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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:
Azantac, Bismo-ranit, Novo-ranitidine, Nu-ranit, Pylorid, Raniplex, Ranitic, Ranitidina, Ranitidinum, Rantec, Zaedoc, Zantic

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Axid, Pepcid, Tagamet , Pepcid, Fluxid, Pepcid AC

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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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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 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.

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Histamine (10-7 to 10-4 M) concentration-dependently stimulated the production of IL-18 and IFN-gamma and inhibited the production of IL-2 and IL-10 in human PBMCs. Histamine in the same concentration range did not induce the production of IL-12 at all. The stimulatory or inhibitory effects of histamine on cytokine production were all antagonized by H2 receptor antagonists ranitidine and famotidine in a concentration-dependent manner, but not by H1 and H3 receptor antagonists. Selective H2 receptor agonists, 4-methylhistamine and dimaprit, mimicked the effects of histamine on five kinds of cytokine production. The EC50 values of histamine, 4-methylhistamine, and dimaprit for the production of IL-18 were 1.5, 1.0, and 3.8 microM, respectively. These findings indicated that histamine caused cytokine responses through the stimulation of H2 receptors. All effects of histamine on cytokine responses were also abolished by the presence of either anti-IL-18 Ab or IL-1beta-converting enzyme/caspase-1 inhibitor, indicating that the histamine action is dependent on mature IL-18 secretion and that IL-18 production is located upstream of the cytokine cascade activated by histamine. The addition of recombinant human IL-18 to the culture concentration-dependently stimulated IL-12 and IFN-gamma production and inhibited the IL-2 and IL-10 production. IFN-gamma production induced by IL-18 was inhibited by anti-IL-12 Ab, showing the marked contrast of the effect of histamine. Thus histamine is a very important modulator of Th1 cytokine production in PBMCs and is quite unique in triggering IL-18-initiating cytokine cascade without inducing IL-12 production.

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Though adjudication of outcomes such as VAP is time-consuming, consistent decision-making requires strict criteria, training, and calibration. Patients should be assigned to adjudication teams through random allocation.

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A combination with ranitidine and amoxicillin is an effective and well tolerated therapy in H. pylori infected duodenal ulcer patients. The eradication rate does not seem to be further improved by a ranitidine dose higher than 600 mg daily.

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Ninety-four patients undergoing elective surgery received ranitidine 100 mg or 50 mg intravenously one hour pre-operatively, or acted as controls. A gastric aspirate pH in excess of 2.5 one to two hours after administration was achieved in 93% of patients given 100 mg, 88% of those given 50 mg, and 61% of controls. There were no significant differences in the volumes of gastric aspirate.

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394 patients with endoscopically diagnosed duodenal ulcer were randomly allocated to treatment with ranitidine 150 bid o ranitidine 300 mg bid in a prospective double-blind multicenter trial conducted in seven LatinoAmerican countries. Endoscopy at 4 weeks showed complete ulcer healing en 171 of 196 patients (87.2%) treated with ranitidine 150 mg bid and 178 of 198 (89.9%) treated with ranitidine 300 mg bid. Both treatment regimens were equally effective at rapidly reducing the incidence of ulcer-related symptoms. It is possible that higher dosage regimen of ranitidine would be useful in patients with more severe duodenal ulcer disease.

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Gastric bleeding in children is associated with critical illness, shock, and physical trauma. Histamine-2 receptor antagonist therapy is used prophylactically to treat gastric bleeding, but it is not known whether bolus dosing or continuous infusion dosing is more effective.

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We have previously shown that ranitidine bismuth citrate (RBC)-based triple therapy is comparable to proton pump inhibitor-based triple therapy in eradicating Helicobacter pylori infection.

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The number of PPI prescriptions decreased during the intervention and was sustained at least three quarters afterward. This low-intensity, practice-based intervention may serve as a model for other health care systems.

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Histamine has long been recognised as a classical inducer of pruritus. However, the specific mechanism of histamine-induced itch has still not been fully understood. The H1 and H4 receptor appear to be key components in the induction of itch. The specific role of the H3 receptor in histamine-induced itch remains unclear. The aim of our study was to investigate the role of the four known histamine receptors (H1-4) in acute itch in mice. Intradermal injection of the selective H3R inverse agonist pitolisant induced strong itch in mice. Pitolisant (50 nmol/injection)-induced pruritus could be completely blocked by a combined treatment with the H1R antagonist cetirizine (15 mg/kg) and the H4R antagonist JNJ 7777120 (15 mg/kg), whereas the H2R antagonist ranitidine (15 mg/kg) failed to inhibit the scratch response. Next, expression and function of histamine receptors on sensory neurons isolated from dorsal root ganglia of mice were investigated. As the itch sensation results from the excitation of sensory nerves in the skin, we further focused on skin specific sensory neurons. Therefore, neurons were retrograde labelled from the skin by means of a fluorescent tracer. Expression of H1R, H3R and H4R on skin innervating sensory neurons was detected. By single-cell calcium imaging, it was demonstrated that histamine induces a calcium increase in a subset of (skin-specific) sensory neurons via activation of the H1R and H4R as well as inhibition of the H3R. It is assumed that the decreased threshold in response to H3R antagonism activates H1R and H4R on sensory neurons, which in turn results in the excitation of histamine-sensitive afferents and therefore elicits the sensation of itch.

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Retrospective study.

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In a double-blind multicenter study with 28 centers in Germany, pantoprazole (40 mg before breakfast) was compared with ranitidine (300 mg at bedtime) with regard to healing rates, time until healing, symptom relief, and tolerability. A total of 248 outpatients with benign gastric ulcer were included.

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The acute toxicity of Protonix Suspension FA-Na is very low, it has the effects of antidiarrheal and anti-gastric ulcer.

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The tonic discharge of 71 medial vestibular nucleus (MVN) neurones was Voltaren Gel Reviews recorded in slices of the dorsal brainstem of young adult rats. Bath application of histamine caused a dose-related excitation in 59 of the 71 cells (83%), the remaining 12 (17%) being unresponsive. Dimaprit, a selective H2 agonist, also caused excitation in all 20 cells tested. The histamine-induced excitation and the response to dimaprit were antagonised by the selective H2 antagonist ranitidine, confirming that the H2 subtype of histamine receptor is involved in mediating the effects of histamine on these cells. Triprolidine, a selective H1 antagonist, also antagonised the excitation caused by histamine, at a concentration (0.3 microM) which left the H2 receptor-mediated response to dimaprit unchanged. Thus the excitatory effects of histamine on MVN cells in the rat involve two components mediated through H1 and H2 receptor-linked mechanisms, respectively. Betahistine, a weak H1 agonist and H3 antagonist, had little excitatory action when applied on its own, but significantly reduced the excitation caused by histamine when the two drugs were applied together. The effects of betahistine were consistent with a partial-agonist action at H1 receptors on MVN cells, reducing the excitatory responses to histamine presumably by occupying these receptor sites in competition with the exogenously applied neurotransmitter. This partial-agonist action of betahistine may be an important part of its mechanism of action in the symptomatic treatment of vertigo and motion sickness, since it is likely to occur not only in the MVN but also in many brain regions, including the thalamus and cortex, which express H1 receptors and which are innervated by the hypothalamic histaminergic system. Thus the effectiveness of betahistine and other anti-H1 drugs against motion sickness may be explained by their action in reducing the effects of the excess histamine release induced in such conditions in various brain areas, including the MVN.

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To investigate the effects of multiple dosing with ranitidine (300 mg four times a day) on the absorption of a moderate dose of alcohol (0.5, consumed postprandially or on an empty stomach at different times of day, and Periactin Tabs to investigate if coadministration of ranitidine affects psychomotor function.

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The powder of dried mature unripe Noni fruit was boiled in water until it became a sticky paste and was then dried into a powder by lyophilization. The pharmacological activity of AFE Paxil 50 Mg and pure scopoletin at the same equivalent dose present in AFE was investigated in rat on gastro-esophageal inflammatory models (acid reflux esophagitis, acute gastritis induced by ethanol and serotonin, and chronic gastric ulcer induced by acetic acid); gastric biochemical parameters and gastrointestinal motility.

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One hundred and seven patients who were pretreated with either a conventional premedication regimen (two doses of dexamethasone) or a short premedication regimen (single dose of dexamethasone with oral diphenhydramine and intravenous ranitidine), prior to paclitaxel infusion were retrospectively analyzed Zyrtec Normal Dosage . A modified premedication regimen, consisting of 12.5 ml of Rescalmin (intravenous diphenhydramine 50 mg and calcium bromide 437.5 mg), intravenous ranitidine 100 mg, and intravenous dexamethasone 20 mg, was given 30 min prior to paclitaxel, with oral dexamethasone 8 mg given on the night before the paclitaxel. Patients received paclitaxel intravenously at 175 mg/m(2) over 3 h, followed by carboplatin, AUC 5, over 1 h on day 1 every 3 weeks.

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Administration of omeprazole to healthy volunteers was recently reported to increase proximal duodenal mucosal bicarbonate secretion. As human oesophagus Pamelor 10mg Reviews also secretes bicarbonate, the hypothesis was tested that omeprazole may stimulate oesophageal bicarbonate secretion and thus contribute to the therapeutic efficacy of the drug in gastro-oesophageal reflux disease.

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Elevated aluminum concentrations have been implicated in several disease states in the elderly. We examined the effects of sucralfate, a basic aluminum salt of sucrose sulfate, and ranitidine, administered individually and in combination, on plasma and urine aluminum concentrations in the elderly in a prospective, randomized, three-arm crossover study. Subjects were 20 healthy volunteers over age 65 years, with no clinically significant comorbidities or recent use of aluminum-containing drugs or histamine (H)2-antagonists. The three regimens were ranitidine 300 mg at bedtime, sucralfate 1 g 4 times/day, and ranitidine 300 mg at bedtime plus sucralfate 1 g 4 times/day, administered for 4 weeks, with a washout period of at least 1 week between regimens. Plasma and urine aluminum concentrations were measured on days 0, 1, 7, 14, and 28 of each regimen. After 28 days, mean plasma aluminum concentrations were significantly higher in subjects receiving sucralfate alone (8.5 +/- 1.8 micrograms/L) and sucralfate plus ranitidine (5.1 +/- 1.3 micrograms/L) compared with those receiving ranitidine alone (2.4 +/- 0.7 micrograms/L). Urine aluminum concentrations were significantly higher in subjects receiving sucralfate alone (133.2 +/- 32.8 micrograms/g Motrin Kids Dosage creatinine) and sucralfate plus ranitidine (148.1 +/- 51.9 micrograms/g creatinine) compared with those receiving ranitidine alone (11.0 +/- 3.7 micrograms/g creatinine). There was no significant difference in plasma or urine aluminum concentrations between subjects who received sucralfate alone versus those who received sucralfate plus ranitidine. Sucralfate 4 g/day in elderly subjects produces a significant increase in both plasma and urine aluminum concentrations, compared with ranitidine 300 mg/day. This increase most likely is secondary to gastrointestinal absorption of aluminum in the sucralfate formulation. The clinical relevance of this increase requires further evaluation.

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Factors predisposing to endoscopic Buy Prandin ulcer formation or healing with non-steroidal anti-inflammatory drugs (NSAIDs) have not been well defined.

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Histological oesophagitis was present in 21/90 (23%). The oesophageal reflux index (RI) was >5% and >10% in 21/103 (20%) and 6/103 (6%) infants, respectively. Gastric pH was >4.0 during <50%, >50%, >75% and >90% of the duration of pH monitoring in 33/103 (32%), 70/103 (68%), 22/103 (21%) and 7/103 (7%), respectively. By simple regression analysis, the dosage of ranitidine correlated with the oesophageal RI (r = 0.21; p = 0.05), but not with the duration of time gastric pH was >4.0 (r = 0.09; p = 0.39). Histological oesophagitis did not correlate with ranitidine dosage, duration of treatment, duration gastric pH was >4.0 and oesophageal reflux index.