate and stored at room temperature under fluorescent light. Concentrations of each drug in each admixture were determined by stability-indicating high-performance liquid chromatography immediately and after one, two, and four hours. Aztreonam, ceftazidime, and piperacillin each retained more than 95% of the original concentration for at least four hours when mixed 1:1 with ranitidine. Ranitidine retained more than 90% of its original concentration for at least four hours when combined with each of the other drugs. Ranitidine 1 mg/mL (as the hydrochloride salt) and aztreonam 16.7 mg/mL, ceftazidime 20 mg/mL (with sodium carbonate), or piperacillin 30 mg/mL (as the sodium salt) were stable for at least four hours during simulated Y-site administration.
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To compare the prevalence of drug prescriptions for elderly inpatients, with those for non-elderly inpatients, in order to assess age-related differences in the number of prescribed drugs, drug choices and prescribed doses, and to evaluate the prescription appropriateness for the elderly patients.
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The results of the treatment with the Bulgarian drug biotidin of 30 patients with endoscopically proved duodenal peptic ulcer are presented. The drug was given in a dose of 150 mg twice daily in the course of 20 days. The pain ceased up to the third day in 93.3% of the patients treated and the dyspeptic complaints vanished up to the second day of treatment in 96.6% of the patients. Following the treatment a statistically significant lowering of the indices of gastric secretion (V abd V1) and acid production (BAO, MAO, PAO) was found compared to those before the treatment. Endoscopically full epithelialization was found in 63.3% of the patient, in 33.3% of the patients the size of the ulcer diminished and in only 3.4% of the patients there was no change of the ulcer size. The ulcer epithelialization was related to the initial ulcer size. The results achieved do not differ substantially from those achieved with the English drug Zantac. In the course of treatment with biotidin no side effects were observed and no changes of the basic biochemical indices were found.
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Degranulating mast cells are increased in the airway smooth muscle (ASM) of asthmatics, where they may influence ASM function. The aim of the present study was to determine whether histamine and tryptase modulate ASM cell granulocyte-macrophage colony-stimulating factor (GM-CSF) and RANTES (regulated on activation, normal T-cell expressed and secreted) release and also to examine which receptors are involved in this release. Confluent, quiescent ASM cells from asthmatic and nonasthmatic donors were treated with histamine (1 microM-100 microM) with and without histamine receptor antagonist pre-treatment, or the protease-activated receptor (PAR)-2 agonists tryptase (0.5-5 nM) and SLIGKV (100 and 400 microM). The cells were then stimulated with interleukin (IL)-1beta and/or tumour necrosis factor (TNF)-alpha (10 ng.mL(-1)) or left unstimulated for 24 h. Release of GM-CSF and RANTES was determined by ELISA and prostaglandin (PG)E(2) measured by enzyme immunoassay. Neither histamine nor tryptase induced ASM GM-CSF or RANTES secretion. However, histamine increased IL-1beta-induced GM-CSF release and markedly reduced TNF-alpha-induced RANTES release by both asthmatic and nonasthmatic cells to a similar extent, but did not modulate PGE(2) release. All changes involved activation of the histamine H1 receptor as they were partially or fully blocked by chlorpheniramine, but not ranitidine. Tryptase, via its proteolytic activity, also potentiated GM-CSF, but not RANTES, release from asthmatic and nonasthmatic ASM cells induced by both cytokines. PAR-2 involvement in the tryptase potentiation was unlikely because SLIGKV had no effect. In conclusion, mast cells, through histamine and tryptase, may locally modulate airway smooth muscle-induced inflammation in asthma.
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No significant differences in gastric emptying were noted between the four solutions. In contrast, the presence of 1, 2.5, and 5 g PEG 400 reduced the mean small intestinal transit times of the solutions by 9, 20, and 23%, respectively, against the control. In terms of drug absorption, the mean cumulative amount of ranitidine excreted was reduced by 38% in the presence of both 2.5 and 5 g PEG 400, although it was significantly increased by 41% in the presence of 1 g PEG 400.
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We report a case of severe dyskinetic syndrome, consisting of intense myoclonia movements, associated with choreiform activity involving the face and upper extremities. The abnormal movements occurred in a patient with confusion and visual hallucinations. This syndrome had an abrupt onset in a patient recovering from coronary artery bypass surgery complicated by an early post-operative cardiac arrest and acute renal failure. Dyskinesia appeared several days after intravenous administration of ranitidine for stress ulcer prophylaxis. Several etiologies were raised in this case among which were post-anoxic myoclonia and metabolic encephalopathy. Cessation of histamine receptor blocker therapy for 48 hours was associated with return of normal cognitive function and disappearance of abnormal movements. This confirmed the iatrogenic nature of the syndrome related to administration of ranitidine.
Misoprostol was significantly more effective than ranitidine in the prevention of gastroduodenal lesions in cancer patients receiving diclofenac.
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The full risk to develop stress-related upper gastrointestinal bleeding was realized when two risk factors were present concomitantly. The presence of additional risk factors did not increase the occurrence of bleeding. A continuous infusion of ranitidine at 6.25 mg/hr provided significant protection from bleeding, regardless of the number of risk factors present.
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Eighty-two patients were enrolled into the study between October 2002 and August 2003. The patients were randomly assigned into two groups. One group received ranitidine bismuth citrate 2x400 mg, metronidazole 3x500 mg and tetracycline 2x1000 mg for 14 days (RMT group) and the other group pantoprazole 2x40 mg, bismuth subcitrate 4x300mg, amoxicillin 2x1000 mg and clarithromycin 2x500 mg for 14 days (PBAC group). The eradication was assessed four weeks after completion of the treatment, and the patients underwent endoscopy and were asked whether there were changes in their symptoms. When H. pylori was negative on both histological examination and urease test, the disease was considered eradicated.
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As a factor favoring relapses, noncompliance is particularly crucial to the treatment of peptic ulcer disease, and greater efforts should be made to eliminate or reduce it. To investigate the reasons for noncompliance, we performed two clinical trials involving a total of 592 patients with duodenal ulcer treated with various H 2 antagonists for 12 months. In the first study, 40.3% of patients with uncomplicated duodenal ulcer were noncompliant, compared with only 4.6% who had had previous bleeding episodes. Compliance in the second study averaged 68%. Major reasons for noncompliance among these patients were an absence of symptoms and an inconvenient dosage schedule. On the basis of our clinical experience and a review of the literature, compliance appears to be higher in patients with previous complications of their disease and when the effectiveness of prescribed drugs does not depend on ingestion with the evening meal.
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This prospective, randomized, double-blinded study was performed to evaluate the effects of intravenous metoclopramide and ranitidine on preoperative gastric contents in outpatients receiving intravenous anesthesia for laparoscopic gynecologic surgery. Fifteen minutes before the induction of anesthesia, the Z-M group (n=20) received 50 mg ranitidine and 10 mg metoclopramide intravenously and the control group (n=20) received the same volume of normal saline. Before the surgery, a 14-F multiorifice nasogastric tube was inserted to aspirate the gastric contents of patients under sedation with propofol and midazolam. The mean pH values of the gastric fluid were 2.7 +/- 2.0 (SD) [median 1.6 (range: 1.2-7.2)] in the control group, and 6.1 +/- 1.9 [median 6.8 (range 1.4-7.8)] in the Z-M group. The mean aspirated volumes (mL) were 15.3 +/- 10.4 (SD) [median 11.0 (range: 5.0-44.0)] in the control group, and 6.9 +/- 10.0 (SD) [median 4.5 (range: 0-38.0)] in the Z-M group. There were significantly more high-risk (gastric fluid volumes > 25 mL and pH < 2.5) patients in the control group (4/20, 20%) than in the Z-M group (1/20, 5%). In conclusion, intravenous prophylactic ranitidine and metoclopramide may be an easy and useful method to decrease the volume while increasing the pH of gastric contents, and therefore may reduce the number of patients at risk for aspiration pneumonitis in ambulatory laparoscopic procedures who receive an anesthesia.
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Actions of various drugs have been tested on the gastric acid basal secretion and on the drug (Indomethacin)- induced gastric mucosal damage; however their physiological and pharmacological mechanisms have not been compared.
Six weeks after the start of treatment, 32 of the 35 patients were Helicobacter pylori-negative and their ulcers had all healed completely. Five of the 35 patients reported mild side effects (diarrhea, temporary nausea).
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The aim of this study was to determine the effect of gestational age on pharmacokinetics of ranitidine in newborns with gastroesophageal reflux.
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This study assessed the efficacy of ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene)amino]-4-thiazolyl] methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfonamide, CAS 100981-43-9, FI-3542) versus ranitidine and placebo in preventing gastroduodenal lesions induced by piroxicam. Thirty patients with rheumatic disease, who were divided into 5 groups, received an oral treatment of piroxicam 20 mg once daily for 6 days plus ebrotidine 400 mg/day (Group I); ebrotidine 800 mg/day (Group II); ranitidine 150 mg/day (Group III); ranitidine 300 mg/day (Group IV); or placebo (Group V). Patients were endoscopically examined before and after treatment. Lanza's score was also determined, and laboratory tests were performed. The results of this study showed that the most powerful protective effect against mucosal gastric lesions induced by piroxicam was achieved with 800 mg/day of ebrotidine. Ranitidine at doses of 150 mg/day did not protect gastric mucosa, and the 300 mg/day dose exerted a poor gastroprotective effect.
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Species of Chresta genus- are recognized by the population of northeastern Brazil as traditional herbs used to treat gastric diseases and other disorders.
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Three cases are reported in which resolution of severe esophagitic dyspepsia followed amiodarone therapy for cardiac arrhythmias. This effect has proved long lasting. The mechanism of amiodarone action may be related to its calcium antagonist or nitratelike properties that reduce lower esophageal sphincter tone. An alternate hypothesis calls attention to structural similarities between amiodarone and the histamine antagonist ranitidine, and suggests a previously unrecognized action of amiodarone on histamine receptors.
The effects of ranitidine, a new H2-receptor antagonist, on liver regeneration were investigated using a protocol described previously. The animals in Group I had standard two-thirds hepatectomy. In Group II, the rats received an 8 mg/kg intramuscular dose of ranitidine immediately and 24 and 48 hours after two-thirds hepatectomy. In Group III, the rats had the same amounts of ranitidine after a sham operation. Mortality rate, liver weight restoration, mitotic activities of the residual livers, and serum levels of aminotransferases were examined from 24 hours to 14 days after operation. The mortality was very high in Group II (45 percent), whereas no rats died in Group I, and only 1 of 35 animals died in Group III. Administration of ranitidine after hepatectomy resulted in suppression not only of liver restoration, but also of the mitotic activities of hepatocytes. The serum aminotransferase levels in Group II had a tendency to increase after hepatectomy, compared with the levels in Group I. Using light microscopy, we detected that the hepatectomized group treated with ranitidine (Group II) underwent profound liver steatosis and marked dilatation of sinusoidal spaces. The present and previous observations by us indicate that ranitidine also inhibits, like cimetidine, liver regeneration after hepatectomy. The causes of the inhibitory effects of both cimetidine and ranitidine on hepatocyte cell division have also been discussed herein.