Drugs online research references









Fam Pract. 2001 Jun;18(3):333-8.
Proton pump inhibitors: a study of GPs' prescribing.

Jones MI, Greenfield SM, Jowett S, Bradley CP, Seal R.

Department of Primary Care and General Practice, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

BACKGROUND: There has been a rapid increase in proton pump inhibitor (PPI) prescribing in recent years, and controlling the cost and improving the quality of prescribing is an issue of concern to many GPS: OBJECTIVE: Our aim was to compare GPs' usage of different PPIs and explore how GPs' PPI prescribing changes following the introduction of a cheaper competitor. METHODS: PPI prescribing data (PACT) for 53 GPs, who were selected as regular users of a teaching hospital, were monitored from January 1995 to December 1997. The GPs were located in two adjoining health districts and had been interviewed about influences on their decisions to begin prescribing lansoprazole. The PPI prescribing data were collected for the teaching hospital and the general hospital in the adjoining district. RESULTS: Complete prescribing data were available for 50 GPS: Total PPI prescribing increased throughout the study due mainly to increasing use of the new PPIS: Use of the new PPIs increased from 6 to 24% over 3 years. The proportion of maintenance doses prescribed increased from 3 to 12%. There was a 23-fold difference in total PPI prescribing and an 87-fold difference in lansoprazole prescribing between the highest and lowest prescribers. The uptake of pantoprazole was slower than that of lansoprazole. A rapid increase in the use of lansoprazole by the GPs followed an increase in use in the teaching hospital. CONCLUSION: Hospital prescribing was an important influence on the choice of PPI used by GPS: The wide variation in PPI prescribing suggests that there is scope for improvement in the quality and cost of PPI prescribing.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11356744&dopt=Abstract

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Gastroenterology. 2002 Jan;122(1):119-33.
Genetic or chemical hypochlorhydria is associated with inflammation that modulates parietal and G-cell populations in mice.

Zavros Y, Rieder G, Ferguson A, Samuelson LC, Merchant JL.

Howard Hughes Medical Institute, University of Michigan, Ann Arbor, Michigan, USA.

BACKGROUND & AIMS: Reduced gastric acid predisposes the stomach to colonization by bacteria and inflammation. Therefore, we investigated how the chronic gastritis in mice made hypochlorhydric by either gastrin deficiency or omeprazole treatment modulates epithelial cell function. METHODS: The gastric pathology of 16-week-old wild-type gastrin-expressing (G+/+) and gastrin-deficient (G-/-) mice maintained in conventional housing was compared. G-/- mice were then treated with antibiotics for 20 days. In a separate experiment, G+/+ mice were treated with omeprazole for 2 months or treated with omeprazole and antibiotics. RESULTS: Compared with the G+/+ animals, the hypochlorhydric G-/- mice showed significant inflammation that resolved after 20 days of antibiotic treatment and correlated with a decrease in bacterial overgrowth. Elevated G- and parietal-cell numbers in the G-/- mice, quantified by flow cytometry, normalized after antibiotic treatment. G+/+ mice treated with omeprazole had increased bacteria and mucosal lymphocytes that resolved after antibiotic therapy. Quantitation of the gastric cells in these omeprazole-treated mice revealed a significant increase in G- and parietal-cell numbers. On resolution of the gastritis, a decrease in parietal and gastrin-expressing (G) cells was observed despite sustained hypochlorhydria in the presence of omeprazole. CONCLUSIONS: Genetic or chemical hypochlorhydria predisposes the stomach to bacterial overgrowth resulting in inflammation. The specific changes in parietal and G cells correlate with the presence of inflammation and not directly with gastric acid. Thus, the normal stomach responds to inflammation by increasing the number and function of cell types that are able to maximize gastric acid output.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11781287&dopt=Abstract

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mb.kyoto-phu.ac.jp

We examined the local effect of several drugs against secretagogue-stimulated acid secretion in dogs. Test drugs were applied to denervated gastric pouches in conscious dogs either for 5 to 30 min beginning 1 hr after or for 30 min before intravenous infusion of gastric secretagogues (histamine, pentagastrin, or carbachol). The antisecretory effect of test drugs delivered by an intravenous or oral route was also examined. Local application of acid pump inhibitors (omeprazole, leminoprazole) for 30 min beginning 1 hr after histamine infusion significantly inhibited gastric acid secretion. The effect of leminoprazole persisted for more than 8 hr after a 30 min application. A mast cell stabilizer (FPL 52694) applied to pouches for 15 to 30 min also potently inhibited histamine-stimulated gastric acid secretion in a time-dependent manner. The duration of the antisecretory effect of such drugs after a 30 min application was greater than 4 hr. Locally applied leminoprazole and FPL 52694 for 30 min also significantly inhibited pentagastrin- and carbachol-stimulated gastric acid secretion. Although intravenous omeprazole and leminoprazole exerted a potent antisecretory effect on histamine-induced acid secretion FPL 52694 had little or no antisecretory effect following intravenous or oral administration. 16,16-dimethyl prostagladin E2 also locally inhibited histamine-stimulated acid secretion. Acid stable local anesthetics (tetracaine, ethyl-4-aminobenzoate), histamine H2-receptor blockers (cimetidine, ranitidine, and famotidine), and a muscarinic M1-receptor antagonist (pirenzepine) did not exhibit local antisecretory effects. Such results strongly suggest that the apical membrane of parietal cells possesses a pharmcologically sensitive portion similar to the basolateral membrane, which usually mediates gastric acid secretion. The apical membrane represents an intriguing target for new antisecretory drugs, as well as a new medium for further elucidating the functional features of parietal cells.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11787764&dopt=Abstract

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