Effects Of Famotidine Research Articles

The effects of famotidine combined with vitamin K1 on the therapy of neonatal alimentary tract hemorrhage

Objective To observe the therapeutic efficacy of famotidine combined with vitamin K1 on neonatal alimentary tract hemorrhage. Methods 69 neonates with neonatal alimentary tract hemorrhage were divided into control group (24 neonates who accepted the conventional therapy combined with vitamin K,) and therapy group (45 neonates who got the treatment of control group combined with famotidine). The effects were evaluated by the offtime of hemorrhage. Results The total curative effect of the therapy group was 95.6% .which significantly higher than that in control group(70. 8% ) ,P < 0.05. Conclusion Famotidine combined with vitamine K1 could improve the therapeutic efficacy of the treatment of neonatal alimentary tract hemorrhage. It was a safe and effective method in the treatment of neonatal alimentary tract hemorrhage. Key words: Gastrointestinal hemorrhage; Famotidine; Vitamine K1; Infant,newborn

Famotidine Versus Pantoprazole for Preventing Bleeding in the Upper Gastrointestinal Tract of Critically Ill Patients Receiving Mechanical Ventilation

Mechanical ventilation increases risk for bleeding in the upper part of the gastrointestinal tract. Proton pump inhibitors, although they are more potent and longer acting inhibitors of gastric acid production than are histamine(2) antagonists, also are generally more expensive. Data comparing the 2 types of agents for preventing gastrointestinal bleeding in critically ill patients are limited. To compare the effectiveness of famotidine (a histamine(2) antagonist) and pantoprazole (a proton pump inhibitor) in preventing stress ulcers in critically ill patients receiving mechanical ventilation. Data were collected from the Project Impact database. All patients who received mechanical ventilation for more than 48 hours from November 2002 to June 2006 and were treated with either drug were included. Patients receiving other drugs or with known bleeding in the upper part of the gastrointestinal tract, thrombocytopenia, or coagulopathy were excluded. A total of 522 patients who received famotidine and 95 who received pantoprazole were included. Bleeding in the upper part of the gastrointestinal tract was more common in patients receiving pantoprazole than in patients receiving famotidine (0.38% vs 3.2%, P= .03). Although scores on the Acute Physiology and Chronic Health Evaluation II were higher in patients who received pantoprazole (P= .01), other outcome measures did not differ significantly between groups. Bleeding in the upper part of the gastrointestinal tract was more frequent among dialysis patients receiving pantoprazole than among those receiving famotidine. Famotidine and pantoprazole are similarly effective for preventing bleeding in the upper part of the gastrointestinal tract in patients receiving mechanical ventilation.

Effect of famotidine and lansoprazole on serum phosphorus levels in hemodialysis patients on calcium carbonate therapy

Histamine H2 receptor antagonists (HRA) or proton pump inhibitors (PPI) are frequently administered to patients on hemodialysis, because their intestinal mucosa is fragile. Although three studies have indicated that concomitant HRA administration causes a decrease in the binding of phosphate by calcium carbonate, the HRA doses tested in these studies were 2-4 times higher than the recommended dose for hemodialysis patients. In addition, it remains unclear whether PPI therapy affects serum phosphate levels in hemodialysis patients taking calcium carbonate. Accordingly, the aim of this study was to evaluate the influence of lansoprazole and the recommended dose of famotidine on serum phosphate and calcium levels in hemodialysis patients. The study included 115 hemodialysis patients who were taking calcium carbonate and who were also treated with either famotidine (10 mg/day) or lansoprazole (30 mg/day). Changes of the mean serum phosphate and calcium levels over 2 months before and after the start of famotidine or lansoprazole therapy were compared. The same parameters were also compared when famotidine was switched to lansoprazole. The mean serum phosphate level increased significantly after administration of either famotidine or lansoprazole (by 6.6 +/- 21.9% or 13.0 +/- 26.3%, p = 0.032 and p = 0.029, respectively). The mean serum calcium level was unchanged after administration of famotidine, but showed a significant decrease after administration of lansoprazole (by 3.44 +/- 7.73%, p = 0.013). Therefore, the calcium x phosphorus product was significantly increased by administration of famotidine, but not by administration of lansoprazole (6.68 +/- 23.37% and 8.73 +/- 27.41%, p = 0.046 and p = 0.251, respectively). When famotidine was switched to lansoprazole, the serum phosophate level did not change, but serum calcium decreased significantly by 3.8 +/- 13.0% (p = 0.0006). Not only administration of 20 mg/ day of famotidine as previously reported, but also 10 mg/day of this drug (the recommended dose for hemodialysis patients) caused a significant increase of serum phosphate in patients taking calcium carbonate. PPIs have been reported to show no effect on the serum phosphate level, but 30 mg/day of lansoprazole also caused a significant increase of serum phosphate in patients taking calcium carbonate.

In vivo γ-rays Induced Initial DNA Damage and the Effect of Famotidine in Mouse Leukocytes as Assayed by the Alkaline Comet Assay

Ionizing radiation induces a variety of lesions in DNA, each of which can be used as a bio-indicator for biological dosimetry or the study of the radioprotective effects of substances. To assess gamma ray-induced DNA damage in vivo in mouse leukocytes at various doses and the effect of famotidine, blood was collected from Balb/c male mice after irradiation with 4 Gy gamma-rays at different time intervals post-irradiation. To assess the response, mice were irradiated with doses of gamma-rays at 1 to 4 Grays. Famotidine was injected intra-peritoneally (i.p) at a dose of 5 mg/kg at various time intervals before irradiation. Four slides were prepared from each sample and alkaline comet assay was performed using standard protocols. Results obtained show that radiation significantly increases DNA damage in leukocytes in a dose dependent manner (p < 0.01) when using appropriate sampling time after irradiation, because increasing sampling time after irradiation resulted in a time dependent disappearance of DNA damage. Treatment with only 5 mg/kg famotidine before 4 Gy irradiation led to almost 50% reduction in DNA damage when compared with those animals which received radiation alone. The radioprotective capability of famotidine might be attributed to radical scavenging properties and an anti-oxidation mechanism.

Influence of famotidine on verapamil pharmacokinetics in rats

The effect of famotidine (4 mg/kg, p.o.) on the kinetic profile of co-administered verapamil (20 mg/kg(-1), p.o.) was studied in the rat. Plasma verapamil levels were collected serially for 12 h and measured using sensitive HPLC method. The pharmacokinetic parameters (elimination half-life, area under the plasma concentration-time curve, peak plasma levels and the times to attain these plasma levels) of verapamil were evaluated in the rat. The results indicate that co-administered famotidine did not significantly alter the pharmacokinetic profile of verapamil in the rat. The present finding suggests that famotidine may safely be co-administered with verapamil but clearly further studies in human subjects are needed to reliably rule out the potential interaction of these two drugs.

Effect of famotidine on recurrent bleeding after successful endoscopic treatment of bleeding peptic ulcer

We investigated the effect of acid suppression therapy on recurrent bleeding after successful endoscopic treatment of bleeding peptic ulcer. A total of 400 patients with bleeding peptic ulcer received either intravenous infusion of famotidine (40 mg/day) (n = 207, 163 males, 44 females, mean age 61.5 years) or drip infusion of omeprazole (40 mg/day; n = 193, 134 males, 59 females, mean age 59.8 years) after successful endoscopic treatment. The fasting duration, hospital stay, volume of transfused blood, incidence of rebleeding and mortality were compared between the two groups. The incidence of rebleeding did not differ significantly between the famotidine group (9%) and the omeprazole group (8%). The mean hospital stay was significantly shorter in the omeprazole group (18.4 days) than in the famotidine group (21.5 days, P = 0.009). However, there was no statistically significant difference in fasting duration, volume of transfused blood or mortality. Our findings indicate that intravenous infusion of famotidine after successful endoscopic treatment is equivalent to drip infusion of omeprazole for prevention of recurrent bleeding.

Effect of Famotidine After Endoscopic Treatment on Bleeding Peptic Ulcers

Background and Aim: Peptic ulcers are the most common cause of upper gastrointestinal bleeding. The aim of our study was to investigate the effect of acid suppressive therapy after endoscopic treatment on bleeding peptic ulcer diseases. Patients and Methods: The 398 patients with bleeding peptic ulcers were divided into two groups those receiving drip infusion of PPI (40 mg/day) (n=165, 116 men, 49 women, mean age 59.8 yrs) and those receiving infusion of famotidine (40 mg/day) (n=233, 188 men, 45 women, mean age 61.5 yrs) after initial endoscopic treatment.

Famotidine does not induce long QT syndrome: experimental evidence from in vitro and in vivo test systems

The effects of famotidine on the cardiac repolarization process were assessed using four different levels of test systems described in the draft stage guideline ICH S7B. A supratherapeutic concentration of famotidine (10 −5 M), which is >8 times higher than C max obtained after its therapeutic dose, neither inhibited human ether-a-go-go-related gene (HERG) K + current expressed in human embryonic kidney 293 (HEK293) cells nor affected any of the action potential parameters of guinea pig papillary muscles. Therapeutic (0.3 mg/kg, i.v.) to supratherapeutic doses (3–10 mg/kg, i.v.) of famotidine did not affect the repolarization process of the halothane-anesthetized canine model, while only supratherapeutic doses exerted the positive chronotropic, inotropic and dromotropic effects without affecting the mean blood pressure. Moreover, supratherapeutic doses of famotidine (1–10 mg/kg, i.v.) neither induced torsades de pointes nor prolonged QT interval in the canine chronic atrioventricular conduction block model. These results suggest that famotidine possesses no cardiovascular effects at a therapeutic dose, while it may exert cardiostimulatory actions after drug overdoses that might potentiate the proarrhythmic potential of co-administered cardiotonic agents by increasing the intracellular Ca 2+ concentration.

Gastric Mucosal Cell Proliferation in Ethanol-Induced Chronic Mucosal Injury Is Related to Oxidative Stress and Lipid Peroxidation in Rats

The oxygen free radicals-induced lipid peroxidation (LP) has been implicated in the pathogenesis of acute ethanol-induced gastric mucosal lesions. However, the role of LP in the generation of chronic gastric mucosal injury is unknown. We have developed a model of chronic mucosal injury induced by continuous ethanol ingestion for 5 days and characterized by marked alterations in plasma membranes from gastric mucosa. Therefore, LP was evaluated in this experimental model. Indicators of peroxidative activity, mucosal glutathione content, thymidine kinase activity (an index of cell proliferation), and histamine H2-receptor (H2R) binding constants were quantified in animals undergoing gastric mucosal damage. The effect of famotidine, a H2R antagonist that readily ameliorates the chronic mucosal injury, was also tested. Increased free radicals and LP levels were detected during gastritis; however, a second, higher peak of LP was noted in mucosal plasma membranes after ethanol withdrawal (recovery period). This further increase of LP coincided with active cell proliferation, decreased mucosal glutathione levels, and diminished specific cimetidine binding by H2R. Administration of famotidine accelerated the mucosal proliferative process, inducing the second lipoperoxidative episode sooner, and preserved the content of glutathione. In addition, LP correlated directly with cell proliferation and inversely with mucosal membrane cimetidine binding. In conclusion, LP seems to be involved in chronic ethanol-induced gastric mucosal injury. However, a further enhancement of plasma membrane LP occurred, associated with increased DNA synthesis and diminished cimetidine binding by membrane H2R. Therefore, increased LP could also participate in the compensatory mucosal proliferation initiated after ethanol withdrawal.

The Effect of Famotidine on Lowering Gastric Acidity in Gastric Carcinoma Patients

The Effect of Famotidine on Lowering Gastric Acidity in Gastric Carcinoma Patients

Plasma concentration of itraconazole in patients receiving chemotherapy for hematological malignancies: the effect of famotidine on the absorption of itraconazole

Plasma concentration of itraconazole in patients receiving chemotherapy for hematological malignancies: the effect of famotidine on the absorption of itraconazole

Effects of Famotidine vs Antacid on Gastric Acidity: Onset of Action and Symptom Relief

To the Editor. —The article by Dr Feldman 1 compares the acid-reducing capacities of over-the-counter famotidine with calcium carbonate antacid. We have confidence in Feldman's overall findings as they pertain to the relative duration of effects of each agent on gastric acidity; however, one should exercise great caution before extrapolating the findings from a highly controlled, pharmacodynamic assessment of gastric acidity to an interpretation of clinically relevant symptom relief. The results of several large symptom-based heartburn studies contradict the reported delayed onset of famotidine's antisecretory action in the article by Feldman. These studies clearly demonstrated the efficacy of low-dose famotidine both in treating and in preventing heartburn symptoms in a far earlier time frame than suggested by Feldman's pharmacodynamic data. In 2 such studies 2 (N. Laird, PhD, written communication, March 26, 1996), data collected from 1100 patients with heartburn demonstrated significant symptom relief (vs placebo) as early as 15

Effects of famotidine vs antacid on gastric acidity: onset of action and symptom relief

Effects of famotidine vs antacid on gastric acidity: onset of action and symptom relief

Controlled Study of the Putative Interaction Between Famotidine and Theophylline in Patients with Chronic Obstructive Pulmonary Disease

The effects of famotidine (80 mg per day), cimetidine (1600 mg per day), and placebo on theophylline pharmacokinetic parameters in chronic obstructive pulmonary disease (COPD) patients were compared. This was an open-label, randomized, three-period cross-over study, in which each subject first underwent a seven-day theophylline washout period, and thereafter received three single intravenous doses of theophylline (5 mg/kg infused over 30 minutes) during the study. Each of the experimental treatments was administered orally every 12 hours for a total of 9.5 days (19 doses). Theophylline was infused after the 17th dose of each treatment. Fourteen serial blood samples were collected before the start of each infusion, and for 30 hours after the end of each infusion. Plasma samples were assayed for theophylline, pharmacokinetic parameters were estimated, and treatment effects on each parameter were compared. Fourteen COPD patients completed all three periods of the investigation. Famotidine treatment had virtually no effect on any of theophylline's pharmacokinetic parameters. In contrast, cimetidine treatment significantly altered every pharmacokinetic parameter of theophylline as follows: Cimetidine decreased theophylline geometric mean CL from 2.74 L/h to 2.07 L/h (P < .001), and prolonged theophylline harmonic mean half-life from 6.6 to 9.6 hours (P < .001) and mean residence time from 10.8 to 15.0 hours (P < .001). Cimetidine treatment slightly increased theophylline volume of distribution by approximately 10%, and that change also was statistically significant (P = .032). The authors conclude that the treatment effects of cimetidine on theophylline pharmacokinetic parameters were in accord with those reported by others, and that famotidine treatment had no effect on any of theophylline's pharmacokinetic parameters in COPD patients.

NMDA receptor hypofunction and schizophrenia

famotidine 20 mg twice a day as adjunctive therapy in an open-label study. SPEM were recorded for 60 seconds at baseline, after 3 weeks on famotidine, and 1 week after discontinuation, using a 0.4 Hz/10 degree amplitude stimulus. SPEM outcome measures included In signal/noise, saccade number, and percent error. We found no statistically significant effect of famotidine on any of our outcome measures, although there was considerable intersubject variability. To determine if SPEM changes meaningfully reflect clinical response, we are currently analyzing the correlation of SPEM findings with BPRS and SANS scores, as well as the heterogeneity of the responses. Further studies might explore the utility of SPEM as a potentially valuable and noninvasive tool for the monitoring of response to novel pharmacologic therapies for schizophrenia.

Effect of famotidine on ciprofloxacin pharmacokinetics after single intravenous and oral doses in rats

The effect of intravenous (3.5 mg/kg) and oral (5 mg/kg) famotidine on ciprofloxacin pharmacokinetics after single (i.v.) intravenous (5 mg/kg) and oral (20 mg/kg) doses were examined in the rat. Famotidine co-administration significantly increased the terminal elimination half-life of ciprofloxacin (54% and 29% following i.v. and oral administration, respectively) and tended to reduce the total body clearance by 27% and 34% following i.v. and oral routes, respectively. The area under the plasma concentration-time curve and the mean residence time in the body after i.v. and oral doses were significantly increased following famotidine co-administration. No changes in the steady-state apparent volume of distribution was observed after i.v. administration. The maximum plasma concentration and the time to peak concentration after oral dosing were also unaffected. These results suggest a possible reduction in the total clearance of ciprofloxacin, owing to inhibition of its renal tubular excretion by famotidine. Further studies are warranted to determine whether this interaction occurs in humans.

Famotidine increases plasma alcohol concentration in healthy subjects

The effect of famotidine on plasma alcohol concentration was studied in 24 healthy male subjects who demonstrated high apparent ethanol first-pass metabolism after oral (p.o.) and intravenous (i.v.) ethanol administration (i.e. AUC(po) < or = 40% of AUC(i.v.), where AUC is area under the plasma ethanol concentration-time curve). Six of the original 30 subjects screened (20%) did not demonstrate high first-pass metabolism and were excluded. In a randomized open crossover study, oral ethanol pharmacokinetics were assessed after breakfast in the morning following a 3-day regimen of famotidine, 40 mg/day, and following a no-drug control period. Famotidine increased the area under the plasma ethanol concentration-time curve (AUC0-t) by 29% (7.1 vs 5.5 mg.h/dL, P = 0.006) and maximal plasma concentration (Cmax) by 23% (9.2 vs 7.5 mg/dL, P = 0.013). The changes in ethanol AUC0-t and Cmax may have been associated with changes in gastric emptying, as they were inversely correlated with changes in the time at which maximal plasma concentration was attained. There was considerable intra-individual variation in ethanol AUC and Cmax. As a result, regression to the mean is a potentially confounding problem in ethanol pharmacokinetic studies when subjects are selected on the basis of having low AUC(po), and properly controlled randomized studies of substantial size are required to detect modest drug effects. Small effects on ethanol pharmacokinetics have now been demonstrated with all four of the major H2-receptor antagonists, but these effects are seen only under specific experimental conditions and appear to be unimportant clinically.

Effect of famotidine on renal transplant patients treated with ciclosporine A.

The influence of a 7-day course of 40 mg famotidine administered orally on the pharmacokinetics of ciclosporine A at steady-state has been investigated in 10 renal transplant patients. Famotidine did not appear to significantly alter the pharmacokinetics of ciclosporine A. This might be ascribed to the limited potential of famotidine for inhibiting microsomal enzyme function. Moreover, plasma creatinine concentrations and creatinine clearance remained stable. Our results suggest that famotidine has no noticeable interaction with ciclosporine A.

Effects of famotidine on various immunological parameters in patients with rheumatic diseases: decreased lymphocyte DR expression by famotidine.

We examined the effect of famotidine, a histamine-type 2 receptor antagonist, on the immunocompetent cells. The number of DR(+) cells were significantly decreased in patients with systemic lupus erythematosus (P less than 0.05) by parenteral administration of famotidine (40 mg/days for 4 weeks). However, total lymphocyte number and monocyte number did not change. Immunoglobulin levels of patients with rheumatoid arthritis and normal male did not change. Furthermore, phytohemagglutinin induced lymphocyte proliferation was increased by addition of famotidine (10 ng/ml). Nonetheless, famotidine did not have mitogenic function itself to lymphocyte and did not affect IL-2 production.

Effect of famotidine on gastrin cell, somatostatin cell, and prostaglandin E2 concentration of stomach in experimental pyloric stenosis model

Effect of famotidine on gastrin cell, somatostatin cell, and prostaglandin E₂ concentration of stomach in experimental pyloric stenosis model