Drugs online research references
Am J Clin Pathol. 1998 Nov;110(5):615-21.
Proton pump inhibitor-associated gastric polyps: a retrospective analysis of their frequency, and endoscopic, histologic, and ultrastructural characteristics.
Choudhry U, Boyce HW Jr, Coppola D.
Center for Swallowing Disorders, Division of Digestive Diseases, University of South Florida College of Medicine, Tampa 33612-9497, USA.
Since 1992 there have been reports of proton pump inhibitors being associated with fundic gland-type gastric polyps. Endoscopic and histologic characteristics and natural history of these polyps have not been clearly defined. We performed a retrospective study of patients on long-term treatment with proton pump inhibitors who developed gastric polyps. Gastric polyps developed in 17 (10 males and 7 females, 7.3%) of the 231 patients who underwent 2 or more upper endoscopies for complicated gastroesophageal reflux disease and who were receiving long-term treatment with proton pump inhibitors. The mean interval of proton pump inhibitor use after which an endoscopy revealed gastric polyps was 32.5 months. In 1 patient, discontinuation of treatment resulted in disappearance of the polyps within 3 months. The polyps recurred 4 months after the treatment was restarted. Endoscopy established that typical polyps were generally small (<1 cm), sessile, multiple, and whitish pink with a mottled partially translucent surface. The polyps were most often present in the proximal/midgastric body. Of the 15 polyps removed endoscopically, 9 were of the fundic gland type, 4 were of the hyperplastic type, and 2 were of the inflammatory type. Eight of 9 polyps with typical endoscopic appearance were of the fundic gland type. None of the polyps contained dysplasia or carcinoma. Long-term use of proton pump inhibitors may be associated with the presence of small gastric fundic gland polyps and hyperplastic polyps. A prospective study is required to establish their incidence, natural history, and clinical significance.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9802346&dopt=Abstract
note: kwd match prilosec online literature
Biochem Pharmacol. 1991 Jul 5;42(2):347-55.
The H+, K(+)-ATPase inhibitor pantoprazole (BY1023/SK&F96022) interacts less with cytochrome P450 than omeprazole and lansoprazole.
Simon WA, Budingen C, Fahr S, Kinder B, Koske M.
Byk Gulden Pharmazeutika, Konstanz, Germany.
The gastric acid antisecretory compound omeprazole (5-methoxy-2-((4-methoxy- 3,5-dimethyl-2-pyridinylmethyl)-sulphinyl)-1H-benzimidazole), a member of the new class of H+, K(+)-ATPase inhibitors, is known to interact with the metabolism of other drugs in vitro and in vivo. In this study, two other substituted benzimidazoles, pantoprazole (5-difluoromethoxy-2-((3,4-di-methoxy-2-pyridinylmethyl)-s ulp hinyl)-1H- benzimidazole) and lansoprazole (2-((3-methyl-4-(2,2,2-trifluoroethoxy)-2-pyridinylmethyl)- sulphinyl)-1H-benzimidazole) are compared for their ability to inhibit cytochrome P450 dependent biotransformation in vitro with regard to three representative reactions: O-dealkylation of 7-ethoxycoumarin (EC), N-demethylation of ethylmorphine (EM) and hydroxylation of lonazolac (Lona). These reactions can be seen in microsomes from phenobarbital pretreated rats representing the cytochrome P450IIB1 subfamily. As shown in presence of known inhibitors of cytochrome P450, e.g. SK&F 525A, metyrapone, chlorpromazine and nitrendipine, different enzymes seem to be responsible for these three indicator reactions of the cytochrome P450IIB1 complex. These reactions are inhibited to a different extent by the three H+, K(+)-ATPase inhibitors. Pantoprazole shows the lowest inhibitory activity versus the three reactions (Ki, mumol/L): EC, 138; EM, 104; Lona, 128. A greater effect is observed with omeprazole: EC, 38; EM, 68; Lona, 20. Lansoprazole exceeds omeprazole in inhibiting the three cytochrome P450 dependent enzymes: EC, 17; EM, 34; Lona, 8. In microsomes from untreated rats with the predominant cytochrome P450IIA1 subfamily as well as in microsomes from isopropanol treated rats (induction of cytochrome P450IIE1) which catalyse only lonazolac hydroxylation to a detectable amount, the latter reaction was inhibited by pantoprazole with a somewhat lower Ki of 77 whereas the values for omeprazole and lansoprazole remained unchanged in comparison to those found in microsomes from phenobarbital pretreated rats. The biotransformation rate of the substituted benzimidazoles themselves in microsomes from control and induced rats is lowest for pantoprazole followed by lansoprazole and omeprazole.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1650212&dopt=Abstract
note: kwd match prilosec online literature
hama-med.ac.jp
BACKGROUND: The acid inhibitory effect of lansoprazole depends on the S-mephenytoin 4'-hydroxylase (CYP2C19) genotype status. The effect of famotidine is independent of this genotype. AIM: To investigate the acid inhibitory effects of lansoprazole vs. famotidine during the daytime and night-time with reference to different CYP2C19 genotypes. METHODS: Fifteen healthy volunteers were given 20 mg famotidine twice a day or 30 mg lansoprazole once a day for 8 days. On post-dose day 8, 24-h intragastric pH monitoring was performed. RESULTS: During the daytime, the intragastric pH with lansoprazole was significantly higher than that with famotidine in the heterozygous extensive metabolizer group, whereas no significant difference was observed in the homozygous extensive metabolizer group. During the night-time, the intragastric pH with famotidine was quite similar to that with lansoprazole in the heterozygous extensive metabolizer and poor metabolizer groups. However, during the night-time, the intragastric pH with famotidine was significantly higher than that with lansoprazole in the homozygous extensive metabolizer group. CONCLUSIONS: An insufficient acid inhibition by lansoprazole during the night-time in the homozygous extensive metabolizer group could be compensated for by famotidine. CYP2C19 genotype testing appears to be useful for predicting the optimal acid inhibitory drug treatment collated with circadian intragastric pH change.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11929404&dopt=Abstract
note: kwd match prilosec online literature
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