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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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A search of all published trials on H. pylori eradication therapy performed in The Netherlands was conducted via electronic database search, hand-searching of abstracts from scientific meetings and checking reference lists of pharmaceutical companies. Full papers and abstracts were included. Data on anti-H. pylori therapies were pooled based on duration and combination of drugs. Only triple and quadruple eradication regimens were studied. Dual therapies were excluded, except for ranitidine bismuth citrate-based dual therapies.

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Pediatric patients who present with symptoms of gastroesophageal reflux and severe eosinophilic esophagitis may be unresponsive to aggressive anti-reflux medical therapy. In order to determine whether the degree of eosinophilia predicts anti-reflux treatment response and possibly distinguishes different etiologies, we reviewed the initial biopsies of patients with esophageal eosinophilia and compared the number of eosinophils with the response to anti-reflux treatment. Over a 1-year period, 102 patients with a biopsy demonstrating at least 1 intraepithelial eosinophil were identified among patients undergoing initial endoscopy for symptoms of reflux. All patients were treated with H2 blockers and prokinetic agents. Treatment response was classified into three categories: improvement, relapse, and failure. There were significant differences between the group who improved (mean eosinophil count [MEC] 1.1 +/- 0.3 SEM) and those who failed (24.5 +/- 6.1 SEM, P < 0.0025) or relapsed 6.4 +/- 2.4 SEM, P < 0.05). A threshold MEC value of > or = 7 provided a sensitivity of 61.3%, a specificity of 95.7%, and a predictive value for treatment failure of 86.1. A MEC value of < 7 provided an 85% predictive value of successful therapy. From these data we made the following conclusions: (1) The number of eosinophils has a predictive value of treatment response with > or = 7 per high power field offering a valuable clinical threshold for predicting outcome of conventional therapy. (2) The variable response to conventional reflux treatment may reflect different etiologies. (3) Alternate medical treatment modalities may be appropriate in the presence of severe eosinophilia, before considering surgical intervention.

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A prospective, double-blind parallel study was performed in 85 patients endoscopically diagnosed of duodenal ulcer H. pylori positive. Patients were randomized to a 7-days triple therapy (group A) or omeprazole plus antibiotic placebo (group B). All patients were treated only with omeprazole for the next three weeks. Patients with ulcer healing after treatment were entered in a one-year follow up phase with ranitidine placebo (group A) or ranitidine (group B). Endoscopy and biopsies were performed at baseline, after treatment (5 weeks) and after 12 months of follow-up or when relapsing symptoms appeared.

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25 patients with Helicobacter pylori-associated active duodenal ulcer disease (bleeding: n = 5, penetrating: n = 1, stenosis of the bulb: n = 4, frequent ulcer relapse: n = 18) were treated with 3 x 600 mg bismuth subsalicylate (BSS), 3 x 400 mg metronidazole and 3 x 500 mg tetracycline in addition to 300 mg ranitidine. 23 out of 25 patients (92%) proved to be Helicobacter pylori-negative four weeks after cessation of study medication as judged from negative urease test, specific culture and histology after modified Giemsa staining. 24/25 ulcers (96%) had healed after six weeks. In one patient on NSAIDs a small duodenal ulcer was detected on the final endoscopic examination despite successful Helicobacter pylori eradication. Twelve out of 25 (48%) patients complained side effects that did not lead to discontinuation of therapy. In conclusion, oral triple therapy with BSS, metronidazole and tetracycline is highly effective in Helicobacter pylori eradication, but there was a rather high rate of more or less serious side effects, diminishing the attractiveness of this therapeutic regimen.

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While dyspeptic patients in primary care often receive empirical treatment with antisecretory drugs, a substantial number suffer from motility disturbances which may be associated with their complaints. We aimed to compare the effectiveness of treatment with antisecretory treatment with a prokinetic agent in uninvestigated dyspepsia.

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Healing of peptic ulcers can be achieved by using a variety of anti-ulcer medications. The most commonly used agents include the histamine-2 receptor antagonists (H2RAs) and the proton pump inhibitors. They are also efficacious in preventing ulcer recurrence providing maintenance treatment is given. The ideal treatment for peptic ulcers today is aiming at eradication of Helicobacter pylori infection. Successful elimination of the latter not only heals the ulcers but also provides a cure for the disease, so that the patients will no longer require lifelong maintenance medical therapy.

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Twenty-three patients treated with misoprostol and 26 treated with ranitidine concluded the study. The M group showed a significantly (P < .02) lower incidence of gastroduodenal lesions (two patients; 8.7%) than the R group (10 patients; 38.5%). Gastric ulcers occurred in one (4%) misoprostol-treated patient and in six (23%) ranitidine-treated patients. Six of seven patients with ulcers were asymptomatic. Seventy-one percent and 86% of ulcers occurred in patients older than 60 years and in those who received greater than 3.1 mg/kg of diclofenac, respectively.

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Prolonged ambulatory pH studies in GERD patients were reviewed. Group A: 60 patients (mean age 53 years, male 30) taking either omeprazole 20 mg or lansoprazole 30 mg b.d. Group B: 45 patients (mean age 49 years, male 23) on proton pump inhibitor b.d. (omeprazole 20 mg or lansoprazole 30 mg) plus an H2-blocker at bedtime (ranitidine 300 mg, famotidine 40 mg or nizatidine 300 mg). Eleven patients were evaluated during treatment with both regimens (group C). The percentage time of nocturnal and daytime intragastric pH > 4 and per cent of patients with gastric NAB were analysed. In the patients with NAB, its duration and associated oesophageal acid exposure also were analysed.

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Histamine (1-100 microM) induced a concentration-dependent increase in intracellular cyclic AMP in monolayer cultures of human, canine and foetal-bovine articular chondrocytes. The dose-response curve for histamine in each culture was progressively displaced to the right with increasing concentrations of cimetidine, an H2-receptor antagonist. The histamine-induced cyclic AMP elevation in human articular chondrocytes was also significantly decreased by ranitidine, another H2 antagonist, but not by the H1 antagonists mepyramine and chlorpheniramine. These findings indicate that histamine activates chondrocyte adenylate cyclase through an H2 receptor. The cyclic AMP response of human chondrocytes to histamine was many times greater than that measured for synovial fibroblasts under similar conditions. Such findings suggest that mast-cell-chondrocyte interactions in vivo may contribute to changed chondrocyte metabolism in joint disease.

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A case report of hematologic toxicity following the administration of MTX and flurbiprofen at our institution is presented. Six previously published case reports and five pharmacokinetic studies regarding MTX and NSAID interactions are available to assist in the evaluation of this potential interaction.

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Two hundred and twenty-six patients with endoscopically confirmed duodenal ulcers > or = 5 mm in diameter entered a double-blind randomized trial comparing 20 mg omeprazole administered once daily in the morning with 300 mg ranitidine administered once daily at night. The patients were assessed endoscopically and symptomatically after 2 weeks, and those whose ulcers had healed terminated the study. Patients with unhealed ulcers continued treatment for a total of 4 weeks. Omeprazole produced significantly higher healing rates than ranitidine at both 2 weeks (57 vs 28%, P < 0.0001) and 4 weeks (93 vs 80%, P = 0.006). Similarly, significantly higher 'effective healing rates' (defined on the criteria established by the Japanese Society of Digestive Endoscopy) were observed with omeprazole compared with ranitidine at 2 and 4 weeks. After 2 weeks, there were significantly fewer reports of both day-time and night-time epigastric pain by omeprazole-treated patients compared with ranitidine-treated patients (22 vs 44%, P < 0.0001 for day-time pain; 24 vs 35%, P = 0.025 for night-time pain). Both drugs were well-tolerated and no major adverse effects were recorded during either treatment. In conclusion, 20 mg omeprazole administered once daily was superior to 300 mg ranitidine administered once daily for duodenal ulcer healing and symptom relief.

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Antisecretory drugs (ASDs) are prescribed for preventing and treating nonsteroidal, antiinflammatory drug (NSAID)-induced gastrointestinal adverse effects and for stress ulcer prophylaxis (SUP). The suitability of long-term use of ASDs has been evaluated elsewhere but not in the Kingdom of Saudi Arabia (KSA).

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Animals were randomly divided into several experimental groups. Each group consisted of 10 animals. The control group received PVP vehicle (720 mg x kg(-1), po) throughout the course of the experiments. The treatment groups received different doses of curcumin SDs (equivalent to curcumin 10, 30 and 90 mg x kg(-1), po), and ranitidine (27 mg x kg(-1), po) was used as the positive control. In acetic acid-induced gastric ulcers model, serum NO, plasma ET and gastric ulcer indexes of rats were measured after oral administration for 14 d. In rat ulcer model induced by pylorus-ligature, gastric volume pepsin and gastric ulcer indexes of rats were measured after oral administration for 3 d and pylorus-ligature inducement for 16 h. Gastric ulcer indexes of mice were measurement after oral administration for 3 d and subcutaneous injection reserpine 10 mg x kg(-1).

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The purpose of this study was to determine whether the bradycardic response to peripheral hyperosmolality in conscious rats is dependent on afferent baroreceptor mechanisms and whether central histamine H2 receptors play a role in baroreflex-mediated changes in heart rate (HR). Mean arterial pressure (MAP) and HR were recorded continuously during a 30-min infusion of 2.5 M NaCl (10 microliters.100 g-1.min-1) hypertonic saline (HTS). HTS infusion significantly increased MAP (21 +/- 4 mmHg) and reduced HR (-62 +/- 10 beats/min) in rats with intact arterial baroreceptors. In sinoaortic-denervated rats, HR remained unchanged from control despite a significant increase in MAP. After intracerebroventricular (lateral ventricle) administration of cimetidine or ranitidine (H2-receptor antagonists) in intact rats, HTS infusion significantly increased MAP (19 +/- 2 and 17 +/- 2 mmHg, respectively) but the bradycardia was abolished (-12 +/- 10 and -10 +/- 10 beats/min, respectively). In contrast, central H2-receptor blockade did not alter reflex HR responses to the intravenous administration of phenylephrine and nitroprusside or to the central administration of histamine or angiotensin II. These results indicate that the bradycardic response to HTS infusion is mediated through the arterial baroreceptor reflex and involves in part a selective histaminergic pathway.

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There is conflicting evidence regarding whether lower esophageal sphincter and esophageal contractile pressures are affected by changes in the severity of gastroesophageal reflux disease. We compared the manometric and endoscopic findings from 30 patients before and after treatment for esophagitis. Before treatment, the grade of esophagitis (I-III) was significantly correlated (r = -0.37; p less than 0.05) with lower esophageal sphincter pressure, but not with esophageal contractile pressure. After treatment, the grade of esophagitis did not change or became worse in 15 patients, and became better in 15 patients. Of these, seven healed. The group that showed no endoscopic improvement demonstrated no change in lower esophageal sphincter or esophageal contractile pressures. The group that did show endoscopic improvement also demonstrated no increase in lower esophageal sphincter or esophageal contractile pressures, and this was particularly evident in those whose esophagitis healed. These data suggest that healing of esophagitis does not result in improvement of esophageal motor function.

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The in vitro reaction of nitrite with the histamine H2-receptor antagonist ranitidine, in acidified solutions or in human gastric juice, resulted in the formation of genotoxic derivatives, mainly eliciting base-pair substitutions in his-Salmonella typhimurium and trp- Escherichia coli and inducing an increased lethality in DNA repair-deficient bacteria. The mutagenic response was better expressed in the presence of rodent (rat, mouse) and even more of human liver preparations. The patterns of this reaction, e.g., the optimal pH, temperature and time of preincubation, doses of precursor compounds, effect of inhibitors (ascorbic acid), the genotoxic mechanisms and in vitro metabolic trends were investigated and compared with those resulting from nitrosation of cimetidine under the same experimental conditions. Although the reaction proceeded under conditions simulating the gastric environment, an excess of nitrite was needed, in the case of ranitidine, for optimal formation of mutagenic derivatives. Gastric juice samples from fasting individuals treated with ranitidine were devoid of mutagenic activity, and the addition of nitrite to these samples was also without a reproducible effect. Conversely, under the same conditions, most samples from both untreated and ranitidine-treated individuals induced mutations of different genetic specificity (frameshift errors), resulting from nitrosation of physiological components of gastric juice.

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The purpose of this work was to investigate the involvement of carrier-mediated apical (AP) uptake and efflux mechanisms in the absorptive intestinal transport of the hydrophilic cationic drug ranitidine in Caco-2 cells.

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In the control group there was no significant difference between the mean intra-gastric pH values pre-operatively and post-operatively (P> 0.05). In the treatment group the level of intra-gastric pH was much higher than that in the control group (P< 0.05). In the control group, the level of plasma endothelin significantly higher and the level of calcitonin gene-related peptide significantly lower than that pre-operatively (P< 0.01), but the level of plasma endothelin significantly was lower and the level of calcitonin gene-related peptide obviously higher in the post-operative treatment group than that pre-operatively (P< 0.01).

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Patients undergoing biliopancreatic diversion (BPD) may develop gastric ulcers, particularly within the first postoperative year. The prophylactic use of antisecretory compounds at the usual therapeutic doses, mainly conventional H2-receptor antagonists such as ranitidine, may reduce the incidence of this complication, which occurs in approximately 5% of patients after BPD.

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The concept of an alkaline tide which compensates for gastric acid secretion suggests the possibility of indirect measurement of gastric acid secretion. This study was designed to determine whether postprandial changes in renal and respiratory function could be used to assess gastric secretion in healthy adults. Volunteers ate one of three standard (low, medium or high protein) breakfasts on separate days. A fall in urine acid output was observed during 2 h after the high protein meal, but not after the medium or low protein meal. Fasting subjects showed a similar fall in urine acid output over a 2-hour period. Pretreatment with ranitidine 150 mg b.i.d. had no effect on basal or postprandial urine acid output. We conclude that changes in urine acid output are not related to the gastric secretory response to food. In a separate study, treatment with omeprazole 20 mg daily had no effect on postprandial respiratory function (minute ventilation; mixed expired CO2; minute volume of CO2; respiratory exchange ratio; venous blood pH, pCO2 or bicarbonate; and end tidal CO2). Thus we were unable to detect a respiratory alkaline tide after a standard breakfast. These findings suggest that any respiratory or urinary compensation for gastric acid secretion is too small to be of physiological or clinical significance.

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1. We have investigated the effects of inflammatory mediators on visceral afferent discharge and afferent responses to bradykinin (BK) in rat jejunum using a novel in vitro technique. 2. Prostaglandin E2 (1 microM) augmented responses to BK without affecting basal firing, while histamine (100 microM) and adenosine (100 microM) activated basal discharge and enhanced BK responses. In contrast, 5-HT (100 microM) increased basal discharge without influencing responses to BK. 3. Afferent discharge induced by histamine was inhibited by both H1 (pyrilamine) and H3 (thioperamide) but not H2 (ranitidine) receptor antagonists at 10 microM. In contrast, sensitization to BK induced by histamine was inhibited by ranitidine (10 microM). 4. Afferent discharge induced by adenosine was blocked by the A1 receptor antagonist DPCPX (10 microM) but remained unaffected by A2A receptor blockade with ZM241385 (10 microM). In contrast, sensitization of BK responses by adenosine was unaffected by both antagonists. Basal discharge and BK-induced responses were unaffected by the A3 receptor agonist IB-MECA (1 microM). While involvement of A2B receptors is not excluded, adenosine may activate afferent discharge through A1 receptors, while sensitization to BK could involve a receptor other than A1, A2A or A3, possibly the A2B receptor. 5. Inhibition of cyclo-oxygenase with naproxen (10 microM) prevented sensitization after histamine but not adenosine. 6. Sensitization was mimicked by dibutyryl cAMP. This occurred without changes in basal firing and was unaffected by naproxen. 7. In conclusion, afferent discharge induced by BK is augmented by histamine, adenosine and PGE2, but not by 5-HT. Evidence suggests that sensitization involves separate mechanisms from afferent activation. Sensitization may be mediated by increases in cAMP following direct activation by mediators at the nerve terminal or through indirect pathways such as the release of prostaglandins.

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These data suggest that the eradication rate of H. pylori with PCA or RCA treatment is lower in patients with type 2 diabetes than in nondiabetics and that successful eradication could decrease dyspeptic symptoms.

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Weak and reversible inhibitors of cholinesterase, when co-administered in large doses, can act in a protective manner against more potent inhibitors such as organophosphates. The clinically widely used histamine type 2 (H2) receptor blocker ranitidine is among H2 blockers the most potent inhibitor of acetylcholinesterase but roughly three to four orders of magnitude less potent than paraoxon (an irreversible organophosphate esterase inhibitor) or pyridostigmine (a reversible carbamate esterase inhibitor). We have previously shown that in vitro ranitidine confers some protection against inhibition of cholinesterases by paraoxon and that in vivo it both increases the number of rats surviving an acute paraoxon exposure and also protects to some degree the cholinesterases from organophosphate inhibition. The purpose of the study was to compare in a prospective non-blinded study, in a rat model of acute high-dose paraoxon exposure, ranitidine with pyridostigmine either administered simultaneously or 30 min. before exposure. There were 36 rats in each of the 5 groups. All substances were applied intraperitoneally. Additional analysis included data from a similar experiment carried out in 2005, in which 54 rats were exposed to paraoxon only (G1) and 54 to paraoxon+ranitidine simultaneously (G2). All groups (except controls; G6 & G7) received 1 micro Mol paraoxon (approximately LD75); groups 2-5 received in addition to paraoxon: G2: 50 micro Mol ranitidine within 1 min. of paraoxon, G3: 1 micro Mol pyridostigmine within 1 min. of paraoxon, G4: 50 micro Mol ranitidine 30 min. before paraoxon, G5: 1 micro Mol pyridostigmine 30 min. before paraoxon. Groups 6 & 7 received only ranitidine and pyridostigmine respectively, group G1 received only paraoxon. Mortality was recorded at 30 min., 1, 2, 3, 4, 24 and 48 hr. Mortality data were compared using Kaplan-Meier plots and logrank tests. No Bonferroni correction for multiple comparisons was applied and an alpha < or = 0.05 was considered significant. All statistical analysis was performed by using SPSS 12.0 statistical software (SPSS Inc., Chicago, IL, USA). Simultaneous administration of ranitidine or pyridostigmine with paraoxon does not significantly affect mortality. Pretreatment (30 min. before) with both ranitidine or pyridostigmine statistically and significantly reduced mortality. When administered before paraoxon, pyridostigmine is statistically significantly superior to ranitidine. Both ranitidine and pyridostigmine are protective against acute paraoxon toxicity provided they are administered before paraoxon. Pyridostigmine results are statistically significantly superior to ranitidine (< or =0.05).

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Paired studies of hepatic microsomal function were conducted in eight subjects during treatment with two histamine H2 antagonists, cimetidine and ranitidine. Cimetidine but not ranitidine inhibited the metabolism of antipyrine (phenazone) and demethylation of aminopyrine (aminophenazone) as measured by breath 14CO2 production after intravenous injection of 14C-aminopyrine. These results suggest that the metabolic inhibitory actions on the liver may be separated from H2 antagonist effects, and that ranitidine has an advantage over cimetidine by not inhibiting microsomal drug oxidative function.

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Approximately 80-90% of patients show healing of reflux esophagitis after 8 weeks of once-daily PPI therapy. Patients taking PPI therapy twice daily still have nocturnal acid breakthrough (periods of gastric pH <4 lasting for > or =60 min during the night) as much as 70% of the time. The clinical application of this finding has not been shown. One trial has shown that omeprazole in the morning plus ranitidine at bedtime is not as effective as omeprazole twice daily given before the morning and evening meals at controlling nocturnal acid breakthrough. Further, 1 small trial in healthy subjects without GERD showed that the addition of a 1-time dose of ranitidine at bedtime to a twice-daily regimen of omeprazole may decrease the occurrence of nocturnal acid breakthrough. However, the clinical significance of this finding is not clear.

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The effects of pretreatment with selective histamine receptor antagonists on changes in sympathoadrenal activity and haemodynamics, induced by 60-min immobilization stress, were studied in conscious rats. Using adrenomedullary microdialysis, it was shown that ranitidine (5 mg/kg, i.v.), a histamine H2 receptor antagonist, selectively suppressed stress-stimulated noradrenaline secretion without affecting adrenaline response, whereas triprolidine (10 mg/kg, i.v.), a histamine H1 receptor antagonist, had little effect on stress-induced secretion of both catecholamines. Neither triprolidine nor ranitidine changed the pressor response to 60-min stress. The stress-induced increase in heart rate was not altered by triprolidine, whereas ranitidine reduced it after 30 min of stress. To test whether the anti-secretory effect of ranitidine could be of peripheral origin, in a separate experimental series, a local catecholamine secretion was stimulated by histamine (0.5 mM) perfused through the adrenomedullary dialysis probe. It appeared that triprolidine, but not ranitidine, reduced this effect of histamine. Thus, the present results suggest that during stress, the activity of the central histaminergic system, via histamine H2-receptors, may selectively modulate noradrenaline secretion by the adrenal gland.

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Twenty patients with symptoms and endoscopic changes of gastro-oesophageal reflux were randomly allocated to treatment with either ranitidine 150 mg bd, or 300 mg bd for 8 weeks. Symptoms, endoscopic appearances, histopathology of oesophageal biopsies and 22-h intra-oesophageal pH profile in ambulant patients on standard diets were recorded before and at the end of the treatment period. Symptoms improved rapidly and markedly on either dose of ranitidine. Both doses produced significant improvement of the endoscopic appearances, but there were no differences in symptomatic and endoscopic improvement related to the dose. Biopsy appearances and the 22-h oesophageal pH profile remained unchanged on either dose of ranitidine.

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There was a statistically significant difference in favour of 150-mg ranitidine effervescent tablets in terms of time to adequate symptom relief and the proportion of patients who achieved adequate symptom relief for the first episode. A greater proportion of patients in the famotidine group liked the type of formulation than in the ranitidine group.

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The efficacy of omeprazole in preventing gastric mucosal injury induced by hemorrhagic shock in rats and the putative mechanisms involved in this effect were investigated in the present study. Omeprazole did not affect mean arterial blood pressure under both basal conditions and induction of hemorrhagic shock, but it evoked a marked increase in Alcian blue recovery from gastric preepithelial mucus. The morphometric analysis of histological sections revealed that omeprazole caused a significant reduction of hemorrhagic shock-induced damage of gastric mucosa. Ranitidine, used as the reference drug, failed to affect mean arterial blood pressure, Alcian blue recovery from gastric mucus, or hemorrhagic shock-induced damage of gastric mucosa. Both omeprazole and ranitidine exerted a significant inhibition of gastric acid output from anesthetized pylorus-ligated rats. Overall, the present results indicate that omeprazole is effective in protecting gastric mucosa from necrotic damage induced by hemorrhagic shock and suggest that an enhancement of gastric mucus secretion contributes to this protective action.

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In a randomized study, the efficacy of anti-H. pylori treatment versus sucralphate was tested in patients with NUD. One hundred and twelve patients with NUD, 62 positive and 50 negative for H. pylori were studied. Of 62 patients positive for H. pylori, 32 were treated with triple therapy (colloidal bismuth subcitrate, tetracycline and metronidazole) for 2 weeks and the remaining 30 were treated with sucralphate (1 g, q.i.d.) for 4 weeks. Of 50 patients negative for H. pylori, 25 each were treated with either sucralphate (1 g, q.i.d.) or ranitidine (150 mg, b.d.) for 4 weeks.

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zantac tablet 2015-04-07

In the stomach of a gastric ulcer patient who had been administered an anti-acid, a gram-negative and urease-negative bacillus similar in size to Helicobacter pylori was infected together with H. pylori. According to biochemical test and 16S rRNA gene analysis, the urease-negative bacterium was identified as Kingella denitrificans, a human nasopharyngeal commensal. In contrast to the standard strain of K. denitrificans, the isolate showed catalase activity, did not produce acid from glucose, and exhibited acid tolerance. Acid tolerance of H. pylori was increased by cocultivation with the K. denitrificans isolate, but not with buy zantac other isolates of K. denitrificans. Disruption of physiological and immunological niche by dysbiotic colonization of bacterium may provide pathological attributes to human stomach. Collectively, a careful administration of anti-acids to the elderly, especially those with atrophic gastritis, is necessary to avoid repression of the gastric barrier to bacteria.

zantac renal dosing 2015-06-29

Each buy zantac tablet of ranitidine bismuth citrate 400 mg contains 162 mg of ranitidine base, 128 mg of trivalent bismuth, and 110 mg of citrate. It uses the acid-suppressive actions of ranitidine and the antimicrobial and mucosal protective effects of bismuth to eradicate HP. Ranitidine bismuth citrate in conjunction with clarithromycin represents one of four treatment regimens currently approved in the US for duodenal ulcer associated with HP infection. In four double-blind, randomized trials, this agent has achieved HP eradication rates of 73-94% and duodenal ulcer healing rates of 73-89%. It is given twice daily for 28 days, and is associated with very low rates of adverse effects.

colic syrup zantac 2015-12-02

In a patient with a carcinoid crisis and ARDS refractory to conventional therapies buy zantac , substantial hemodynamic and oxygenation improvements were observed following methylene blue administration. This case highlights the potential pathophysiologic role of bradykinin and methylene blue as an adjunct therapeutic option in carcinoid crises.

zantac tablets 2017-07-19

Pantoprazole is an irreversible proton pump inhibitor which, at the therapeutic dose of 40mg, effectively reduces gastric acid secretion. In controlled clinical trials, pantoprazole (40mg once daily) has proved superior to ranitidine (300mg once daily or 150mg twice daily) and equivalent to omeprazole (20mg once daily) in the short term (< or = 8 weeks) treatment of acute peptic ulcer and buy zantac reflux oesophagitis. Gastric and duodenal ulcer healing proceeded significantly faster with pantoprazole than with ranitidine, and at similar rates with pantoprazole and omeprazole. The time course of gastric ulcer pain relief was similar with pantoprazole, ranitidine and omeprazole, whereas duodenal ulcer pain was alleviated more rapidly with pantoprazole than ranitidine. Pantoprazole (40mg once daily) showed superior efficacy to famotidine (40mg once daily) in ulcer healing and pain relief after 2 weeks in patients with duodenal ulcer in a large multicentre nonblinded study. In mild to moderate acute reflux oesophagitis, significantly greater healing was obtained with pantoprazole than with ranitidine and famotidine, whereas similar healing rates were seen with pantoprazole and omeprazole. Pantoprazole showed a significant advantage over ranitidine in relieving symptoms of heartburn and acid regurgitation. Reflux symptoms were similarly alleviated by pantoprazole and omeprazole. Preliminary results indicate that triple therapy with pantoprazole, clarithromycin and either metronidazole or tinidazole is effective in the treatment of Helicobacter pylori-associated disease; however, these findings require confirmation in large well-controlled studies. Pantoprazole appears to be well tolerated during short term oral administration, with diarrhoea (1.5%), headache (1.3%), dizziness (0.7%), pruritus (0.5%) and skin rash (0.4%) representing the most frequent adverse events. The drug has lower affinity than omeprazole or lansoprazole for hepatic cytochrome P450 and shows no clinically relevant pharmacokinetic or pharmacodynamic interactions at therapeutic doses with a wide range of drug substrates for this isoenzyme system. In conclusion, pantoprazole is superior to ranitidine and as effective as omeprazole in the short term treatment of peptic ulcer and reflux oesophagitis, has shown efficacy when combined with antibacterial agents in H. pylori eradication, is apparently well tolerated and offers the potential advantage of minimal risk of drug interaction.

zantac dosing information 2017-06-24

This study documented gastric pH and volume and the number of patients at risk of acid aspiration of gastric contents in a group of mothers undergoing emergency cesarean section under general anesthesia. Patients were randomized in a double-blind fashion to receive ranitidine, 50 mg intravenously, or placebo at the time of decision to proceed to cesarean section. In addition, all patients received 30 mL of 0.3 M sodium citrate on entry into the operating room. Aspiration of gastric contents was undertaken immediately after endotracheal intubation (PI) and before tracheal extubation. Patients with both pH < 3.5 and volume > 25 mL were deemed to be at risk of acid buy zantac aspiration should regurgitation occur. Postintubation, 12 patients (4%) were at risk in the citrate-alone group and 7 patients (2.3%) were at risk in the ranitidine/citrate group (not significant). Preextubation, 17 patients (5.6%) were at risk in the citrate-alone group and 1 patient (0.3%) was at risk in the ranitidine/citrate group (P < 0.05). PI pH in patients receiving ranitidine/citrate (mean 5.2, SD 0.8) was significantly higher than in patients receiving citrate alone (mean 4.9, SD 1.1). None of the patients who received ranitidine more than 30 min before the PI sample were at risk compared to 6 (3.2%) in the citrate alone group (P = 0.05). We conclude that 50 mg of intravenous ranitidine given at the time of decision to proceed to cesarean section reduces the risk of acid aspiration provided that at least 30 min have elapsed from injection to induction of anesthesia.

zantac overdose 2017-12-11

The effect of preoperative oral and intramuscular ranitidine administration on intragastric pH and volume was evaluated in children. Thirty healthy inpatients whose ages were 2-13 years, were randomly assigned to three groups. Twelve hours before the elective operation apple juice was given to the control group, and apple juice with 0.4 mg.kg-1 ranitidine to the second group (Oral group). For the third group (IM group) an intramuscular injection of 0.1 mg.kg-1 ranitidine was done. Intragastric pH was significantly elevated and gastric volume was also significantly reduced in IM group, and serum ranitidine concentration showed a high level of 359. buy zantac 4 +/- 85.6 ng.dl-1 (mean +/- SD). In oral group ranitidine effect on pH and volume was not significant, and the drug serum concentration was 31.6 +/- 13.3 ng.dl-1 which was slightly lower than the effective level. Though the intramuscular injection guaranteed safer gastric content, a painful injection is stressful for children. With the knowledge of elimination rate of serum ranitidine we recommend oral ranitidine (0.4 mg.kg-1) six hours preoperatively for pediatric premedication.

zantac dosing pediatrics 2015-06-11

We conducted a double-blind study comparing two dosage regimens of a prokinetic drug, cisapride (10 mg q.d.s. and 20 mg b.d.), with a low dose of a H2-receptor antagonist (150 mg ranitidine b.d.) in the treatment of 155 patients with reflux oesophagitis as determined by endoscopy. The active treatment took 8 to 12 weeks depending on whether complete healing was found at endoscopy. Improvement in oesophagitis grades buy zantac from baseline to endpoint was observed in 68% of patients in the 10 mg cisapride q.d.s. group, 83% in the cisapride 20 mg b.d. group and 81% in the ranitidine group (N.S.). At endpoint, the percentages of endoscopically cured patients with initial grades I or II were 52% for 10 mg cisapride q.d.s., 71% for 20 mg cisapride b.d. and 80% for ranitidine (N.S.). The proportional improvement of the overall reflux symptom score (60%) also showed no significant difference between the three groups. In the treatment of mild reflux oesophagitis (grades I and II) similar results can be expected from 20 mg cisapride b.d. and 150 mg ranitidine b.d. As the results of the two dosage regimens of cisapride were not different, the 20 mg twice daily regimen is preferred because it will improve patient compliance. It is concluded that in reflux oesophagitis grades I and II, the efficacy of 20 mg cisapride b.d. and 150 mg ranitidine b.d. are broadly similar.

zantac 450 mg 2016-01-11

Thirty-three of 35 enrolled patients were buy zantac available for evaluation; using the protocol-specified modified intention-to-treat analysis, five failed treatment, two were lost to follow-up (cure rate per-protocol = 85.7%, intention-to-treat = 78.7%). The cure rate among metronidazole-susceptible strains was 100% (22 of 22) (95% confidence interval 84-100%) compared with 55% (five of nine intention-to-treat) (95% confidence interval 21-86%) among metronidazole-resistant strains. In four cases, therapy was truncated at 4-7 days because of side-effects; yet the treatment was effective in three. The three metronidazole-susceptible but clarithromycin-resistant infections were cured.

zantac 150 tablets 2015-12-31

The antisecretory effects of a new histamine H2-receptor antagonist, ranitidine hydrochloride, have been investigated on basal and pentagastrin-stimulated acid secretion in healthy volunteers 5 and 10 h after oral administration of 150 mg. In addition, the 24-h intragastric pH-profiles have been measured in patients undergoing parenteral nutrition after three doses of 150 mg ranitidine per day. A 40% inhibition of basal acid buy zantac output has been noted even 10 h after drug intake. The intragastric pH-values were raised above 5 for at least 24 h. The new H2-antagonist ranitidine has been proven to be a potent and long-acting antisecretory compound.

zantac dosage infant 2017-05-07

Successful Helicobacter pylori eradication was found to induce a better response in peptic ulcer healing, regardless of diagnosis: gastric ulcer 88% vs 73% (odds ratio [OR] 2.7, p < 0.01), duodenal ulcer 95% vs 76% (OR 5.6, p < 0.0001), and peptic ulcer 95% vs 76% (OR 6. buy zantac 6, p < 0.0001), for patients having their HP infection successfully cured versus those remaining HP-positive, respectively (Fisher's exact test). For all evaluated time points (< or = 6, 7-8, and 10-12 wk after beginning treatment), HP-negative patients had higher healing rates than HP-positive patients (95% vs 82%, 94% vs 69%, and 96% vs 78% with corresponding OR of 4.2, 6.5, and 7.4, all p < 0.0001, Fisher's exact test). The use of concomitant acid suppression therapy during initial HP eradication provided a benefit on peptic ulcer healing only for patients with persistent HP infection (improved healing rates of 78% vs 67%; otherwise rates were 94-96%). Likewise, prolonged acid inhibition in HP treatment failures after the initial HP treatment phase resulted in 7-20% improved healing rates, whereas patients becoming HP-negative did not profit.

zantac 150 dosage 2017-04-15

Two hundred and forty-two patients were assigned to either empirical or antimicrobial sensitivity testing-based treatment; within each group, subjects were further randomized to receive buy zantac ranitidine bismuth citrate, 400 mg b.d., tinidazole, 500 mg b.d., and clarithromycin, 500 mg b.d., or omeprazole, 20 mg b.d., clarithromycin, 500 mg b.d., and amoxicillin, 1 g b.d., for 1 week, with substitution of the resistant antibiotic in the antimicrobial sensitivity testing-based treatment group.

medicine zantac 2015-01-14

1 microM histamine produced a 2- to 3-fold selective increase in PDE4 activity in U-937 cells after 4 hours of incubation. Enzyme activation was reversible, concentration buy zantac - and time dependent. Cycloheximide (10 microM) prevented histamine-induced stimulation of PDE4. The H2-receptor antagonist, ranitidine, but not the H1-receptor antagonist, diphenhydramine, prevented histamine-induced activation of PDE4 in a concentration-dependent manner. Inhibition of cAMP degradation in the presence of histamine plus rolipram after 4 h of incubation further increased cAMP levels and PDE4 activity.

dosage zantac infant 2016-02-20

Most animal models of nonsteroidal Tegretol Xr Prices anti-inflammatory drug (NSAID) induced gastric injury are characterized by acute, superficial erosions in the corpus region, whereas the clinically significant injury in man is the deep, antral ulcer. The purpose of this study was to characterize a model of NSAID-induced antral ulceration that more closely resembles the type of damage seen in man. Rabbits received indomethacin subcutaneously every 12 h. The progression of ulcer formation was followed by killing groups of animals after one to seven doses of indomethacin. The dose dependency of ulcer formation was assessed by giving indomethacin at doses of 1 to 20 mg/kg. Healing of antral ulcers was determined by examining the stomach at various times after administering the seventh dose of indomethacin (20 mg/kg). The effects of prophylactic treatment with misoprostol or ranitidine on ulcer formation were assessed. Indomethacin administration initially produced superficial erosions in the corpus and antrum, but with time, ulcers became apparent in the antrum. The formation of these ulcers was dependent upon the number of times indomethacin was administered and the dose. Similar ulcers could be induced with a second NSAID, diclofenac. Misoprostol treatment resulted in a significant reduction in the extent of indomethacin-induced antral ulceration, but ranitidine had no effect. Antral ulcers healed progressively following cessation of indomethacin administration and were almost completely resolved by 108 h after the final dose of indomethacin. These results demonstrate that subcutaneous NSAID administration to rabbits is a simple and reproducible method for producing ulcers that bear striking macroscopic resemblance to NSAID-induced antral ulcers in man.(ABSTRACT TRUNCATED AT 250 WORDS)

zantac 1 mg 2017-01-28

Histamine interacts with the stress response in eukaryotes. This study investigated the effects of antihistamines on the heat shock (HS) response in yeast, thereby exploring their functions in a well-established histamine receptor (H(x) R)-free Elavil Dosage Cats model.

zantac 50 mg 2016-03-15

The introduction in 1990 of the Minimum Pricing Policy without allowing generic substitution had a relatively small impact on the selection of medicines within the Pharmaceutical Benefits Scheme. However the effect of generic substitution at the pharmacist level, which was introduced in December 1994, resulted in a marked increase in the percentage of eligible PBS items dispensed at benchmark. Case studies showed a larger premium resulted in a greater shift of patients Indocin 15 Mg from drugs with a brand premium to the benchmark alternative.

zantac pediatric dose 2016-05-29

Eradication of H Duphaston Dose . pylori cures peptic ulcer disease. Bismuth and antibiotics in various combinations were tested at a single university hospital.

zantac 300mg tablets 2017-08-09

The cations (all associated with the acetate anion) inhibited bitterness when mixed with pharmaceutical solutions to varying degrees. The sodium cation significantly (P < 0.003) inhibited bitterness of the pharmaceuticals more than the other cations. The anions (all associated with the sodium cation) also inhibited bitterness to varying degrees. With the exception of salicylate, the glutamate and adenosine monophosphate anions significantly (P < 0.001) inhibited Mestinon Xr Generic bitterness of the pharmaceuticals more than the other anions. Also, there were several specific inhibitory interactions between ammonium, sodium and salicylate and certain pharmaceuticals.

zantac tabs 2015-09-05

20 outpatients with acute peptic ulcer were treated with ranitidine 50 mg i.v. twice daily in an open trial. 92% of the duodenal ulcers and 80% of the gastric ulcers were healed after four weeks treatment. The rapid symptomatic improvement noted during the Effexor Dosage Forms patients daily visits was particularly impressive. The results of our study show that the commonly practised intravenous treatment of peptic ulcers is also practicable with a modern drug possessing a clearly defined mode of action.

zantac infant dose 2015-03-25

We studied the pharmacological actions of combined histamine H1/H3 receptor blockade on the increase in nasal airway resistance (NAR) and decrease in nasal cavity volume produced by nasal exposure to compound 48/80, a mast cell degranulator. In the anesthetized cat compound 48/80 (1%) produced a maximum increase in NAR of 9.1 +/- 0.7 cmH20.L/minute. The increase in NAR in animals pretreated with a combination of the H1 antagonist, chlorpheniramine (CTM; 0.8 mg/kg i.v.) and increasing doses of the H3 antagonist, thioperamide (THIO; 1.0, 3.0, and 10.0 mg/kg i.v.) were 6.1 +/- 2.1, 4.2 +/- 1.0 and 2.2 +/- 0.7 cmH20.L/minute, respectively. A second H3 antagonist, clobenpropit (CLOB; 0.03, 0.3, and 1.0 mg/kg i.v.) combined with CTM (0.8 mg/kg i.v.) also inhibited the nasal effects of compound 48/80. When the nonsedating H1 antihistamine, loratadine (3.0 mg/kg i.v.), was substituted for CTM, it also reduced nasal congestion when given in combination with THIO (10 mg/kg i.v.). In contrast, treatment with CTM (1. Nexium Tablet 40mg 0 mg/kg i.v.) and the H2 antagonist, ranitidine (RAN; 1.0 mg/kg i.v.) were without activity. Loratadine, CTM, CLOB, RAN, or THIO administered alone were inactive. The alpha-adrenergic agonist, phenylpropanolamine (PPA; 1.0 mg/kg i.v.) demonstrated decongestant effects, but in contrast to H1/H3 blockade, PPA produced a significant hypertensive effect. Using acoustic rhinometry (AcR) we found that combined i.v. CTM (1.0 mg/kg) and THIO (10 mg/kg) and combined oral CTM (10 mg/kg) and THIO (30 mg/kg) blocked the decrease in nasal cavity volume produced by intranasal compound 48/80 (1%, 50 microL). We conclude that combined H1/H3 histamine receptor blockade enhances the efficacy of an H1 antagonist by conferring decongestant activity to the H1 antihistamine. We propose that the decongestant activity of combined H1/H3 blockade may provide a novel approach for the treatment of allergic nasal congestion without the hypertensive liability of current therapies.

zantac 300mg dosage 2015-08-23

This case of an unintentional ingestion of an unknown amount of potassium permanganate by a 5-year-old boy, and its sequelae, exemplifies the potential danger of this poison. Due to the wide availability of this agent in over-the-counter preparations and the high potential for serious sequelae, clinicians should be aware of the actions of this agent, as well Biaxin Medicine as the diagnostic and management features associated with it.

zantac reviews 2015-01-16

Background-Repeat prescribing should be limited to drugs which are to be prescribed on a long-term basis to patients whose conditions are stable. Early studies were based on small sample sizes. The definition of repeat prescribing has not been consistent and interpractice variation in repeat prescribing has not been described.Aims-To describe the diagnostic categories and anatomical groups associated with repeat prescriptions; to describe interpractice variation associated with repeat prescribing and to describe the repeat to consultation ratio for the most frequently prescribed diagnoses and drugs.Method-Doctors from a stratified quota sample of 22 Northern Ireland practices recorded their perceived diagnosis for every consultation and for every repeat prescription over a 2-week period.Results-The diagnostic categories significantly associated with repeat prescriptions were digestive, cardiovascular, neurological, psychiatric and metabolic ( p < 0.0001). The anatomical drug categories significantly associated with repeat prescriptions were gastrointestinal drugs, cardiovascular drugs, central nervous system drugs, dressings and appliances (p < 0.0001). There was wide interpractice variation in repeat prescribing (both overall and for individual anatomical groups) and associated diagnoses. Lasix 20mg Tab High repeat to consultation ratios were recorded for ranitidine, temazepam and diazepan.Conclusions-Wide interpractice variation in repeat prescribing and associated diagnoses revealed poor consensus among practices. Therefore, the approach to the management of common conditions - whether to consult or issue a repeat prescription - was not uniform. The implications of these findings require further research. Commonly occurring diagnoses and drugs had unacceptably high repeat to consultation ratios. Copyright (c) 2000 John Wiley & Sons, Ltd.

zantac blue pill 2016-02-23

The effects of Cimetidine, Ranitidine, and Omeprazole on gastric and hepatic alcohol-dehydrogenase (ADH) activity was studied in rat. Two apparent values for Km were found for gastric ADH (220 mmol l-1 and 1043 mmol l-1 respectively) and one for hepatic ADH (0.54 mmol l-1). Cimetidine was shown to exert an uncompetitive inhibition of low Km gastric ADH with a Ki of 0 Buspar Low Dose .167 mmol l-1 and a competitive inhibition of high Km gastric ADH with a Ki 2.3 mmol l-1. Ranitidine was found to present non-competitive inhibition only on low Km gastric ADH with a Ki of 12 mmol l-1. Omeprazole affects only low Km gastric ADH with a Ki of 5.6 mmol l-1 and presents a linear-mixed type of inhibition. Hepatic ADH was shown to be competitively inhibited only by Cimetidine with a Ki of 6.0 mmol l-1 whereas no inhibition for either Ranitidine and Omeprazole was observed. These results confirm the inhibitory action of Cimetidine on both gastric and hepatic ADH; Ranitidine and Omeprazole show minor effects on ADHS activity and probably on first-pass metabolism.

zantac generic equivalent 2017-04-14

Up to 4 wk of treatment with rabeprazole 20 mg q.a.m. produced significantly greater healing rates, compared to treatment with ranitidine 150 mg b.i.d. (83% vs 73%; p = 0.017). Significant differences between treatment groups were also observed for secondary efficacy indices. At wk 2, rabeprazole was more likely than ranitidine to produce complete resolution of duodenal ulcer pain (39% vs 25%; p = 0.006), improvement in duodenal ulcer nighttime pain severity (76% vs 65%; p = 0.044), and improvement in overall well-being (55% vs 41%; p = 0.009). At wk 4, the proportion of patients with normalization of overall well-being was significantly higher in the rabeprazole group than in the ranitidine group (45% vs 29%; p = 0.003). Rabeprazole was safe and well tolerated in this study.

zantac generic target 2017-03-17

We report three cases of hemorrhagic gastritis in term infants that led to massive bleeding of life--threatening proportions in the first 24 hours of life. In all three cases, bleeding was controlled by conservative therapeutic management. Management of this unusual entity in the newborn infant is discussed.

zantac 300 mg 2015-06-19

Histamine in food has been shown to induce intolerance reactions mimicking food allergy. These reactions seem to be due to impaired histamine metabolism caused by reduced diamine oxidase activity. To validate routine serum diamine oxidase assessment, daily variations of diamine oxidase were evaluated.

zantac dosage pediatric 2016-03-05

The rates at which wastewater treatment plant (WWTP) microbial communities biotransform specific substrates can differ by orders of magnitude among WWTP communities. Differences in taxonomic compositions among WWTP communities may predict differences in the rates of some types of biotransformations. In this work, we present a novel framework for establishing predictive relationships between specific bacterial 16S rRNA sequence abundances and biotransformation rates. We selected ten WWTPs with substantial variation in their environmental and operational metrics and measured the in situ ammonia biotransformation rate constants in nine of them. We isolated total RNA from samples from each WWTP and analyzed 16S rRNA sequence reads. We then developed multivariate models between the measured abundances of specific bacterial 16S rRNA sequence reads and the ammonia biotransformation rate constants. We constructed model scenarios that systematically explored the effects of model regularization, model linearity and non-linearity, and aggregation of 16S rRNA sequences into operational taxonomic units (OTUs) as a function of sequence dissimilarity threshold (SDT). A large percentage (greater than 80%) of model scenarios resulted in well-performing and significant models at intermediate SDTs of 0.13-0.14 and 0.26. The 16S rRNA sequences consistently selected into the well-performing and significant models at those SDTs were classified as Nitrosomonas and Nitrospira groups. We then extend the framework by applying it to the biotransformation rate constants of ten micropollutants measured in batch reactors seeded with the ten WWTP communities. We identified phylogenetic groups that were robustly selected into all well-performing and significant models constructed with biotransformation rates of isoproturon, propachlor, ranitidine, and venlafaxine. These phylogenetic groups can be used as predictive biomarkers of WWTP microbial community activity towards these specific micropollutants. This work is an important step towards developing tools to predict biotransformation rates in WWTPs based on taxonomic composition.