Drugs online research references
amy.hi-ho.ne.jp
In this study, the influence of omeprazole on the adhesive activity of neutrophils, provided by an extract of Helicobacter pylori, was determined. Human neutrophils were collected from peripheral blood and labelled with a fluorochrome. Helicobacter pylori (NCTC 11637) was cultured and its water extract was obtained by centrifugation of the bacterial suspension. Neutrophils were incubated with the extract in a plastic plate. Percentage adherence was calculated by measuring the fluorescence of floating and adherent cells. Rat mesenteric venule was prepared on an intravital microscope and the number of neutrophils which adhered to venular endothelium was counted. Neutrophil adherence to the plastic plate was increased by the presence of H. pylori extract. Pretreatment with omeprazole significantly decreased this adherence in a dose-dependent manner (10(-6)-10(-4)mol/L). Neutrophil adherence to the mesenteric venule was also increased by H. pylori extract and significantly inhibited by omeprazole. These results indicate that the neutrophil-endothelial adhesive interaction is inhibited by omeprazole, suggesting that omeprazole prevents neutrophil recruitment to the gastric mucosa associated with H. pylori infection.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10029274&dopt=Abstract
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Gastroenterology. 1999 Apr;116(4):813-22.
Omeprazole and dietary nitrate independently affect levels of vitamin C and nitrite in gastric juice.
Mowat C, Carswell A, Wirz A, McColl KE.
University Department of Medicine and Therapeutics, Western Infirmary, Glasgow, Scotland.
BACKGROUND & AIMS: Hypochlorhydria is associated with an increased risk of gastric cancer. We have studied the effect of pharmacologically induced hypochlorhydria on the gastric juice ascorbate/nitrite ratio, which regulates the synthesis of potentially carcinogenic N-nitroso compounds. METHODS: Saliva, gastric juice, and serum from 20 healthy volunteers (9 positive for Helicobacter pylori), with a mean age of 30 years (range, 20-47 years), were analyzed for nitrite, ascorbic acid, and total vitamin C before and for 2 hours after ingestion of 2 mmol [corrected] nitrate (nitrate content of a standard salad meal). This was repeated after 4 weeks of treatment with omeprazole, 40 mg daily. RESULTS: Before omeprazole treatment, the nitrate meal lowered gastric ascorbic acid levels from 3.8 to 0.9 microg/mL (P < 0.05) and increased median salivary nitrite levels from 44 to 262 micromol/L (P < 0.001); gastric nitrite concentration remained undetected in 10 subjects. Omeprazole increased median fasting gastric nitrite levels from 0 to 13 micromol/L (P = 0.001) and decreased fasting gastric ascorbic acid levels from 3.8 to 0.7 microg/mL (P < 0.001). With omeprazole treatment, gastric nitrite levels after the nitrate meal were markedly increased at 154 micromol/L (range, 49-384 micromol/L; P < 0.001). In H. pylori-infected subjects, omeprazole also decreased total vitamin C levels in both gastric juice and serum. CONCLUSIONS: Omeprazole and dietary nitrate independently decrease the ascorbate/nitrite ratio. This may lead to an increased risk of gastric cancer.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10092303&dopt=Abstract
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numico-research.nl
BACKGROUND & AIMS: This study evaluated the effect of long-term gastric acid suppressive therapy with omeprazole on intragastric levels of carcinogenic N-nitrosamines and related parameters. METHODS: Forty-five patients on long-term omeprazole medication (mean, 35 months) and 13 healthy subjects without medication participated. Volatile N-nitrosamines were determined in gastric juice and urine. Intragastric pH, nitrite, nitrate, and H. pylori status were determined. DNA isolated from gastric biopsy specimens was analyzed for precarcinogenic alkyl-DNA adducts. RESULTS: The intragastric pH in patients was significantly higher compared with controls (P = 0.0001). Gastric nitrite levels in patients were nonsignificantly higher. There was no difference in total levels of intragastric volatile N-nitrosamines between patients and controls, however, urinary N-nitrosodimethylamine excretion was higher in patients (P = 0.001). On omeprazole, Helicobacter pylori-positive vs. -negative patients had a nonsignificantly higher intragastric nitrite level and higher urinary N-nitrosodimethylamine excretion. No alkyl-DNA adducts could be detected in gastric epithelium. CONCLUSIONS: Increased intragastric pH caused by long-term treatment with omeprazole does not result in increased intragastric levels of nitrite and volatile N-nitrosamines. The significantly higher urinary N-nitrosamine excretion implies the risk of increased endogenous formation of N-nitrosamines during long-term omeprazole treatment. This risk may be higher in H. pylori-positive patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11522734&dopt=Abstract
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