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Zantac (Ranitidine)

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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.


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.


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.


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.


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.


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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Bismuth compounds remain useful for Helicobacter pylori eradication therapy. These include colloidal bismuth subcitrate (CBS), bismuth subsalicylate (BSS) and, most recently, ranitidine bismuth citrate (RBC). CBS appears to prevent the development of imidazole resistance when coadministered with nitroimidazoles. Traditional triple therapy with bismuth, metronidazole and tetracycline or amoxicillin (BMT/A) only partially overcomes metronidazole resistance. However, the addition of a PPI to bismuth triple therapy largely overcomes established metronidazole resistance if treatment is given for at least one week or more. When RBC rather than PPI is used with clarithromycin, this dual regimen appears to be more effective in preventing the development of secondary clarithromycin resistance. The triple combination of RBC, metronidazole and clarithromycin appears to be effective against metronidazole resistant strains of H pylori. Thus, overall, there is some evidence that bismuth compounds may prevent the development of antibiotic resistance and that existing antibiotic resistance may at least be partially overcome in vitro and in vivo. With the growing emergence of H pylori resistance to metronidazole and clarithromycin, further research to clarify the role of bismuth compounds is required.

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A 17-bed intensive care unit in a university teaching hospital. PATIENTS. In phase 1 there were 736 patients and in phase 2737. Those in the two phases were comparable in age and reason for admission; clinically significant gastrointestinal bleeding rates did not differ between the two phases, but patients in phase 2 were more severely ill.

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The effects of pirenzepine and ranitidine alone and combined, on gastric acid secretion and gastrin release stimulated by liquid peptone meal were evaluated in 12 duodenal ulcer patients. Six patients received placebo and ranitidine 150 mg per os and the other six patients were given placebo, pirenzepine 50 mg and pirenzepine 50 mg plus ranitidine 150 mg per os, according to randomized sequences. In the first experiment ranitidine markedly inhibited (69%) gastric acid secretion for entire two hours period (p less than 0.01). In the second experiment acid secretion after pirenzepine, was reduced by 39% while the combination of pirenzepine plus ranitidine almost completely inhibited the meal stimulated acid secretion (99%). Mean integrated gastrin responses after pirenzepine and ranitidine alone as well as pirenzepine plus ranitidine were not significantly different from placebo. The results of these studies show that in duodenal ulcer patients, the simultaneous block of muscarinic and H2-receptors, suppresses meal stimulated gastric acid secretion, without affecting gastrin release. This therapeutic combination might be used in clinical situations (non-responders, Zollinger-Ellison syndrome) in which complete inhibition of gastric acid secretion is needed.

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Reactive oxygen species (ROS) have been implicated in the etiology of indomethacin-induced gastric mucosal damage. This study investigated ascorbic acid (vitamin C)'s protective effects against oxidative gastric mucosal damage induced by indomethacin. Ascorbic acid is a powerful antioxidant because it can donate a hydrogen atom and form a relatively stable ascorbyl free radical. We have investigated alterations in the levels of myeloperoxidase, antioxidant system enzymes (glutathione S-transferase, superoxide dismutase, glutathione reductase, catalase, glutathione peroxidase), lipid peroxidation and glutathione, as markers for ulceration process following oral administration of ascorbic acid, famotidine, lansoprazole, and ranitidine in rats with indomethacin-induced ulcers. In the present study, we found that (1) ascorbic acid, famotidine, lansoprazole and ranitidine reduced the development of indomethacin-induced gastric damages; (2) the administration of indomethacin caused a significant decrease in the levels of superoxide dismutase, glutathione peroxidase, glutathione S-transferase and glutathione, and an increase in the lipid peroxidation level; (3) the administration of ascorbic acid reversed the trend, inducing a significant increase of these enzymes' levels and a reduction in lipid peroxidation level in tissues; and (4) catalase, glutathione reductase and myeloperoxidase activities, increased by indomethacin, were found to be lower in the ascorbic acid, famotidine, lansoprazole and ranitidine-treated groups. The results indicate that the gastroprotective properties of ascorbic acid could be related to its positive effects on the antioxidant system and myeloperoxidase activity in indomethacin-induced gastric ulcers in rats.

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Peptic ulcers can be treated successfully with antisecretory drugs and drugs which have a protective effect. Thanks to their good tolerance and a form of administration acceptable to patients, the H2-receptor antagonists have won a leading position amongst the other ulcer therapeutics. It remains to be seen whether the substituted benzimidazoles will develop into a serious competitor. Until now the clinical experiences with the prostaglandins in the treatment of ulcers are not very encouraging.

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Stress-related gastric mucosal damage is a common occurrence in intensive care unit (ICU) patients. Because of the significant morbidity and mortality associated with this mucosal damage, many ICU patients routinely receive prophylactic therapy, usually with histamine H2-receptor antagonists (H2RAs). Gastric acid secretion occurs in a circadian pattern, with late afternoon and evening surges. H2RAs by continuous infusion may control this uneven pattern of secretion more effectively than H2RAs given by bolus injection. More studies are needed to identify the target ICU population for prophylactic treatment.

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A 17-year-old boy who developed a symptomatic duodenal ulcer at 10 years of age with melena, and was then treated continuously for 6 years with ranitidine therapy that only partially controlled symptoms and peptic lesions, came to us with vomiting due to duodenal bulb stenosis and active ulcer. Four months of omeprazole (40 mg/die o.m.) did not modify the endoscopic picture. The diagnosis of H. pylori infection and its treatment with triple therapy led to the cure of both duodenal ulcer and bulbar stenosis. Afterwards he remained asymptomatic without any lesions or complications for 18 months. This case illustrates that H. pylori eradication: a) is able to cure refractory duodenal ulcer; b) resolves severe complications such as duodenal stenosis.

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Gastroesophageal reflux (GER) and tracheal aspiration of acid may increase morbidity and mortality in patients undergoing thoracotomy. This randomized, double-blinded, placebo-controlled study demonstrates frequent incidences of both acid GER and tracheal acid aspiration during surgery that are significantly reduced by premedication with ranitidine.

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Numerous environmental and genetic factors have been implicated in the pathogenesis of peptic ulcer disease. Although the cause of this disorder has not been established, acid pepsin has been acknowledged at least as a permissive factor in its development. More important, inhibition of nocturnal or 24-hour intragastric acidity is predictably associated with ulcer healing. Famotidine 40 mg at bedtime maintains approximately one-third of pH readings at or above 3.5, reduces pepsin activity, and has no adverse effect on mean total serum gastric concentrations after one week of therapy. In addition, the effect of this dose of famotidine is comparable to ranitidine 300 mg at bedtime and predicts comparable rates of ulcer healing. Thus, monitoring of intragastric pH levels may be useful in identifying potent healers of peptic ulcer disease and in selecting optimal doses or timing of drug administration. Studies of famotidine using such measurements have suggested that this new H2-receptor antagonist is comparable to ranitidine in the healing of duodenal ulcers.

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To evaluate the clinical efficacy of available therapies directed towards Helicobacter pylori eradication.

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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 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.

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We report a patient--a 42-year-old man--who had suffered from recurrent duodenal ulcer for about 20 years. Successful curative therapy for Helicobacter pylori infection was performed for 2 weeks with new triple omeprazole, anoxicillin, clarithromycin (OAC) treatment in October 1995, and cure of the infection was repeatedly confirmed by histology, culture, and the 13C urea breath test. One month after the curative therapy, recurrence of a small duodenal ulcer was observed and in February another duodenal ulcer and reflux esophagitis occurred, with severe symptoms, despite the continuous administration of ranitidine. None of the examinations to reconfirm cure of the infection revealed the presence of H. pylori. As the patient experienced continual psychological stress and smoked more frequently during the recurrent episode and had not used nonsteroidal anti-inflammatory drugs, stress and smoking appeared to play important roles in the relapse of duodenal ulcer in this patient after cure of H. pylori infection.

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Combination preparation plays an important role in clinical treatment because of its better and wider curative synergism and weaker side effects. However, the existence of incompatibility between active ingredients or between active ingredients and excipients presents a serious obstacle in the preparation of such combination solid dosage forms. In this study, aspirin and ranitidine hydrochloride, between which there existed a chemical interaction, were selected as model drugs. Aspirin powders without any additives were granulated with hydroxypropyl methyl cellulose (HPMC) water solution as a binder using a Wurster coating apparatus and the operation conditions were optimized by Artificial Neural Network (ANN) analysis. Under these conditions, the aspirin granules prepared showed good flowability and compressibility. On the other hand, ranitidine hydrochloride was coated with Aquacoat (ethyl cellulose aqueous dispersion) after preliminary granulation with the Wurster coating apparatus. The aspirin granules and coated ranitidine hydrochloride particles were compressed into tablets with suitable excipients. The combination tablets showed good dissolution, content uniformity and improved stability of active ingredients.

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Levodopa (l-dopa) remains the best drug in the treatment of Parkinson's disease (PD). Unfortunately, long-term l-dopa caused motor complications, one of which is l-dopa-induced dyskinesia (LID). The precise mechanisms of LID are not fully understood. We have previously reported that ranitidine could reduce LID by inhibiting the activity of protein kinase A pathway in a rat model of PD. It is demonstrated that neurotransmitters such as γ-aminobutyric-acid (GABA) and glutamate (Glu) are also involved in the expression of LID. But whether ranitidine could reduce LID by remodeling the neurochemical changes is unknown.

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Polymorphs of a similar purity yielded virtually identical moisture sorption profiles. In contrast, samples containing higher levels of impurities had both enhanced moisture sorption below RH0 and a lowered value of RH0.

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Echocardiography laboratory at a university hospital.

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When HL-60 cells were stimulated with histamine, a significant differentiation of the cells toward neutrophils was elicited. Histamine increased phagocytic activity, but it reduced myeloperoxidase activity of HL-60 cells. Histamine-induced differentiation in HL-60 cells was inhibited not only by H2 antagonists, such as cimetidine, ranitidine and famotidine, but also by an inhibitor of protein kinase A (A kinase), KT-5720. Histamine increased the cAMP level and A kinase activity in HL-60 cells; both increases preceded the cell differentiation. Histamine also enhanced phosphorylation of a 160 kD protein in HL-60 cells, while H2 antagonists and KT-5720 inhibited this phosphorylation. The results of the present study indicate that an activation of A kinase via H2 receptor stimulation may cause the phosphorylation of a 160 kD protein and that this phosphorylation is probably involved in the process leading to differentiation of HL-60 cells.

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This study was to investigate the gastrokinetic activity of Morinda citrifolia aqueous fruit extract (AFE) in human subjects by examining the GI absorption of ranitidine, a putative indicator of GI motility and to elucidate its possible gastrokinetic mechanism of action in rats.

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The aim of this study was to compare in an open trial the efficacy of 2 x 500 mg clarithromycin + 2 x 1000 mg amoxicillin + 40 mg pantoprazole/day given for 7 days (I. group, 48 cases), with that of 2 x 500 mg clarithromycin + 2 x 400 mg ranitidine bismuth citrate/day given for 14 days (II. group, 51 cases). The diagnosis of peptic ulcer was established endoscopically. HP infection was confirmed the modified Giemsa stain and rapid urease test. After eradication all patients were given 2 x 150 mg ranitidine for one month. Controls were performed 4-6 weeks after eradication. Peptic ulcer healing was proven in the group I in 93.0% and in the group II in 91.6% (p > 0.05). On intention-to-treat basis, HP was eradicated in 80.3% (confidence interval, CI: 73-92.7%) in the I. and 80.3% (confidence interval: 76-95%) in the II. group (p > 0.05). Per protocol analysis revealed eradication rates of 88.3% (CI: 81-97.6%) and 85.4% (CI: 80-97%) (p > 0.05). Side effects were recorded in 9.5% and 14.5% of the cases. Both regimens were equally effective in the eradication of HP and healing of peptic ulcers.

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The efficiency of stress ulcer prophylaxis in the prevention of gastrointestinal bleeding in critically ill patients has led to its widespread use. The lower incidence of stress ulcer bleeding, the side-effects and the cost of the prophylaxis have made it necessary targeting this preventive therapy to those patients most likely to benefit. Metaanalysis of studies on patients who received no stress ulcer prophylaxis showed few critically ill patients with important gastrointestinal bleeding.

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Currently, ranitidine dose recommendations are based on children's weights. However, our findings suggest that a dosing scheme that takes into consideration both weight and cardiac failure/surgery would be more appropriate in order to avoid administration of higher or more frequent doses than necessary.

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To assess the cost effectiveness of a multidrug prepackaged regimen for Helicobacter pylori, the Hp-PAC (lansoprazole 30mg, clarithromycin 500 mg, amoxicillin 1 g, all twice daily), relative to alternative pharmacological strategies in the management of confirmed duodenal ulcer over a 1-year period from 2 perspectives: (i) a strict healthcare payer perspective (Ontario Ministry of Health) excluding the patient copayment; and (ii) a healthcare payer perspective including the patient copayment.

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1 Ranitidine single dose pharmacokinetics and absolute bioavailability have been studied in five healthy male volunteers. Following an overnight fast, 150 mg was given intravenously as a bolus injection or orally as a tablet formulation to each subject on separate occasions. 2 Following intravenous administration, plasma levels declined biexponentially. The mean (+/- s.d.) distribution half-life (t 1/2 alpha) was 6.6 +/- 1.6 min; plasma half-life (t 1/2 beta) was 1.7 +/- 0.2 h; the volume of distribution (V) was 96 +/- 9 1; total body clearance (CL) was 647 +/- 94 ml/min and renal clearance (CLR) 520 +/- 123 ml/min. 3 Following oral administration plasma levels showed a bimodal pattern with a first peak at 1.1 +/- 0.4 h and a second peak at 3 +/- 0 h. The absolute availability was 60 +/- 17%. The plasma half-life (t 1/2) of 2.3 +/- 0.4 h was significantly longer (P less than 0.05) after oral than after i.v. administration. 4 Renal excretion of unchanged ranitidine accounted for 79 +/- 9% of the dose after i.v. administration and for 27 +/- 7% after oral administration. 5 Our results suggest a more extensive biotransformation of ranitidine and biliary excretion of metabolites after oral administration while i.v. administration ranitidine is preferentially excreted unchanged in the urine.

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Acid secretion inhibitors are of dubious value to most patients with functional dyspepsia but might be effective in a subset. The aims of the trial were to compare the effect of ranitidine with that of placebo in selected subsets of patients.

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Parietal cell sensitivity is increased in patients with active duodenal ulcer. It has been shown to increase in healthy volunteers after a 4-week treatment with H2-receptor blockers. Metaanalyses of therapeutic trials have indicated that time to first relapse was longer after ulcer healing with prostaglandins (PG) than after healing with H2-receptor blockers, which might be due to a different effect of the two treatments on parietal cell sensitivity. OBJECTIVES--To study, in healthy volunteers, basal gastric acid secretion, acid secretory responses and parietal cell sensitivity to histamine before and after a 4-week treatment with enprostil (E) and ranitidine (R). METHODS--This was a randomized double-blind double-dummy crossover study. Twelve male healthy volunteers (22-44 years) were randomly assigned to receive a 4-week treatment with either E (35 micrograms bid) or R (150 mg bid). After a 2-month washout period, they were crossed to the alternate treatment. Basal acid output (BAO), acid secretory responses to low-dose histamine infusion (histamine dihydrochloride 2.5 micrograms/kg/h) (LDAO), to a high-dose histamine infusion (25 micrograms/kg/h) (HDAO) and parietal cell sensitivity (PCS = LDAO/HDAO x 100) were measured 24 hours before the first administration and 72 hours after the last administration of each medication. RESULTS--All secretory parameters were similar before treatment with E and R. As compared to pretreatment values: a) HDAO tended to increase after both treatments (NS); b) LDAO (m +/- sem) slightly increased after R (18.4 +/- 2.6 vs 13.9 +/- 3.3 mEq) (NS) but not after E (12.5 +/- 1.8 vs 13.2 +/- 1.9 mEq); c) PCS (m +/- sem) was unchanged after R (36 +/- 4 vs 33 +/- 6) but decreased after R (30 +/- 6 vs 36 +/- 0.5; P < 0.02). When secretory parameters after treatment with R and treatment with E were compared, the difference was significant for LDAO (P < 0.02) and PCS (P < 0.05). CONCLUSIONS--If also found in patients with duodenal ulcer disease, these results might, at least partly, explain the lesser propensity of the ulcers to relapse early after healing with PG than after healing with H2-receptor blockers. However enprostil has been with-drawn from the market and it is now well established that one factor influencing the relapse rate is the efficiency of the treatment given to achieve ulcer healing in eradicating Helicobacter pylori. Consequently, the interest of our results is presently mostly physiological.

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Helicobacter pylori is the causative agent of gastritis and a co-agent in other gastroduodenal diseases. Gastroduodenal ulcer and MALT-lymphoma in particular, regress when patients are administered antimicrobial agents to eradicate infection. Sometimes eradication is not definitive and is difficult to check. The aim of our study was to test the antimicrobial activity of omeprazole on H. pylori in comparison with ampicillin and other anti-H2 drugs (ranitidine and famotidine), and to evaluate their interference with bacterial adhesion of H. pylori. We also compared results of the agar dilution antibacterial sensitivity test on H. pylori to those obtained using a bacteria adherence to cell monolayers model, to see if drug activity was different against adhered bacteria. We evaluated omeprazole and ampicillin MIC90s (minimum inhibitory concentrations) against 20 H. pylori isolates by traditional agar dilution method and by exposing previously adhered bacteria to an Hep-2 monolayer to different drug concentrations. The activity against bacteria adhered to cell lines was evaluated by counting viable adhered bacteria after 1, 6, 12 hours of contact with drug. Interference with adherence to Hep-2 cells was also tested. Omeprazole and ampicillin MICs were comparable to other findings (omeprazole MIC90 was 12.5 microg/ml and ampicillin MIC90 was 0.016 microg/ml), while higher concentrations were necessary (4 x MIC90) against adhered bacteria. These findings suggest that MICs evaluated with traditional assays can have different predictivity than tests on adhered H. pylori.

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Basophils are circulating granulocytes, best known as effector cells in allergic reactions. Recent studies in mice suggest that they might also participate in the suppression of chronic inflammation. The aim of this study was to assess the ability of purified human basophils to modulate monocyte responses upon IL-33 and IgE triggering. Activation of human basophils with IL-33 induced the production of IL-4 and the release of histamine, and enhanced their IgE-mediated activation. In addition, basophils triggered with IL-33 and anti-IgE significantly suppressed the LPS-induced production of the proinflammatory cytokine TNF-α and the upregulation of the costimulatory molecule CD80 by monocytes. These effects were mainly explained by the release of histamine, as they could be inhibited by the histamine receptor 2 antagonist ranitidine, with a smaller contribution of IL-4. In contrast, basophil-derived IL-4 and histamine had opposing effects on the expression of the inhibitory Fc γ receptor IIb and the production of IL-10 by monocytes. Our data show that basophils can influence monocyte activation and suggest a previously unrecognized role for human basophils in the modulation of monocyte-mediated immune responses, through the balanced secretion of histamine and IL-4.

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A double-blind, multicenter, randomized study was performed in 75 patients with endoscopically documented reflux esophagitis. Patients were randomly given 1 g sucralfate four times a day or the combination of sucralfate three times a day and 300 mg ranitidine after dinnertime. Endoscopy was performed at the beginning of the study, after 8 weeks, and, if, the reflux esophagitis was not healed, after 16 weeks. Four patients had to be excluded from evaluation; 71 patients could therefore be evaluated. Both groups showed symptomatic improvement to similar extents. Endoscopy showed symptomatic improvement in 67% of the patients treated with sucralfate and in 74% of the combination therapy group. Complete healing or Savary-Miller stage 1 was seen in 26.5% and in 31.4%, respectively. We conclude that sucralfate monotherapy in patients with milder forms of reflux esophagitis is comparable with a combination of sucralfate during the day and ranitidine after dinnertime. This study does not support the commonly used combination of sucralfate and H2-receptor antagonists in reflux esophagitis.

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Histamine type-2 receptor antagonists (H-2RA) have been used chronically to prevent dyspepsia in cancer patients subjected to immunotherapy with chronic indomethacin (Indo) and intermittent IL-2 in our cancer centre. We tested the effects of these agents during immunotherapy of C3H/HeJ mice transplanted s.c. with 5 x 10(5) C3L5 mammary adenocarcinoma cells. Tumor-transplanted mice were divided into groups receiving: (1) Indo (14 micrograms/ml); (2) H-2RA, i.e. (a) ranitidine at 28.6 micrograms/ml (Ran-lo) or 143 micrograms/ml (Ran-hi), or (b) famotidine (Fam) at 4.3 micrograms/ml, or (c) cimetidine (Cim) at 107 micrograms/ml, all in the drinking water on days 5-24; (3) IL-2 (1.5 x 10(3) Cetus U i.p. every 8 h on days 10-14 and 20-24); (4) combinations of H-2RA + Indo; or (5) combinations of H-2RA + Indo + IL-2. Animals were killed on day 24 for examination of primary s.c. tumor growth, secondary lung metastasis and splenocyte cytotoxicity against YAC-1 lymphoma cells (51Cr release assay). Results revealed: (1) primary tumor growth was reduced in mice treated with Fam + Indo, Indo + IL-2 and any of the H-2RA + Indo + IL-2 (no difference observed within the last two groups); (2) lung metastases decreased in mice treated with IL-2 alone, Indo + IL-2, and Indo + IL-2 + Ran-hi; (3) splenic cytotoxicity was suppressed in tumor-bearing controls, with partial restoration seen in Ran (both doses), Ran-lo + Indo, Ran-lo + Indo + IL-2, and Cim + Indo + IL-2 treated groups. Nearly complete restoration was seen in Cim, Cim + Indo, Indo + IL-2, Ran-hi + Indo + IL-2, and Fam + Indo + IL-2 groups. Thus, addition of H-2RA did not alter the overall therapeutic efficacy of the standard Indo + IL-2 tumor immunotherapy.

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zantac generic target 2015-01-02

Ranitidine kinetics in renal failure were evaluated in six patients undergoing continuous ambulatory peritoneal dialysis (CAPD). On separate occasions each patient received either 50 mg intravenously (i.v.) or 150 mg orally of ranitidine HCl. Following i.v. administration, the plasma concentration vs time curve was best described by a two compartment model with firstorder elimination. The mean +/- SD distribution and elimination rate constants were 2.47 +/- 0.78 and 0.098 +/- 0.013 h, respectively. The area under the serum concentration vs time curve after the i.v. dose was 5979 +/- 2870 micrograms X h X l-1, resulting in a mean volume of distribution of 76.8 l and a total body clearance of 126 ml X min-1. Following oral administration the observed maximum plasma concentration was 904 +/- 483 micrograms X l-1 at 4.2 +/- 1.8 h, and the bioavailability was 69.7 +/- 35.6%. The peritoneal clearance of ranitidine was 3.2 +/- 0.7 and 2.6 +/- 0.6 ml X min-1 for buy zantac online the i.v. and oral groups, respectively. The amount of drug removed by dialysis was 561.2 +/- 336.2 micrograms for the i.v. and 1197.1 +/- 602.3 micrograms for the oral group. Four patients in the i.v. group had urine output during the study period with renal ranitidine clearance values of 9.9 +/- 9.9 ml X min-1. Two patients in the oral group had urine output and corresponding renal ranitidine clearance values of 5.1 and 20.1 ml X min-1. A dosage regimen for ranitidine is proposed based on ranitidine kinetics in patients undergoing CAPD.

zantac 75 dosage 2016-06-14

Thirty-six patients in whom an asymptomatic duodenal ulcer had been detected endoscopically were followed up clinically and endoscopically during the following months. Ten of the patients were receiving either no treatment or placebo, and 26 patients were receiving maintenance treatment with either 150 mg ranitidine or 400 mg cimetidine at night. Treatment remained unchanged during the follow-up period. The cumulative annual rate of spontaneous healing was approximately one quarter, whether or not patients were receiving active maintenance therapy. However, the likelihood of developing symptoms during the year after detection of the asymptomatic ulcer was significantly greater in those patients receiving no treatment or placebo (77%) than in those receiving active maintenance therapy (27%). One patient, receiving no treatment, bled from his ulcer during the follow-up period. We conclude that routine endoscopic reexamination, to detect asymptomatic ulcer recurrences in patients receiving buy zantac online maintenance treatment for duodenal ulceration, is probably unnecessary, since the recurrences rarely cause clinical problems, despite prolonged failure to heal.

zantac iv dose 2015-05-11

The effect of histamine and of some H2-antagonists on isolated gastric mucosal preparation from immature (14-18 days) rats, was investigated. Basal secretion varied, in our experimental conditions, between 1.06 and 3.54 mumol cm-2 h-1, reaching higher values (approximately 4.6 mumol cm-2 h-1) only in a small percentage of animals (10%). Histamine exerted a concentration-dependent stimulation of acid secretion in concentrations varying between 2 X 10(-6) and 1.6 X 10(-4) M. The response to histamine was competitively antagonized by ranitidine (pA2 value = 6.78) and by 4(5)-(4- isopropylaminomethyleniminophenyl ) imidazole (compound marked DA 4577) (pA2 value = 7.37). Oxmetidine acted as a competitive antagonist only for concentrations as low as 10(-8) M; higher concentrations (10(-7) and 10(-6) M) determined a non-competitive inhibition. Ranitidine and compound marked DA 4577 did not affect basal secretion up to concentrations of 3 X 10(-4) M. On the contrary oxmetidine exerted a concentration-dependent inhibition starting from 10(-5) M. Since in our experimental conditions the role of calcium ions in the regulation of basal secretion could not be established, the mechanism of action of oxmetidine was not completely clarified, even if an interference in the utilization of calcium ions may be suggested. In any case it is deemed of interest that this H2-antagonist was the only buy zantac online compound capable of inducing a reversible complete inhibition of basal acid secretion (only KSCN, in very high concentrations, had a similar behaviour).

zantac drug interactions 2015-12-18

The effect of perioperative buy zantac online ranitidine on postoperative change in plasma interleukin-6 (IL-6) and serum C-reactive protein (CRP) levels was assessed in 23 women undergoing elective abdominal hysterectomy. The patients were randomized to receive intravenous ranitidine, 100 mg twice a day from skin incision, for two days, followed by oral ranitidine, 150 mg twice a day, for a further three days, or no ranitidine. Interleukin-6 and CRP were analyzed in plasma and serum, respectively, drawn preoperatively and six, 24, 48, and 120 hours after skin incision.

zantac 300mg tablets 2015-06-25

In chronic intractable diarrhea, colonic or duodenal biopsy specimens may appear unremarkable on routine hematoxylin- buy zantac online eosin staining, but increased mast cells may be demonstrated by immunohistochemistry for mast cell tryptase, with the novel term mastocytic enterocolitis describing this condition. Similar increases in mast cells are not apparent in control populations or in patients with other specific diseases that cause chronic diarrhea. The cause of the increased mast cells remains to be elucidated.

cold medicine zantac 2016-04-13

A traditional Chinese Medicine (TCM) formula, HZJW, has been applied in clinics in China for gastrointestinal disorders. However, the therapeutic mechanism underlying its efficacy and safety remained to be defined. The present investigation was undertaken to evaluate the formula HZJW for its gastroprotective potential, possible effect on Helicobacter pylori along with safety to justify its anti-ulcer action and safe buy zantac online clinical application.

zantac po dosing 2017-08-02

Chronobiology is devoted to the study of biological rhythms. It is buy zantac online possible that a given medication may be therapeutic and safe when administered at some time, but subtherapeutic or poorly tolerated at another.

8 mg zantac 2016-01-18

1. Acid secretion for each dog has reached a near maximum (100%) at the 6th samples, 90 min after the intravenous infusion of histamine (10 mu ghr-1, or approximately equal to 0.3 mghr-1). 2. 0.5 mgkg-1 buy zantac online Cimetidine had produced a mean inhibition of 47% on the stomach. 3. 0.1 mgkg-1 Ranitidine (D 14,951) could only inhibit a maximum of 28%, and the secretion had return to normal in just 30 min. 4. 0.025 mgkg-1 Tiotidine (D 15,104) had inhibited 53% acid secretion within 15 min of exposure. Recovery was quite similar to that of Cimetidine, at 150 min. 5. At a dosage one fifth of Cimetidine (0.1 mgkg-1) D 15,144 had depressed 35% of acid secretion at the first 15 min. The inhibition is gradually increased to about 43% (at 30 min), and was maintained for the next 105 min.

zantac chewable tablets 2017-05-24

Neuroanatomical studies have revealed a direct hypothalamocerebellar histaminergic pathway, and our previous studies have demonstrated an excitatory effect of histamine on granule and Purkinje cells of the cerebellar cortex. In this study, we further investigated the effect of histamine on the neuronal firing of cerebellar interpositus nucleus (IN) by using cerebellar slice preparations. Eighty-seven IN cells were recorded from 38 slices. The vast majority of the cells responded to histamine stimulation with an excitatory response (79/87, 90.8%), and the rest of them showed no reaction (8/87, 9.2%). The histamine-induced excitation was not blocked by application of low-Ca(2+)/high-Mg(2+) medium (n=8), supporting a direct postsynaptic action of histamine. The histamine H(2) receptor antagonist ranitidine effectively blocked the excitatory response of IN cells to histamine (n=23), but the histamine H(1) receptor antagonist triprolidine could not significantly block the histamine-induced excitation, or only very slightly decreased the excitatory effect of histamine on the cells (n=21). On the other hand, the highly selective histamine H(2) receptor agonist dimaprit mimicked the excitatory effect of histamine on IN cells and the dimaprit-induced excitation was also blocked by ranitidine (n=14). Successively perfusing slices with the medium containing ranitidine and triprolidine, respectively, we found that ranitidine exhibited the same blocking effect on the dimaprit-induced excitation, but triprolidine had no such effect (n=8). Moreover, the histamine H(1) receptor buy zantac online agonist 2-pyridylethylamine did not show any effect on the IN cells (n=9). These results demonstrate that histamine excites cerebellar IN cells via the histamine H(2) receptor mechanism. Together with our previous results, we suggest that the hypothalamocerebellar histaminergic fibers may modulate neuronal activities of the cerebellar cortex and deep nuclei in parallel. The significance of the excitatory effect of histamine on the cerebellar nuclear cells is discussed.

zantac dosing directions 2015-01-25

Neuropathic pain was induced in rats by partial ligation of the buy zantac online left sciatic nerve, and changes in the extracellular concentration of histamine in the right striatum were examined by a microdialysis procedure 2 weeks later. The nociceptive threshold was determined with von Frey tests, and effects of histaminergic ligands were examined.

zantac suspension 2015-08-31

In the experiments performed on Wistar rats it was found that histamine (0.05 and 0.5 mg/kg i.p.) caused an acceleration of the turnover of serotonin (5-HT) in the stomach. After the lowest dose of ranitidine (3 mg/kg i.p.) a decrease in the rate of 5-HT turnover in the stomach was observed, whereas the higher doses (15.0 and buy zantac online 30 mg/kg i.p.) accelerated the turnover of this amine. In the duodenum, both doses of histamine accelerated the turnover of 5-HT, however, ranitidine in all doses induced a reduction in the rate of 5-HT turnover in this part of the alimentary tract. In the intestine, both doses of histamine enhanced the turnover of 5-HT but after all doses of ranitidine a decrease of the turnover was observed. The blockade of histamine H2 receptors with ranitidine did not completely abolish the effects of histamine on the 5-HT system, in the parts of the rat digestive system studied which suggests also an indirect activity of other receptors in presented observations. In the rat brain, an acceleration of the turnover of 5-HT after both doses of histamine was found. However, ranitidine only reduced the rate of 5-HT turnover at the lowest dose. In animals treated with ranitidine (15 mg/kg i.p.) for three days, histamine did not produce any change in the turnover of 5-HT in rat brain. These experiments show, that in the alimentary tract a relationship exists between histaminergic and serotoninergic systems.

zantac renal dosing 2015-12-13

The 1-day survey (May–July 2014) regarded 220 newborn infants admitted to 36/107 Italian neonatal intensive care units: 191 prematures and 29 born at term. In total, 720 prescriptions (corresponding to 79 different drugs) were analysed: 191 (26.5 %) followed the terms of the product license, 529 (73.5 %) were off-label or unlicensed: 193/220 newborns (87.7 %) received at least one off-label/unlicensed prescription. Antiinfectives were the most common medicine used, followed by respiratory drugs and antianaemics; in an off-label manner buy zantac online , the most common was cardiovascular and central nervous system (CNS) drugs, gastrointestinals and antiinfectives. The most common categories of off-label use were age (34.4 %) and dosing frequency (20.6 %). Compared to ISN practical guide, prescriptions adhered more frequently to indications (100 % for ampicillin/sulbactam, >80 % for ampicillin, fluconazole, fentanyl, ranitidine and vancomicin).

zantac pediatric dose 2015-02-20

In conscious rats implanted with a lateral brain ventricle cannula, the effect of intracerebroventricular (i.c.v.) injection of histamine (2.5, 10, and 40 μg), and chlorpheniramine and ranitidine at the same doses of 5, 20, and 80 μg were investigated on visceral pain. Visceral nociception induced buy zantac online by intraperitoneal (i.p.) injection of acetic acid (1 mL, 1%), and the number of complete abdominal wall muscle contractions accompanied with stretching of hind limbs (writhes) were counted for 1 h.

zantac cost 2017-03-10

Adding ranitidine enhanced P2Y(12)-mediated platelet reactivity to ADP assessed by the PRI (mean PRI+/-SEM: before ranitidine 28+/-5%; after ranitidine 37+/-5%, p=0.0025). Similarly, prostaglandin E1 (PGE(1))-mediated inhibition of ADP-induced aggregation was abrogated in the presence of ranitidine (Agg(max)+/-SEM: before PGE(1) 41+/-2%; after PGE(1) 29+/-2 buy zantac online %, p<0.01 vs. before PGE(1); after PGE(1)+ranitidine 42+/-2%, p<0.01 vs. after PGE(1)).

zantac dosage infants 2015-04-14

The efficacy of anti-Helicobacter pylori treatment Anafranil Reviews and cytoprotective drugs in H. pylori-positive and -negative non-ulcer dyspepsia (NUD), respectively, is debatable.

zantac dosing infants 2016-12-07

Triple therapy regimens including two antibiotics plus acid suppression have become the new standard therapy in Helicobacter pylori eradication because of success rates of about 90%. However, these regimens are still costly, duration is about one week or less, and side-effects are not negligible. We therefore evaluated a new Propecia Cost Usa quadruple therapy, because theoretically a shorter duration of treatment may result in reduced costs, fewer side-effects, and possibly in a lower potential for antibiotic resistances.

zantac mg 2017-08-12

To estimate the pharmacokinetic (PK) properties of posaconazole in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) undergoing Zyrtec Generic Dosage chemotherapy in a clinical setting.

toddler zantac dosage 2017-02-05

Even though conventional systemic doses of cimetidine and other histamine H(2) antagonists display minimal brain penetration, central nervous system (CNS) effects (including seizures and analgesia) have been reported after administration of these drugs in animals and man. To test the hypothesis that cimetidine-like drugs produce these CNS effects via inhibition of GABA(A) receptors, the actions of these drugs were studied on seven different, precisely-defined rat recombinant GABA(A) receptors using whole-cell patch clamp recordings. The H(2) antagonists famotidine and tiotidine produced competitive and reversible inhibition of GABA-evoked currents in HEK293 cells transfected with various GABA(A) receptor subunits (IC(50) Aciphex Tablets values were between 10-50 microM). In contrast, the H(2) antagonist ranitidine and the cimetidine congener improgan had very weak (if any) effects (IC(50) > 50 microM). Since the concentrations of cimetidine-like drugs required to inhibit GABA(A) receptors in vitro (greater than 50 microM) are considerably higher than those found during analgesia and/or seizures (1-2 microM), the present results suggest that cimetidine-like drugs do not appear to produce seizures or analgesia by directly inhibiting GABA(A) receptors.

drug zantac 2016-04-17

Eighty patients with endoscopically proven active duodenal ulcer were randomized to take ranitidine or lansoprazole for 4-8 wk, Topamax 25 Mg together with clarithromycin 250 mg b.i.d. and metronidazole 500 mg for the first 2 wk. Endoscopic controls, as well as histological and urease tests for H. pylori, were performed at entry and after 4 and 8 wk.

zantac pediatric dosing 2016-06-10

To examine Lopid Tabs and compare the effects of omeprazole, lansoprazole, and ranitidine on the DNA synthesis of peripheral blood mononuclear cells.

zantac drug 2015-03-15

The possible role of brain histamine in the release of prolactin, ACTH and corticosterone following acute restraint, was pharmacologically evaluated in adult male rats. Fifteen min of restraint caused marked increases in the plasma levels of these hormones. alpha-Fluoromethyl histidine (FH), a histidine decarboxylase inhibitor which depleted hypothalamic histamine, inhibited the enhancement of plasma prolactin levels. In contrast, plasma ACTH levels were not modified. FH treatment decreased plasma corticosterone concentrations in animals submitted to stress or in rest; this suggests a direct action of FH on the adrenal. Intraventricular (IVT) injection of ranitidine (H2 antagonist) blunted the prolactin response to restraint stress whereas its systemic administration had no effect. On the contrary, pyrilamine (H1 antagonist) given systemically decreased slightly, but significantly, the prolactin rise but when injected IVT it was ineffective. Pyrilamine was also unable to affect the ranitidine action. ACTH and corticosterone levels in plasma of restrained rats were not modified by the histamine antagonists. It is concluded that histamine is Cymbalta Canada Cost involved, mainly through central H2 receptors, in the enhancement of plasma prolactin levels produced by an acute stress. The failure of both antihistaminic compounds and a histamine depletor to alter the ACTH stimulation suggest that histamine has no participation in the hypophysio-corticoadrenal response to acute restraint.

zantac 500 mg 2016-04-10

Patients were prospectively randomized to treatment with total Aldactone Reviews Ascites parenteral nutrition, either alone, with sucralfate, or with ranitidine.

zantac brand name 2015-03-11

Of the 94 patients restudied, with a follow-up period Eulexin 500 Mg range of 48-96 months or a total of 549.8 yr, only two (2.2%) were again H. pylori positive. This gives an effective reinfection rate of 0.36% per patient year. In the two H. pylori-positive patients, one had normal mucosa endoscopically, whereas duodenitis without active ulceration was present in the other. The former was asymptomatic, whereas the latter patient was using ranitidine daily for symptom control.

zantac 600 mg 2016-06-10

A silicone stent of 7-, 9-, or 12.7-mm external diameter is built coaxially on a Depakote Sprinkle Capsules nasogastric tube that guarantees the correct position. The 2 ends are tailored to allow food passage between stent and esophageal wall. All patients received dexamethasone (2 mg/kg per day) for 3 days and ranitidine/proton-pump inhibitors. Study approval was obtained from our ethical board.

zantac dosing 2016-04-10

Nociceptin/orphanin FQ (N/OFQ) is the endogenous ligand for the N/OFQ peptide receptor (NOP). N/OFQ causes hypotension and vasodilation, and we aimed to determine the role of histamine in inflammatory microvascular responses to N/OFQ. Male Wistar rats (220-300 g, n = 72) were anesthetized with thiopental (30 mg/kg bolus, 40-90 mg x kg(-1) x h(-1) iv), and the mesentery was prepared for fluorescent intravital microscopy using fluorescein isothiocyanate-conjugated BSA (FITC-BSA, 0.25 ml/100 g iv) or 1 microm fluorescently labeled microspheres. N/OFQ (0.6-60 nmol/kg iv) caused hypotension (SAP, baseline: 154 +/- 11 mmHg, 15 nmol/kg N/OFQ: 112 +/- 10 mmHg, P = 0.009), vasodilation (venules: 23.9 +/- 1.2 microm, 26.7 +/- 1.2 microm, P = 0.006), macromolecular leak (interstitial gray level FITC-BSA: 103.7 +/- 3.4, 123.5 +/- 11.8, P = 0.009), and leukocyte adhesion (2.0 +/- 0.9, 15.2 +/- 0.9/100 microm, P = 0.036). Microsphere velocity also decreased (venules: 1,230 +/- 370 microm/s, P = 0.037), but there were no significant changes in blood flow. Flow cytometry measured a concurrent increase in neutrophil expression of cd11b with N/OFQ vs. controls (Geo mean fluorescence: 4.19 +/- 0.13 vs. 2.06 +/- 0.38, P < 0.05). The NOP antagonist [Nphe(1),Arg(14),Lys(15)]N/OFQ-NH(2) (UFP-101; 60 and 150 nmol/kg iv), H Levaquin 1000mg Dose (1) and H(2)antagonists pyrilamine (mepyramine, 1 mg/kg iv) and ranitidine (1 mg/kg iv), and mast cell stabilizer cromolyn (1 mg x kg(-1) x min(-1)) also abolished vasodilation and macromolecular leak to N/OFQ in vivo (P < 0.05), but did not affect hypotension. Isolated mesenteric arteries (approximately 200 microm, n = 25) preconstricted with U-46619 were also mounted on a pressure myograph (60 mmHg), and both intraluminally and extraluminally administered N/OFQ (10(-5) M) caused dilation, inhibited by pyrilamine in the extraluminal but not the intraluminal (control: -6.9 +/- 3.8%; N/OFQ: 32.6 +/- 8.4%; pyrilamine: 31.5 +/- 6.8%, n = 18, P < 0.05) experiments. We conclude that, in vivo, mesenteric microvascular dilation and macromolecular leak occur via N/OFQ-NOP-mediated release of histamine from mast cells. Therefore, N/OFQ-NOP has an important role in microvascular inflammation, and this may be targeted during disease, particularly as we have proven that UFP-101 is an effective antagonist of microvascular responses in vivo.

zantac medication 2017-01-09

The glyceroglucolipids content of basal and pentagastrin-stimulated gastric secretion was measured in male patients with gastric (12) and duodenal (12) ulcer. Six patients in each group received twice daily for a period of 4 weeks 150 mg of ranitidine, whereas the other patients received placebo. The glyceroglucolipids output in the basal secretion of patients with gastric and duodenal ulcer before treatment was similar and increased 2.7-fold after pentagastrin stimulation. In all patients treated with ranitidine, the mean output of glyceroglucolipids after pentagastrin stimulation increased from 1.38 to 2.05 mumol/h (P less than 0.05). This increase, however, was more pronounced in the duodenal ulcer group than in the gastric ulcer patients. No change in glyceroglucolipids output was noted in the patients treated with placebo. The ratio of glyceroglucolipids to HCl increased significantly (P less than 0.02) only in the ranitidine-treated patients.

zantac syrup 2015-08-24

Following the administration of ranitidine there was a rise in gastric pH by 1-2 pH units over the duration of the study period (pH range 2.2-5.2 without ranitidine and 3.5-6.0 with ranitidine). There was no difference in the pharmacokinetic parameters of temozolomide or MTIC with or without the concomitant administration of ranitidine. There was however, a lower C(max) for temozolomide and MTIC for patients receiving ranitidine on day 1 and 2 versus day 4 and 5. Temozolomide was rapidly absorbed [time to maximum plasma concentration (t(max)) 1.8 h] and eliminated [elimination half-life (t(1/2)) 1.8 h] and MTIC followed a similar pattern with a t(max) of 1.9 h and a t(1/2) of 1.9 h. Overall, the AUC of the MTIC represented about 2-4% of the AUC for temozolomide.

medication zantac 2016-09-01

CWPO has proved to be effective for the treatment of representative pharmaceuticals (sulfamethoxazole, atenolol, metronidazole, diltiazem, trimethoprim and ranitidine) in different water matrices (ultrapure water, surface water, WWTP effluent and hospital wastewater). Complete removal of the pollutants and the aromatic intermediates was achieved using the stoichiometric dose of H2O2, a catalyst (Fe3O4/γ-Al2O3) load of 2gL(-1), pH 3 and temperature of 50-75°C. Accordingly, the ecotoxicity was reduced to negligible values. The degradation was faster when the pharmaceuticals were together, being the reaction time for the elimination of the most refractory species (metronidazole) shortened from 4h to 1h. The mineralization of the drugs was fairly different, being the most reactive species those containing several aromatic rings (XTOC∼80%) and the most refractory that bearing an imidazolium ring (XTOC∼35%). The water matrix affected the kinetics of the process but in all cases complete conversion of the drugs was reached within 1h. The presence of dissolved organic matter (surface water) seemed to promote drugs degradation while the occurrence of inorganic ions (real WTTP and hospital effluents) partially inhibited it due to scavenging effects. Remarkably, the process was successfully operated at the typical concentrations of main micropollutant sources (μgL(-1)).

zantac infant dose 2016-01-26

An oral controlled release formulation matrix for highly water-soluble drugs was designed and developed to achieve a 24-hour release profile. Using ranitidine HCl as a model drug, sodium alginate formulation matrices containing xanthan gum or zinc acetate or both were investigated. The caplets for these formulations were prepared by direct compression and the in vitro release tests were carried out in simulated intestinal fluid (SIF, pH 7.5) and simulated gastric fluid (SGF, pH 1.2). The release of the drug in the sodium alginate formulation containing only xanthan gum completed within 12 hours in the SIF, while the drug release in the sodium alginate formulation containing only zinc acetate finished almost within 2 hours in the same medium. Only the sodium alginate formulation containing both xanthan gum and zinc acetate achieved a 24-hour release profile, either in the SIF or in the pH change medium. In the latter case, the caplet released in the SGF for 2 hours was immediately transferred into the SIF to continue the release test. The results showed that the presence of both xanthan gum and zinc acetate in sodium alginate matrix played a key role in controlling the drug release for 24 hours. The helical structure and high viscosity of xanthan gum might prevent zinc ions from diffusing out of the ranitidine HCl--sodium alginate--xanthan gum--zinc acetate matrix so that zinc ions could react with sodium alginate to form zinc alginate precipitate with a cross-linking structure. The cross-linking structure might control a highly water-soluble drug to release for 24 hours. Evaluation of the release data showed the release mechanism for the novel formulation might be attributed to the diffusion of the drug.