Drugs online research references
Scand J Gastroenterol. 1995 Mar;30(3):216-8.
Omeprazole and dry mouth.
Teare JP, Spedding C, Whitehead MW, Greenfield SM, Challacombe SJ, Thompson RP.
Gastrointestinal Laboratory, Rayne Institute, St Thomas' Hospital, London, UK.
BACKGROUND: Omeprazole causes irreversible inhibition of the hydrogen/potassium adenosine triphosphatase enzyme, leading to a marked reduction in both acid secretion and volume of gastric juice. Reported side-effects include nausea, vomiting, diarrhoea, constipation, and headache. We report the development of dry mouth during omeprazole therapy. METHODS: We have identified six patients taking omeprazole for more than 6 weeks who complained of a dry mouth. Salivary production was measured as whole salivary flow produced over a 10-min period spat into a collecting vessel and as 5% citric acid-stimulated parotid salivary flow collected with a Lashley cup device placed over the parotid duct. Flow rates were evaluated both during and after cessation of treatment. Saliva produced was then cultured for microbes. RESULTS: Four of the six had subnormal parotid or whole salivary flow rates on treatment that recovered after stopping treatment. The increase after treatment was marked in four. Significant amounts of Candida albicans grew from the saliva of the three patients with the lowest salivary flows; one saliva also grew Staphylococcus aureus. CONCLUSION: Salivary flow is reduced in some patients treated with omeprazole, returning to normal after cessation of treatment. This reduction may predispose to opportunistic infection, particularly in the edentulous.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7770709&dopt=Abstract
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Dig Dis Sci. 1996 Sep;41(9):1845-52.
Effect of omeprazole on movement of intravenously administered metronidazole into gastric juice and its significance in treatment of Helicobacter pylori.
Veldhuyzen van Zanten SJ, Pollak PT, Kapoor H, Yeung PK.
Division of Gastroenterology, Faculty of Medicine, Dalhousie University, Victoria General Hospital, Halifax, Nova Scotia, Canada.
Four healthy, Helicobacter-negative volunteers were studied to determine the effect of omeprazole on the movement of metronidazole across the gastric mucosa into the gastric lumen. Each received a 500-mg intravenous infusion of metronidazole and repeated serum, and gastric juice samples were obtained concomitantly over an 8-hr study via indwelling intravenous catheter and nasogastric tube. The same protocol was repeated following one week of oral omeprazole 20 mg twice daily. Metronidazole concentrations were measured by high-performance liquid chromatography. The results demonstrated that: metronidazole moves rapidly from serum into gastric juice; omeprazole causes a marked reduction in total metronidazole concentrations in gastric juice, completely accounted for by pH-related shifts in the proportion of ionized metronidazole, but does not alter concentrations of nonionized metronidazole, which remain above the MIC level against H. pylori; and even under conditions where no pH-related drug trapping occurs (pH > 4), concentrations of metronidazole were higher in gastric juice than in serum during most of the study, indicating that a special transport mechanism may be operational. The practical implication of this effect of omeprazole in combination therapy with metronidazole remains to be established.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8794805&dopt=Abstract
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Antimicrob Agents Chemother. 1997 Aug;41(8):1797-801.
Basis for the selective antibacterial activity in vitro of proton pump inhibitors against Helicobacter spp.
Sjostrom JE, Kuhler T, Larsson H.
Department of Cell Biology, Preclinical Research and Development, Astra Hassle AB, Molndal, Sweden.
Proton pump inhibitors of the benzimidazole type exert a specific antibacterial activity against Helicobacter pylori in vitro. In the present study, the basis for this selectivity was investigated, and in particular, various factors affecting the in vitro antibacterial activity of sulfide analogs of benzimidazoles were studied. Upon preincubation of omeprazole for a period of up to 72 h in a buffer at pH 7, a product was formed that was bactericidal for H. pylori but had no effect on urease activity. Sulfide constitutes the main end product of degradation. The sulfide analog of omeprazole (H 168/22) exerted a bactericidal activity specifically against both resting (in buffer) and growing (in broth) Helicobacter spp., and time-kill in buffer at pH 5 was enhanced compared to that at pH 7. There was no or very low covalent binding of 3H-labeled H 168/22 to Helicobacter spp. or to other gram-negative and gram-positive bacteria. In the presence of fetal calf serum (FCS) under the same conditions, binding was only slightly lowered while the killing activity was markedly reduced, indicating a probably nonspecific interaction with proteins and/or protection of bacterial target(s) by FCS. Addition of H 168/22 (four times the minimum bactericidal concentration [MBC]) to exponentially growing H. pylori immediately stopped growth, and after an incubation period of 20 h viable counts were reduced by >7 log10. One-hour exposure of H. pylori to the drug followed by repeated washing retarded growth by about 2 h, indicating that the effect is reversible after short-term exposure. MICs and MBCs of various sulfide structures were lower than those obtained in broth after the addition of the corresponding sulfoxide. Thus, the MBC of the sulfide structure of omeprazole against 140 clinical isolates of H. pylori ranged from 8 to 32 microg/ml, compared to an MBC of omeprazole of 32 to 128 microg/ml. A similar potency was also recorded against other helicobacters. In conclusion, formation of sulfides of benzimidazoles in culture media is the reason for the selective antibacterial effect against H. pylori. The sulfides rapidly exerted a reversible antibacterial activity, which was specific against both resting and growing Helicobacter spp. without any covalent protein binding.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9257764&dopt=Abstract
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