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Zantac

Generic Zantac is a high-quality medication which is taken in treatment of intestines, ulcers in the stomach, Zollinger-Ellison syndrome, gastroesophageal reflux disease (GERD) and other conditions of heartburn. Generic Zantac acts by decreasing the amount of acid produced in the stomach. It is a heartburn medicine.

Other names for this medication:

Similar Products:
Axid, Pepcid, Tagamet , Pepcid, Fluxid, Pepcid AC

 

Also known as:  Ranitidine.

Description

Generic Zantac is a perfect remedy in struggle against intestines, ulcers in the stomach, Zollinger-Ellison syndrome, gastroesophageal reflux disease (GERD) and other conditions of heartburn.

Generic Zantac acts by decreasing the amount of acid produced in the stomach. It is a heartburn medicine.

Zantac is also known as Ranitidine, Monorin, Histac, Ranitil.

Generic name of Generic Zantac is Ranitidine.

Brand names of Generic Zantac are Zantac, Zantac 150, Zantac 300, Zantac 300 GELdose, Zantac 75, Zantac EFFERdose, and Zantac GELdose.

Dosage

Generic Zantac is available in tablets (150 mg, 300 mg), capsules, syrup.

Before swallowing, fizzy tablets of 25 ml should be dissolved in 1 teaspoon of water.

Before drinking Generic Zantac granules should be mixed with 6 to 8 ounces of water.

The treatment can take more than 8 weeks.

Keep Generic Zantac away from children and do not share it with other people.

Take Generic Zantac tablets orally with water.

Do not crush or chew it.

If you want to achieve most effective results do not stop taking Generic Zantac suddenly.

Overdose

If you overdose Generic Zantac and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Zantac overdosage: coordination, feeling light-headed, fainting.

Storage

Store at room temperature between 2 and 30 degrees C (36 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Zantac are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Zantac if you are allergic to Generic Zantac components.

Be careful with Generic Zantac if you're pregnant or you plan to have a baby, or you are a nursing mother.

Generic Zantac can increase a risk of developing pneumonia.

Be careful using Generic Zantac if you are taking triazolam (Halcion).

It can be dangerous to use Generic Zantac if you suffer from or have a history of kidney disease, liver disease, phenylketonuria (PKU), porphyria.

Avoid alcohol.

Do not stop taking Generic Zantac suddenly.

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Six hundred and seventy-nine (4.4% of the total population) were authorized to receive repeat prescriptions for ulcer healing drugs. Six hundred and fifty-one (4.2%) were authorized to receive repeat prescriptions for H2-antagonists. Ranitidine was prescribed in 583 (86% of patients receiving ulcer healing drugs). Endoscopy had been performed in 426 (63%) and barium meal alone in 113 (17%); 140 (21%) had not been investigated. A diagnosis of peptic ulcer disease or oesophagitis was established in 382 (56%). However, 157 investigated patients (23% of all patients on ulcer healing drugs) did not have a peptic diagnosis.

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Data for 560 individual medication orders for oral medicine were collected, 257 from electronic prescribing and 303 from paper charts. Of these 457 were liquid doses, 103 were from products only available as tablets or capsules. Of the 257 electronically prescribed doses, 61 (24%) were not measurable. Of the 303 paper chart doses, 57 (19%) were not measurable.Of the 457 liquid doses 77 only needed up to 4% dose adjustment to become measurable. A further 10 doses required up to 9% dose adjustment.Drugs that were frequently prescribed as non-measurable doses were: diazepam, alimemazine, chloral hydrate, azithromycin, metronidazole, paracetamol & ibuprofen.Some doses were not measurable from tablets and no liquid is available in the Trust: clonidine, omeprazole, lansoprazole, nifedipine SR.19/560 (3.4%) of medication orders required a dose to be measured to two decimal places: diazepam, morphine, clonazepam, furosemide, spironolactone, chloral hydrate, ranitidine, chlorothiazide, azithromycin, erythromycin.

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The aim of the study was to develop a reliable quantification procedure for mixtures of three solid forms of ranitidine hydrochloride using X-ray powder diffraction (XRPD) and Raman spectroscopy combined with multivariate analysis. The effect of mixing methods of the calibration samples on the calibration model quality was also investigated. Thirteen ternary samples of form 1, form 2 and the amorphous form of ranitidine hydrochloride were prepared in triplicate to build a calibration model. The ternary samples were prepared by three mixing methods (a) manual mixing (MM) and ball mill mixing (BM) using two (b) 5 mm (BM5) or (c) 12 mm (BM12) balls for 1 min. The samples were analyzed with XRPD and Raman spectroscopy. Principal component analysis (PCA) was used to study the effect of mixing method, while partial least squares (PLS) regression was used to build the quantification models. PCA score plots showed that, in general, BM12 resulted in the narrowest sample clustering indicating better sample homogeneity. In the quantification models, the number of PLS factors was determined using cross-validation and the models were validated using independent test samples with known concentrations. Multiplicative scattering correction (MSC) without scaling gave the best PLS regression model for XPRD, and standard normal variate (SNV) transformation with centering gave the best model for Raman spectroscopy. Using PLS regression, the root mean square error of prediction (RMSEP) values of the best models were 5.0-6.9% for XRPD and 2.5-4.5% for Raman spectroscopy. XRPD and Raman spectroscopy in combination with PLS regression can be used to quantify the amount of single components in ternary mixtures of ranitidine hydrochloride solid forms. Raman spectroscopy gave better PLS regression models than XRPD, allowing a more accurate quantification.

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In patients with both Barrett's oesophagus and erosive reflux oesophagitis, lansoprazole is significantly more effective than ranitidine in relieving reflux symptoms and healing erosive reflux oesophagitis.

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Sucralfate (Sc) suspension 6 g/day and ranitidine (Rn) tablets, 150 mg, were compared in 125 patients in a double-blind, multicenter, endoscopically controlled trial in the treatment of reflux esophagitis. Inclusion criteria were symptomatic reflux (number and severity of attacks) and endoscopic evidence of esophagitis (grades 1 to 4). Clinical assessments were performed on entry, and at 4 and at 8 weeks, and endoscopy was repeated at 8 weeks. Sc suspension and Rn placebo or Sc placebo and Rn tablets were taken on waking and immediately before retiring at night. Of the 125 patients, 27 were withdrawn because of default (Rn = 4; Sc = 14), noncompliance (Rn = 1; Sc = 2), or the development of congestive cardiac failure (Rn = 1), diarrhea (Rn = 1; Sc = 1), nausea (Sc = 1), constipation (Sc = 1), and hematemesis (Sc = 1). Analysis was performed on the remaining 98 patients, 43 of whom had been treated with Sc and 55 with Rn. Heartburn, acid regurgitation, epigastric pain, dysphagia, and chest pain were relieved in 34% vs 40%, 67% vs 72%, 71% vs 57%, and 86% vs 63% for Sc and Rn, respectively. There was no significant difference between the two groups. Endoscopic healing occurred in 47% of the Sc- and in 31% of the Rn-treated patients (chi 2 = 2.50), and healing or improvement was noted in 81% of the Sc- and 64% of the Rn-treated patients. This difference approached statistical significance (chi 2 = 3.73). There was no obvious endoscopic benefit in 8 of the 43 and 20 of the 55 patients in the groups treated with Sc and Rn, respectively. Although the findings with sucralfate and ranitidine in patients with reflux esophagitis completing the trial suggest a benefit of these agents, the absence of a placebo control group and the high default rates, particularly for those receiving sucralfate, preclude any firm conclusions as to relative or specific efficacy of these agents in this condition.

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The influence of I and M on gastric mucosa integrity was assessed by oral administration in doses of 200mg/kg. The gastroprotective action of I and M in doses of 50, 100 and 200mg/kg was analyzed in the diclofenac and ethanol-induced gastric lesion models in rats. After the treatment, the stomachs of the animals were analyzed (captured by a digital camera). Ulcer scoring, morphometric and histopathological analyses of the stomachs were done.

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Our patient is a 70-year-old white woman with a 20-year history of intrinsic asthma, well controlled on triamcinolone acetonide 400 micrograms, ipratropium bromide 36 micrograms, and pirbuterol acetate 400 micrograms, each inhaled four times daily. She reported no oral steroid use for > 4 years and that she always rinsed her mouth following triamcinolone acetonide inhalation. The patient had gastritis with peptic ulcer disease in the past and developed worsening dyspeptic pain and heartburn. Following discontinuation of cimetidine and initiation of ranitidine without improvement, esophagogastroduodenoscopy was performed. Several small white patches in the mid and distal esophagus could not be removed with pressure. A biopsy confirmed the diagnosis of candidal esophagitis. Following a 4-week course of fluconazole, the patient was clinically improved and follow-up esophagogastroduodenoscopy was normal. There was no evidence of underlying cellular immunosuppression, malignancy, or diabetes mellitus and no history of recent antibiotic usage. Delayed skin tests revealed 5 x 5 mm induration to dermatophytin. Delayed hypersensitivity to Candida and mumps tests was absent. There was strong in vitro lymphocyte transformation and a positive immediate skin test response to Candida. ELISA for human immunodeficiency virus was negative. T and B cell counts were normal with CD4 = 630/mm3, CD8 = 520/mm3, and absolute B cell = 120/mm3. It is possible that this patient's immediate hypersensitivity response to Candida suppressed her delayed response. Candidal esophagitis is a rare, yet important, complication of inhaled corticosteroid use.

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To investigate plasma aluminum levels in critically ill patients requiring continuous venovenous hemofiltration (CVVH), while receiving sucralfate for stress ulcer prophylaxis.

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The regimen RBC, clarithromycin and metronidazole was the most effective and seems suitable as first-line treatment. The internet collaboration yielded data of high quality that disclosed that patients were not uniformly managed. Our collaborative approach seems to be a suitable method for quality assurance and the organisation of simple clinical multicentre trials.

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We have carried out a longitudinal study in order to confirm our preliminary data on the heavier involvement of the duodenum compared to the stomach after non aspirin non-steroidal anti-inflammatory drugs (NSAIDs). 53 patients with upper digestive haemorrhage due to recent intake of NSAIDs without preexisting known peptic pathology -28 p. from aspirin and 25 p. from NSAIDs other than aspirin--were selected. Aspirin and its derivatives mainly affected gastric mucosa whereas non aspirin NSAIDs the duodenum. 42 of these patients have been observed for two more years; independently of the treatment, ranitidine 150 mg daily vs antacids if needed, the annual rate of recurrence has been very low. These findings have further confirmed the accurate selection of our patients without previous peptic pathology (in this case the rate of recurrence would have been much higher) and also suggest a more rational diagnostic and therapeutic approach to these patients. We then observed a consecutive series of 107 patients affected with duodenal ulcer bleeding: 51 by NSAIDs and 56 not by NSAIDs; both groups were given H2-antagonists and blood transfusions if needed. The short term prognosis has been rather positive mainly for the NSAIDs group, in which no mortality has been observed, independently of the number of blood transfusions and length of hospitalization. In our experience the high percentage of NSAIDs duodenal ulcers (about 50%), shows an increase of this pathology, less severe than peptic one, even if expressed by a serious event as digestive bleeding. It is our opinion that these percentages and prognostic evaluations should be considered in therapeutic decision, limiting thus surgical and aggressive endoscopic procedures.

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Ranitidine bismuth citrate is a novel antiulcerant that provides the antisecretory activity of ranitidine and the gastric mucosal protection and antibacterial properties of bismuth.

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The removal of N-nitrosodimethylamine (NDMA) formation potential through a membrane bioreactor (MBR) coupled to a nanofiltration (NF) pilot plant that treats urban wastewater is investigated. The results are compared to the fate of the individual NDMA precursors detected: azithromycin, citalopram, erythromycin, clarithromycin, ranitidine, venlafaxine and its metabolite o-desmethylvenlafaxine. Specifically, the effect of dissolved oxygen in the aerobic chamber of the MBR pilot plant on the removal of NDMA formation potential (FP) and individual precursors is studied. During normal aerobic operation, implying a fully nitrifying system, the MBR was able to reduce NDMA precursors above 94%, however this removal percentage was reduced to values as low as 72% when changing the conditions to minimize nitrification. Removal decreased also for azithromycin (68-59%), citalopram (31-17%), venlafaxine (35-15%) and erythromycin (61-16%) on average during nitrifying versus non-nitrifying conditions. The removal of clarithromycin, o-desmethylvenlafaxine and ranitidine could not be correlated with the nitrification inhibition, as it varied greatly during the experiment time. The MBR pilot plant is coupled to a nanofiltration (NF) system and the results on the rejection of both, NDMA FP and individual precursors, through this system was above 90%. Finally, results obtained for the MBR pilot plant are compared to the percentage of removal by a conventional full scale biological wastewater treatment plant (WWTP) fed with the same influent. During aerobic operation, the removal of NDMA FP by the MBR pilot plant was similar to the full scale WWTP.

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Pediatric Risk of Mortality (PRISM) score and clinical data were collected on admission and pHi daily during their stay in the pediatric ICU. A sigmoid tonometer was used to determine the pHi. Unconditional logistic regression was used to investigate the prognostic value of pHi. On admission, 26 patients presented with low gastric pHi (< or =7.35) and 17 of them had values of <7.30. The mortality rate in children with pHi <7.30 was 47.1% (95% confidence interval, 26.2 to 69) in contrast with an 11.7% mortality rate (95% confidence interval, 4.6 to 26.6) in children having a pHi of > or =7.30 (p=.015). The pHi and PRISM score on admission were independent predictive factors of death. The risk of mortality is increased when the pHi is low (odds ratio=2.5). However, we did not find the pHi to be a predictor for developing MODS.

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1. Freshly isolated hepatocytes from rat and dog have been evaluated as a model for the metabolism of ranitidine in vivo. 2. Isolated hepatocytes from the male and female dog and male Wistar and random hooded rat metabolized ranitidine to ranitidine N-oxide, ranitidine S-oxide, desmethylranitidine and two unidentified minor metabolites. The furoic acid metabolite of ranitidine, previously reported to be a minor metabolite in vivo in rat and dog, was not detected in hepatocytes from either species. 3. The kinetics for ranitidine metabolism in hepatocytes were monophasic for the formation of the three major metabolites in dog and Wistar rat and for N-demethylation of ranitidine in the random hooded rat, but biphasic in this latter strain for the N- and S-oxidation of ranitidine. 4. Ranitidine N-oxide was reduced to ranitidine by Wistar rat hepatocytes but not by hepatocytes from the random hooded rat or dog. Ranitidine S-oxide was metabolized by hepatocytes from both species to one of the unidentified metabolites but was not reduced to ranitidine in either species. Desmethylranitidine was not a substrate for metabolism in hepatocytes from either species. 5. The relative quantitative importance of ranitidine N-oxide, ranitidine S-oxide and desmethylranitidine produced by the hepatocytes was consistent with the profiles of these three metabolites in vivo in rat and dog. The results confirm the value of isolated hepatocytes as a predictive model for in vivo drug metabolism.

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One hundred and ninety-three (193) H. pylori-positive patients were randomly assigned to one of the following 7-day treatments: Group A (N = 64): amoxicillin, clarithromycin and rabeprazole; Group B (N = 64): tinidazole, clarithromycin and ranitidine bismuth citrate; Group C (N = 65): tinidazole, clarithromycin and rabeprazole Eradication was assessed by 13C-Urea Breath Test 6-8 weeks after the end of the therapy. Not-eradicated patients underwent a second cycle with tinidazole, tetracycline, bismuth and rabeprazole. All patients were asked to complete a validated questionnaire regarding presence and intensity of drug side effects.

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Omeprazole is effective in preventing chemotherapy-induced gastroduodenal injury. Ranitidine is effective in reducing the frequency of ulcers and upper gastrointestinal symptoms but is not effective in preventing the global endoscopic worsening caused by chemotherapy. The different efficacy of omeprazole and ranitidine can be explained by their different pharmacodynamics.

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Creation of an animal model of necrotizing enterocolitis (NEC) allowing adjustment of severity and potential recoverability is needed to study effectiveness of prevention and treatment strategies. This study describes a novel model in preterm rabbits capable of adjusting severity of NEC-like histologic changes. Rabbit pups (n = 151) were delivered by cesarean section 2 days preterm. In the treatment groups, tissue adhesive was applied to anal openings to simulate the poor intestinal function and dysmotility of preterm neonates. Pups were placed into five groups: 3INT (3 day intermittent block), 4INT (4 day intermittent block), 3COM (3 day complete block), 4COM (4 day complete block), based on differences in type of anal blockage and day of life sacrificed. The fifth group, 4CON, was comprised of a control arm (n = 28) without anal block, with sacrifice of subjects on day 4. All pups were gavage fed with formula contaminated with Enterobacter cloacae, ranitidine, and indomethacin. Following sacrifice, the intestines were harvested for pathologic evidence of NEC. A blinded pathologist graded histologic changes consistent with NEC using a grading scale 0-4 with 4 being most severe. Fifty-seven pups (57/123) (46%) in the research arm survived to sacrifice, compared to 26/28 (93%) in the control arm of the investigation, p < 0.0001. The incidence and severity of NEC-like damage increased with the duration and completeness of the anal blockage. 44/57 (77%) of survivors revealed various degrees of NEC-like damage to large and small bowel, and 3/26 (12%) exhibited early NEC-like mucosal injury in the research and control arms, respectively. This animal model produces NEC-like pathologic changes in both small and large intestine in preterm rabbits. Because incidence and severity of damage increases with duration and completeness of intestinal dysmotility, this allows future effectiveness studies for nonsurgical treatment and prevention of NEC.

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A 57-year-old white female presented to the emergency department because of a full-body morbilliform rash, which appeared 9 days after initiation of milnacipran 50 mg twice daily. In the emergency department the patient's vital signs were: heart rate 121 beats/min, blood pressure 180/100 mm Hg, and temperature 38.9 °C. The patient reported diarrhea, nausea, dizziness, restlessness, and increased muscle pain. Her history included recurrent breast cancer first diagnosed in 1999, hypertension, fibromyalgia, depression, osteopenia, gastroesophageal reflux disease, insomnia, and endometriosis. Her home medications included milnacipran, fluoxetine, alprazolam, zolpidem, zoledronic acid, anastrozole, doxepin, ranitidine, levocetirizine, doxazosin, tramadol, vitamin D, and ferrous gluconate. The patient's increased heart rate, blood pressure, and temperature, as well as restlessness, self-reported diarrhea and nausea, and self-reported increase in muscle pain, indicated serotonin toxicity. Milnacipran, fluoxetine, and tramadol were discontinued, while doxepin was continued. Treatment consisted of acetaminophen, diphenhydramine, methylprednisolone, promethazine, and hydralazine 10 mg intravenously. The following morning all vital signs were within normal limits and the patient's diarrhea, nausea, dizziness, restlessness, and muscle pain resolved. She was discharged the following morning. The rash had resolved after day 2 of hospital discharge, which was the fourth day after discontinuation of milnacipran.

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Current literature was reviewed analyzing the outcome of peptic ulcer healing in relation to the results of the posttherapeutic Helicobacter pylori (HP) status.

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The aetiology of gastric ulcers is not completely understood and continuous use of anti-ulcer agents leads to many side effects. In this study we evaluated the anti-ulcer efficacy of a polyherbal formulation with potent antioxidant activity in aspirin and pyloric ligature induced gastric ulcers in rats.

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Isosorbide-5-mononitrate administered orally is a safe and effective alternative to propranolol in the prophylaxis of bleeding in cirrhosis.

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In a randomized study 31 patients with advanced cancer disease in whom classical anticancer therapy had been abandoned received a daily combination of subcutaneous histamine and oral H2-antihistaminics. In 27 patients, treatment induced a marked clinical improvement as shown by a large rise in performance status (Karnofsky scale). Ten patients were still alive 3-14 months after initiation of treatment. Average survival in the 31 treated patients (172 +/- 113 days) was significantly longer than in 34 non-treated patients with similar advanced cancer (26 +/- 16 days, P less than 0.00001). In six treated patients, the size of liver and lung metastases decreased. Histamine was perfectly tolerated up to 4 mg/day.

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Before IC, 32 patients (25%) were negative for axillary involvement by both physical and ultrasonographic examinations. After IC, this number increased to 64 (49%). Of these, 31 (48%) were positive by pathology examination. In most cases, however, the residual tumor was minimal.

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Six patients were lost to the follow-up. At the end of the first course of treatment, the overall H. pylori eradication rate was 78% (95% CI: 73-83) and 79% (95% CI: 75-84) at 'intention-to-treat' (ITT) and 'per protocol' (PP) analysis, respectively, without any statistically significant difference between treatment regimens, although a trend for better results with the omeprazole combination was observed. Moreover, H. pylori eradication was achieved in 82% (95% CI: 75-97) (ITT) and 86% (95% CI: 69-94) (PP) of 38 patients re-treated with RBTT regimen.

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The protective action of zinc compounds in Crohn's disease-like inflammatory bowel disease in animals has been shown. A similar action of zinc sulfate on ulcerative colitis has not been defined. The present study aimed to delineate the protective action of zinc sulfate and the pathogenic mechanisms of 2,4-dinitrobenzene sulfonic acid (DNBS)-induced ulcerative colitis in rats. Zinc sulfate at different concentrations was given either orally (p.o.) or rectally (p.r.) to rats at 42, 48, 66 and 72 h following the induction of colonic inflammation by DNBS. Rats were killed 96 h after instillation of DNBS rectally to assess the severity of colonic damage, myeloperoxidase and xanthine oxidase activities. The involvement of mast cell degranulation and histamine release in the pathogenesis of DNBS-induced colitis was determined by using a mast cell stabilizer (ketotifen) and histamine receptor blockers (terfenadine and ranitidine). DNBS given rectally produced inflammation and ulceration in rats with a pathology resembling ulcerative colitis. Myeloperoxidase activity but not xanthine oxidase activity was sharply increased by this agent. Intrarectal administration of zinc solution and parenteral injection of histamine blockers significantly reduced tissue damage and myeloperoxidase but not xanthine oxidase activity. Ketotifen, a mast cell stabilizer, also significantly decreased mucosal injury and myeloperoxidase activity in the colon. In conclusion, mast cell degranulation followed by histamine release plays an important role in the pathogenesis of DNBS-induced ulcerative colitis. Zinc given rectally has a therapeutic effect against this colitis model, perhaps through the reduction of inflammation and inhibition of the above pathogenic mechanisms.

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Thirty min after oral administration, > 50% of the recovered ranitidine mass resided in the lower half of the small intestine in all rats. Ranitidine mass in 5 of 16 rats displayed a bimodal distribution with significant amounts of ranitidine recovered from the stomach 60 to 90 min after dosing. Ranitidine exsorption was more efficient from the lower jejunum and ileum than from the duodenum and upper jejunum. However, intestinal secretion of ranitidine was minor (5% of the IV dose).

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Electrical and chemical stimulation of the dorsal periaqueductal gray matter (dPAG) and the inferior colliculus (IC) induces escape behavior, usually accompanied by autonomic responses and antinociception. Recently, we presented evidence for a tonic inhibitory control exerted by H(2) histamine receptors on defensive behaviors generated in these midbrain tectum sites. Since treatments of these areas that elicit the defensive behavior repertoire frequently also have anxiogenic effects, we here used the elevated plus-maze (EPM) test for assessing the effects of microinjections of histamine (5-40 nmol), dimaprit (5-10 nmol) and ranitidine (10-30 nmol) into either dPAG or IC, which have a relative abundance of histamine-containing cells and histaminergic receptors. Dimaprit is an agonist and ranitidine is an antagonist of H(2) histamine receptors. Immediately after the injections, the animals were submitted to the EPM test. Whereas dPAG injections of dimaprit had no behavioral effects, histamine (40 nmol) caused a significant reduction in exploratory activity. On the other hand, ranitidine alone or following saline had aversive-like effects in both structures, i.e. reduced open arm, but not closed arm, entries. This pattern is usually interpreted as representing an anxiogenic effect. These effects were more pronounced after injection into dPAG than into IC. Freezing, the most prominent effect produced by ranitidine, was significantly inhibited by histamine as well as dimaprit. Thus, H(2) receptor blockade has fear-like action in the midbrain tectum with predominance in the dPAG. Such an action can be understood as a concomitant of defensive behavior, which has been shown to be a consequence of H(2) receptor antagonism in both dPAG and IC. The functional significance of the different effects of H(2) receptor blockade in dPAG and IC is discussed in the light of the probable distinct roles of these structures in the organization of defensive behavior.

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Pre-treatment with reversible acetylcholinesterase (AChE) inhibitors before organophosphorous compound (OPC) exposure can reduce OPC-induced mortality. However, pyridostigmine, the only substance employed for such prophylaxis, is merely efficacious against a limited number of OPCs. In search of more efficacious and broad-range alternatives, we have compared in vivo the ability of five reversible AChE inhibitors (pyridostigmine, physostigmine, ranitidine, tacrine and K-27) to reduce mortality induced by the OPC azinphos-methyl. Protection was quantified using Cox analysis by determining the relative risk (RR) of death in rats that were administered these AChE inhibitors in equitoxic dosage (25% of LD01) 30 min before azinphos-methyl exposure. Azinphos-methyl-induced mortality was significantly reduced by all five tested compounds as compared with the reference group that was only exposed to azinphos-methyl without prior pre-treatment (RR = 1). The most efficacious prophylactic agents were K-27 (RR = 0.15) and physostigmine (RR = 0.21), being significantly more efficacious than ranitidine (RR = 0.62) and pyridostigmine (RR = 0.37). Pre-treatment with tacrine (RR = 0.29) was significantly more efficacious than pre-treatment with ranitidine, but the difference between tacrine and pyridostigmine was not significant. Our results indicate that prophylactic administration of the oxime K-27 may be a promising alternative in cases of imminent OPC exposure.

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8 mg zantac 2016-04-07

Rheumatoid arthritis patients with a history of peptic buy zantac ulcer disease were randomized to receive either ranitidine 300 mg b.d. or placebo for 12 months. Endoscopy was performed at study entry and after 6 and 12 months. End-point was the recurrence of gastric or duodenal ulcers.

generic zantac cost 2017-03-10

Pantoprazole is a new substituted benzimidazole, which is a potent inhibitor of gastric acid secretion by its inhibition of H+,K(+)-ATPase. Pantoprazole, 40 mg, was compared with the H2-receptor antagonist ranitidine, 300 mg, in the healing of acute duodenal ulcer. Two hundred seventy-six patients with endoscopically diagnosed duodenal buy zantac ulcer were studied in this multicenter double-blind study. Patients were reendoscopied after two weeks of treatment, and those patients whose ulcers remained unhealed were also endoscoped after an additional two weeks of treatment. The primary end point was the complete healing of the ulcer. Demographic characteristics were comparable in both treatment groups. After two weeks of treatment, 90/124 (73%) patients in the pantoprazole group had healed ulcers compared with 57/126 (45%) patients in the ranitidine group (P < 0.001, per-protocol analysis). After four weeks, the cumulative healing rates were 92% and 84% in the pantoprazole and ranitidine groups, respectively (P = 0.073). Symptoms were also improved at week 2, with 84% and 72% of patients in the pantoprazole and ranitidine groups, respectively, reporting no ulcer pain (P < 0.05, per-protocol analysis). Both treatments were well tolerated. This study has confirmed the superiority of pantoprazole compared with ranitidine in the healing of duodenal ulcers and pain relief after two weeks of treatment and has shown pantoprazole to be well tolerated in this indication.

zantac 150 mg 2015-01-15

Responses of the toad isolated rectus abdominis muscle to cumulative doses of carbachol were recorded in the absence or presence of varying concentrations of cimetidine or ranitidine. The corresponding cumulative log concentration-response curves for carbachol were then plotted for each antagonist studied. Cimetidine (1 mmol/l) produced a straight and parallel 1.8-fold shift of the carbachol curve to the right of the corresponding control curve with no significant change in the maximal response. Cimetidine, at doses of 2.5 mmol/l and 5 mmol/l, and ranitidine, at doses of 0.1 mmol/l, 0.25 mmol/l and 0.5 mmol/l, produced a concentration-dependent and non-parallel shift of the carbachol curve to the right buy zantac of the corresponding control curve accompanied by a marked decline of maximal responses. The results provide further evidence that ion-channel block may be involved in the neuromuscular blockade produced by cimetidine or ranitidine, the latter being more potent in this respect. Competitive antagonism may also be partly responsible for cimetidine-induced neuromuscular blockade, especially at lower drug concentrations.

zantac dosing instructions 2016-03-25

Diagnostic methods for detecting forms and strains of Helicobacter pylori isolated from biopsy specimens of gastric mucosa in 28 patients with duodenal ulcers and evaluation of its eradication were compared. Biopsy specimens from all patients were tested for the presence of H. pylori by the urease test, histological method, and PCR with species-specific primers before and after treatment. H. pylori infection was detected in all patients before treatment, the mean titer of serum IgG being 36.7+/-16.6 U/ml. Biopsy specimens positive for H. pylori in PCR were subjected to restriction analysis of specific PCR-amplified genes or their fragments. The fingerprint analysis gave electrophoregrams buy zantac of restriction products amplified fragment of flaA gene of H. pylori in 7 patients. Differences in restriction maps indicate the presence of 5 H. pylori strains in the studied samples.

zantac pill picture 2015-12-20

Observational reports have linked vitamin D with chronic urticaria, yet no randomized controlled trial has been buy zantac conducted.

zantac suspension 2015-12-21

To evaluate the efficacy and safety of 4 buy zantac kinds of triple strategy of Helicobacter pylori (Hp) eradication.

zantac 2 tablets 2015-08-07

Diclofenac, nimesulide, and ranitidine were administered in doses of 2, 4, and 6 mg/kg, p.o. once daily for 14 days, and their buy zantac effect on gastric volume, acidity, mean ulcer number, and gastric pH. In addition, histopathological examination was also performed on sections of stomach, kidney and liver.

zantac dose 2015-12-24

Department of Clinical Pharmacology, Jichi buy zantac Medical School.

zantac 60 mg 2016-06-27

N alpha-methylhistamine (N alpha-MH) is one of an unusual metabolite of histamine that was found in Helicobacter pylori-infected stomachs and is believed to interact with specific histamine H(1), H(2) and H(3)-receptors to stimulate gastric acid secretion and gastrin release from isolated G-cells but the effects of N alpha-MH on gastric mucosal buy zantac integrity have been little studied. This study was designed; (1) to compare the effect of exogenous N alpha-MH with that of standard histamine on gastric secretion and plasma gastrin levels in rats equipped with gastric fistula (series A); and (2) to assess the action of N alpha-MH on gastric lesions induced by 100% ethanol (series B) in rats with or without removal of antral portion of the stomach (antrectomy). Rats of series B were pretreated intragastrically (i.g.) or intraperitoneally (i.p.) with N alpha-MH or histamine (0.1-2 mg/kg) 30 min prior to 100% ethanol (1.5 ml, i.g.) with or without: (1) vehicle (saline); (2) RPR 102681 (30 mg/kg i.p.), to block CCK-B/gastrin receptors; and (3) ranitidine (40 mg/kg s.c.) to inhibit histamine H(2)-receptors. The area of gastric lesions was determined planimetrically, gastric blood flow (GBF) was assessed by H(2)-gas clearance method and venous blood was collected for determination of plasma gastrin levels by radioimmunoassay (RIA). N alpha-MH and histamine dose-dependently increased gastric acid output (series A); the dose increasing this secretion by 50% (ED(50)) being 2 and 5 mg/kg i.g or i.p., respectively, and this effect was accompanied by a significant rise in plasma gastrin levels. Both, N alpha-MH and histamine attenuated dose-dependently the area of gastric lesions induced by 100% ethanol (series B) while producing significant rise in the GBF and plasma immunoreactive gastrin increments. These secretory, protective, hipergastrinemic and hyperemic effects of N alpha-MH and histamine were completely abolished by antrectomy, whereas pretreatment with RPR 102681 attenuated significantly the N alpha-MH and histamine-induced protection against ethanol damage and accompanying hyperemia. Ranitidine, that produced achlorhydria and a further increase in plasma gastrin levels, failed to influence the N alpha-MH- and histamine-induced protection and accompanying rise in the GBF. We conclude that (1) N alpha-MH stimulates gastric acid secretion and exhibit gastroprotective activity against acid-independent noxious agents in the manner similar to that afforded by histamine; and (2) this protection involves an enhancement in the gastric microcirculation and release of gastrin acting via specific CCK-B/gastrin receptors but unexpectedly, appears to be unrelated to histamine H(2)-receptors.

zantac 150 tablets 2017-11-21

Tiffany, a 3-year-old girl, was referred to the developmental and behavioral pediatrics service for evaluation of significant and persistent negative behaviors associated with refusal to eat at meal time and constant snacking during the past 3 months. She lost 2 pounds, but her weight for her height was at the 50th percentile. Her mother indicated that Tiffany had frequent night awakenings (>10) and late sleep onset (between 12:00 and 1:00 a.m.). Her mother described her as being "easily frustrated," getting upset and angry very quickly. Tiffany was identified at an early intervention program as having mild to moderate developmental delays in pragmatic speech, gross and fine motor skills, and social interaction skills. Tiffany was born at 33 weeks gestation and was hospitalized for 10 days without significant perinatal problems. She was readmitted at 2 months of age when she was diagnosed with gastroesophageal reflux, lactose intolerance, sleep apnea, and bradycardia. She was discharged with an apnea monitor. A seizure disorder was diagnosed at 1 year of age and reactive airway disease at 2 years of age. At the time of the referral to the developmental and behavioral pediatrics service, Tiffany was followed by multiple services, including cardiology, neurology, gastroenterology, psychology, and pulmonary. Pharmacologic therapies included albuterol and cromalyn inhalers, phenobarbital, valproic acid, levocarnitine, ranitidine, and an inhaled steroid. She continued to use the apnea monitor each night, although three sleep studies demonstrated a normal sleep pattern with no evidence of apnea or bradycardia. A recent electroencephalogram was normal. Tiffany lives with her mother and maternal grandparents. Her mother is morbidly obese with a history of asthma and depression. She was infertile for a 10-year period, which she attributed to the stress associated with living with buy zantac an abusive man. Tiffany was the result of a subsequent, brief relationship with another man; she has not had contact with her father. Her mother is a licensed practical nurse who has not worked as a nurse since Tiffany's birth. An interdisciplinary treatment approach to Tiffany's multiple biological and behavioral problems was implemented by admitting her to a collaborative care unit at a children's hospital.

zantac mg 2015-06-08

N-nitrosodimethylamine (NDMA), a probable human carcinogen, is a disinfection by-product that has been detected in chloraminated drinking water systems. Pre-oxidation of the NDMA precursors prior to chloramination can be a viable approach for water utilities to control the NDMA levels. This study examined the effects of (i) commonly used oxidants (i.e., chlorine, chlorine dioxide and ozone) in water treatment, (ii) oxidant concentration and contact time (CT), and (iii) pre-oxidation pH on the formation of NDMA buy zantac from subsequent chloramination. Fifteen model precursors with NDMA molar yields ranging from approximately 0.1%-90% were examined. Pre-chlorination reduced NDMA formation from most precursors by 10%-50% except quaternary amine polymers (i.e., PolyDADMAC, PolyACRYL, PolyAMINE). Pre-oxidation with chlorine dioxide and ozone achieved the same or higher deactivation of NDMA precursors (e.g., ranitidine) while increasing NDMA formation for some other precursors (e.g., daminozid). The increases with chlorine dioxide exposure were attributed to the release of oxidation products with dimethylamine (DMA) moiety, which may form more NDMA upon chloramination than the unoxidizied parent compound. On the other hand, chlorine dioxide was effective, if a precursors NDMA yield were higher than DMA. The ozone-triggered increases could be related to direct NDMA formation from DMA which are released by ozonation of amines with DMA moiety, amides or hydrazines. However, hydroxyl radicals formed from the decomposition of ozone would be also involved in decomposition of formed NDMA, reducing the overall NDMA levels at longer contact times. pH conditions influenced significantly the effectiveness of deactivation of precursors depending on the type of precursor and oxidant used.

zantac maximum dosage 2016-08-17

First demonstration of the action of antihistamines in the HS response in yeast. The work supports the potential H(x) R-independent functions buy zantac of histaminergic compounds in fungal adaptation and stimulates research on the prospect of their exploitation in eukaryotic (patho)physiology.

zantac max dose 2016-12-05

Fifty-one patients were studied (n = 51), distributed into 25 buy zantac in the AA+H2 group and 26 in the sucralfate group. In the first group mean pH was higher (5.3 +/- 1.7) than in the sucralfate group (3.2 +/- 2.1) (p = 0.006). Nosocomial pneumonia (NP) was suspected on 25 occasions: 20 patients were positive for NP, 11 in the AA+H2 group and nine in the sucralfate group with no significant differences being observed. S. aureus, S. pneumoniae and H. influenzae (n = 14) were the etiology of predominant PMV. The global mortality of the group was of 22%.

zantac 150 dosage 2017-07-26

In this study, the newer PPIs were of similar efficacy to omeprazole in terms of heartburn control, healing Diflucan Buy Online rates, and relapse rates. All the PPIs were superior to ranitidine and placebo in healing erosive esophagitis and decreasing relapse rates.

zantac kids dosage 2017-10-27

Twelve healthy volunteers were randomly allocated to take two of the following treatments; cimetidine, misoprostol (a prostaglandin E1 analogue) and carbenoxolone, for two weeks. A further four subjects took ranitidine. Gastric aspirates were collected before and on the 14th day of therapy for each drug, and analysed for intrinsic factor concentration and total output. Both randitine and cimetidine inhibited pentagastrin stimulated output by 47% and 27% respectively in comparison to control, but had no effect on stimulated mean intrinsic factor concentrations. No changes were observed with misoprostol and Diovan Dosage Forms carbenoxolone treatment.

zantac dosing 2016-02-07

The study included 104 patients of which 49 underwent VR, 43 CABG and 12 who had both procedures performed simultaneously. Six of the 104 patients developed NP (5.7%). Five of these patients had undergone VR where as opposed to only one in the CABG group. Pulmonary hypertension preoperatively was a risk factor for the Prices Viagra Generic development of NP. Of the 49 patients in the VR group, 46 had pulmonary artery pressures (PAP) recorded, and from their 23 (50%) had pulmonary hypertension. However, 4 of the 5 (80%) patients who developed NP had elevated PAP. The mortality among patients with NP was high. Sixty six percent of patients (4/6) with NP died in comparison to the 10 deaths (10.2%) among 92 patients without NP (p = 0.002).

zantac depression medication 2015-12-16

Five patients with gastroesophageal reflux disease (GERD), who also had chronic functional diarrhea and postprandial urgency, unexpectedly noted rapid relief of their diarrhea and urgency when they took lansoprazole for their heartburn. To determine if this surprising result was not fortuitous, all 20 patients seen during the next six months for chronic diarrhea and postprandial urgency due to irritable bowel syndrome (IBS) or functional diarrhea were treated with inhibitors of gastric secretion: 14 with proton-pump inhibitors and 6 with H2 blockers. All patients had rapid, marked improvement. Usually within three days, their symptoms abated and they usually had one to three formed stools per day. Relief continued during the one to six months they were followed on therapy. Five patients stopped therapy, had recurrent diarrhea Lasix 500mg Tablet , and rapid relief upon resuming therapy. Thus, inhibition of gastric secretion effectively controls the diarrhea and postprandial urgency associated with IBS or functional diarrhea, probably by diminishing the gastrocolic or gastroenteric reflex.

zantac overdose 2016-07-09

During a prospective randomized trial, 250 Hp positive patients with either duodenal ulcer, erosive bulbitis, or gastritis and dyspepsia were treated using 14 days of therapy 1) pantoprazole 40 mg daily and clarithromycin 500 mg b.i.d. (PC), 2) pantoprazole 40 mg daily and clarithromycin 500 mg Coumadin 5 Pill b.i.d. plus amoxicillin 1 g b.i.d. (PCA), or 3) bismuth subcitrate 120 mg t.i.d., roxithromycin 150 mg b.i.d., metronidazole 250 mg b.i.d. plus ranitidin 300 mg (BRMR). Hp status was assessed on 3 tests at the inclusion (2-specimen rapid urease test, 2-specimen histology, serology) and 2 tests (2-specimen rapid urease test, 2-specimen histology) 4 weeks after the end of the treatment.

zantac generic target 2015-04-28

Preoperative fasting guidelines do not recommend H2 receptor antagonists or proton pump inhibitors. This study investigated prophylactic Nexium Safe Dosage use of gastric protection and the incidence of dyspeptic symptoms in the immediate postoperative period.

zantac 1 mg 2015-05-21

Choledochoduodenal fistula is an uncommon complication of duodenal ulcer disease. The role of medical therapy is unclear and surgical management has been recommended for the condition. A patient who was treated with ranitidine 150 mg Problems Generic Seroquel twice daily for 8 weeks for a giant duodenal ulcer with a choledochoduodenal fistula is reported. Both the ulcer and the fistula completely healed on medical therapy. Medical therapy may now become the treatment of choice for this condition due to the availability of potent acid-reducing agents.

medicine zantac 2017-04-10

Healing rate was 90.2% in group A and 85.7% in group B. Eradication rate was 78% in group A and 0% in group B. Out of 37 healed patients in group A, eradication was achieved in 29 and only one relapse was found (3.4%). Three out of eight patients with healing but without eradication relapsed at 12 months (35%) (p < 0.05). Histopathological Periactin Drug Class results showed statistically significant differences (p < 0.05) between eradicated and non eradicated patients in terms of severity of inflammation and intestinal metaplasia, but not in terms of atrophy.

zantac user reviews 2016-11-05

Triple therapies with proton pump inhibitor/ranitidine bismuth citrate (RBC), clarithromycin (C) and either amoxicillin (A) or a nitroimidazole (I) are widely accepted as treatment for Helicobacter pylori infection. However, it is not clear which of these Neurontin Cost antibiotic combinations should be preferred.

cold medicine zantac 2016-08-21

To determine the current practice in selected general Prednisone Kids Dosage practices for prescribing long term (> 6 months) treatment to suppress gastric acid secretion.

pediatric zantac dosing 2016-12-21

A rapid and sensitive HPLC method using a monolithic column has been developed for quantification of famotidine in plasma. The assay enables the measurement of famotidine for therapeutic drug monitoring with a minimum detectable limit of 5 ngml(-1). The method involves simple, one-step extraction procedure and analytical recovery was complete. The separation was carried out in reversed-phase conditions using a Chromolith Performance (RP-18e, 100 mm x 4.6 mm) column with an isocratic mobile phase consisting of 0.03 M disodium hydrogen phosphate buffer-acetonitrile Omnicef Dosing Instructions (93:7, v/v) adjusted to pH 6.5. The wavelength was set at 267 nm. The calibration curve was linear over the concentration range 20-400 ngml(-1). The coefficients of variation for inter-day and intra-day assay were found to be less than 8%.

zantac 2 mg 2015-12-04

Eleven studies Coreg Generic Name fulfilled the inclusion criteria and contained data for at least one of the planned comparisons. Persistent or recurrent bleeding was reported in 6.7% (95% CI: 4.9-8.6%) of the patients treated with proton pump inhibitors, and in 13.4% (95% CI: 10.8-16%) of those treated with H2-A (OR 0.4; 95% CI: 0.27-0.59) (chi2-homogeneity test, 18; P=0.09). Surgery was needed in 5.2% (95% CI: 3.4-6.9%) of the patients treated with proton pump inhibitors, and in 6.9% (95% CI: 4.9-8.9%) of the patients treated with H2-A (OR 0.7; 95% CI: 0.43-1.13). Respective percentages for mortality were 1.6% (95% CI: 0.9-2.9%) and 2.2% (95% CI: 1.3-3.7%) (OR 0.69; 95% CI: 0.31-1.57). SUB-ANALYSIS: Five studies evaluated the effect of both therapies given in bolus injections on persistent or recurrent bleeding rate, which was 6% (95% CI: 3.6-8.3%) and 8.1% (95% CI: 5.3-10.9%), respectively (OR, 0.57; 95% CI: 0.31-1.05). Persistent or recurrent bleeding in high risk patients (Forrest Ia, Ib and IIa) occurred in 13.2% (95% CI: 7.9-8%) of the patients treated with proton pump inhibitors and in 34.5% (27-42%) of those treated with H2-A (OR 0.28; 95% CI: 0.16-0.48). In patients not having endoscopic therapy, persistent or recurrent bleeding was reported, respectively, in 4.3% (95% CI: 2.7-6.7%) and in 12% (95% CI: 8.7-15%) (OR 0.24; 95% CI: 0.13-0.43). Less marked differences were observed in patients having adjunct endoscopic therapy: 10.3% (95% CI: 6.7-13.8%) and 15.2% (11.1-19.3%) (OR 0.59; 95% CI: 0.36-0.97). Moreover, the significance disappeared in this group when a single outlier study was excluded.