Disease relevance of pantoprazole

• Gastric Helicobacter pylori infection accelerates healing of reflux esophagitis during treatment with the proton pump inhibitor pantoprazole [1].
• CONCLUSIONS: Patients with reflux esophagitis and H. pylori infection respond significantly better than H. pylori-negative patients to the PPI pantoprazole [1].
• Intravenous pantoprazole rapidly controls gastric acid hypersecretion in patients with Zollinger-Ellison syndrome [2].
• Recurrent anaphylaxis linked to pantoprazole [3].
• In the short-term treatment of patients with gastro-oesophageal reflux disease (GORD), lansoprazole 15, 30 or 60 mg/day was significantly more effective than placebo, ranitidine 300 mg/day or cisapride 40 mg/day and similar in efficacy to pantoprazole 40 mg/day in terms of healing of oesophagitis [4].

Psychiatry related information on pantoprazole

• In the latter patient, the replacement of omeprazole, a strong CYP1A2 inducer, by pantoprazole, a weaker CYP1A2 inducer, could have contributed, in addition to smoking cessation, to the observed strong increase of plasma clozapine concentrations [5].
• Multi-criteria decision making approach and experimental design as chemometric tools to optimize HPLC separation of domperidone and pantoprazole [6].
• The dual pantoprazole and clarithromycin therapy had the highest rate of patient compliance, but is less effective than triple therapy [7].

High impact information on pantoprazole

• In humans, the half-life of the inhibitory effect on acid secretion is approximately 28 hours for omeprazole and approximately 46 hours for pantoprazole [8].
• Pantoprazole was actively transported by Bcrp1 but not by MRP2 [9].
• Some compounds that stimulate E217betaG transport, such as penicillin G or pantoprazole, are not detectably transported by MRP2, suggesting that they allosterically stimulate transport without being cotransported with E217betaG [10].
• On the basis of the fact that blocking the clearance of acidic metabolites are known to induce the cell death, we hypothesized that pantoprazole (PPZ), one of gastric H+/K(+)-ATPase inhibitors used frequently to treat acid-related diseases, could inhibit growth of tumor cells [11].
• To determine the role of cytochrome P450 (CYP) 2C19 in the stereoselective metabolism of pantoprazole, we investigated the pharmacokinetic disposition of (+)- and (-)-pantoprazole in 7 extensive metabolizers and 7 poor metabolizers of S-mephenytoin [12].

Chemical compound and disease context of pantoprazole

• 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 [13].
• 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 [13].
• Pharmacodynamic effects of single doses of rabeprazole 20 mg and pantoprazole 40 mg in patients with GERD and nocturnal heartburn [14].
• METHODS: In an open two-centre study, 60 duodenal ulcer patients were treated with pantoprazole 40 mg b.d., clarithromycin 500 mg b.d. and amoxycillin 1 g b.d. for 1 week [15].
• CONCLUSION: Pantoprazole is more effective than placebo or nizatidine for controlling heartburn and acid regurgitation in patients with erosive oesophagitis [16].

Biological context of pantoprazole

• Stereoselective pharmacokinetics of pantoprazole, a proton pump inhibitor, in extensive and poor metabolizers of S-mephenytoin [12].
• A significant negative correlation was observed between the individual values for log10% urinary excretion of 4'-hydroxymephenytoin and AUC of pantoprazole (rs = -0.816; p < 0.005) [17].
• OBJECTIVES: To assess the possible relationship between the metabolic disposition of pantoprazole and genetically determined S-mephenytoin 4'-hydroxylation phenotype and genotype [17].
• Metabolic disposition of pantoprazole, a proton pump inhibitor, in relation to S-mephenytoin 4'-hydroxylation phenotype and genotype [17].
• Pantoprazole is well tolerated with minimal potential for drug interactions [18].

Anatomical context of pantoprazole

• Pantoprazole selectively blocks gastric parietal cell H+,K(+)-ATPase [19].
• Inhibition by BY 1023/SK&F 96022 was not reversed by dilution in either permeabilized gastric glands or intact gastric vesicles [20].
• Hepatocytes in suspension correctly predict interspecies differences in drug metabolism, which is demonstrated with pantoprazole and propafenone [21].
• It seems unlikely that this moderate hypergastrinaemia during pantoprazole treatment should influence the human enterochromaffin-like (ECL) cell density in a clinically relevant way, but data during long-term therapy are necessary to confirm this conclusion [22].
• Patients (106) with peptic ulceration of the oesophagus, stomach and duodenum, unresponsive to 3 or more months of high-dose treatment with ranitidine, were initially given pantoprazole (40-80 mg, p.o.) daily [23].

Associations of pantoprazole with other chemical compounds

• Pharmacokinetics, metabolism and interactions of acid pump inhibitors. Focus on omeprazole, lansoprazole and pantoprazole [24].
• Few data have been recently published regarding the pharmacokinetics of pantoprazole in children, and none are available for rabeprazole or esomeprazole [25].
• Continuous Infusion of Pantoprazole versus Ranitidine for Prevention of Ulcer Rebleeding: A U.S. Multicenter Randomized, Double-Blind Study [26].
• Patients were randomized to pantoprazole 40 mg once daily or nizatidine 150 mg b.i.d.. Endoscopy was performed before randomization and after 4 wk of therapy [27].
• Inhibition of pentagastrin-induced gastric acid secretion by intravenous pantoprazole: a dose-response study [28].

Gene context of pantoprazole

• CONCLUSIONS: Proton-pump inhibitors interact with and are metabolized by several human cytochromes P450, but only pantoprazole is also metabolized by a sulfotransferase [29].
• These results indicate that the stereoselective metabolism of pantoprazole depends on S-mephenytoin 4'-hydroxylase (CYP2C19) [12].
• Hence, no influence of pantoprazole on the pharmacokinetics of diclofenac was concluded, either by competition with the CYP2C9 or by the reduction of gastric acid secretion [30].
• 2. By Northern and Western blot analysis, omeprazole has been shown to be a more potent inducer of CYP1A1 than both lansoprazole and E3810, whereas pantoprazole did not induce CYP1A1 [31].
• Within one year of the start of the pantoprazole treatment, serum gastrin levels rose to 3 times normal values (189 +/- 32 pg/ml) [23].

Analytical, diagnostic and therapeutic context of pantoprazole

• Four patients required upward dose titration, 2 required 120 mg pantoprazole every 12 hours, and 2 required 80 mg every 8 hours [2].
• In conclusion, subjects receiving pantoprazole after elective EVL had significantly smaller postbanding ulcers on follow-up endoscopy than subjects receiving placebo [32].
• Pantoprazole reduces the size of postbanding ulcers after variceal band ligation: a randomized, controlled trial [32].
• 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 [13].
• A direct stereoselective reversed-phase HPLC method is described for the determination of the enantiomers of a proton pump inhibitor, pantoprazole (PAN), in human serum [33].

References