Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tolerability of omeprazole was compared to control agents in 68 clinical studies that enrolled a total of 4846 patients, of whom 3096 received omeprazole. The incidence of adverse experiences was independent of omeprazole dose administered, the age of the patients, and the disease treated (duodenal ulcer or endoscopically verified gastroesophageal reflux disease). The most common clinical adverse experiences were headache, diarrhea, abdominal pain, and nausea. The most common laboratory adverse experiences were elevated aspartate aminotransferase and elevated alanine aminotransferase. Omeprazole was well tolerated, and the incidence of clinical and laboratory adverse experiences was similar in patients receiving omeprazole, placebo, cimetidine, or ranitidine.
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PMID:Comparative tolerability profile of omeprazole in clinical trials. 191 59

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of omeprazole are reviewed. Omeprazole, a substituted benzimidazole, has a unique site and mechanism of action because it inhibits the proton pump--i.e., hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase)--and consequently blocks the final common step in the gastric acid secretory pathway. Omeprazole inhibits basal and histamine-, gastrin- and pentagastrin-stimulated gastric hydrochloric acid secretion. It produces a dose-dependent reduction in gastric acidity, gastric acid output, and gastric juice volume and has variable effects on pepsin secretion. Omeprazole has no documented effect on esophageal motility or lower esophageal sphincter pressure. Omeprazole is variably absorbed from the gastrointestinal tract, and food appears to decrease the rate, but not the extent, of drug absorption. The drug is approximately 95% bound to plasma proteins and is metabolized to inactive components that are enterohepatically or renally eliminated. Omeprazole is more effective (in most studies) than H2-receptor antagonists in treating duodenal ulcer, at least as effective in treating benign gastric ulcer, and more effective in treating reflux esophagitis. Omeprazole has been used successfully in patients with Zollinger-Ellison syndrome refractory to treatment with H2-receptor antagonists. Gastrointestinal complaints (nausea and diarrhea) are the most commonly reported adverse effects associated with omeprazole therapy. The most frequently reported laboratory abnormality occurring with omeprazole use is elevation of serum aspartate aminotransferase and alanine aminotransferase concentrations. Omeprazole will serve a valuable role in the management of gastrointestinal tract ulcers and hypersecretory conditions.
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PMID:Therapeutic evaluation of omeprazole. 306 85

The effect of omeprazole on liver regeneration was studied in rats following partial (65 per cent) hepatectomy. Omeprazole 0.2 mg/kg increased the relative liver weight (weight of liver as a proportion of body-weight) and mitotic index (P < 0.05). There was no difference in food and water intake. The serum gastrin concentration was significantly higher in animals receiving omeprazole 0.2 mg/kg than in controls (P < 0.05). Omeprazole administration induced an increase in the level of serum alkaline phosphatase (P < 0.05) but had no effect on serum albumin, glutamic-pyruvic transaminase and total bilirubin levels. Omeprazole stimulates liver regeneration after partial hepatectomy and this regeneration may be mediated by gastrin.
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PMID:Liver regeneration is enhanced by omeprazole in rats following partial hepatectomy. 795 55

A 9-year-old male German Shepherd Dog was presented with the primary complaints of vomiting, profuse watery diarrhea, anorexia, and severe weight loss. The dog developed hematemesis and melena, which were unresponsive to treatment with an H2-receptor antagonist and a gastrointestinal protectant. A marked neutrophilia, panhypoproteinemia, hypokalemia, and mildly increased activities of alkaline phosphatase and alanine aminotransferase were the only relevant abnormalities found on a CBC, serum biochemical profile, and urinalysis. An exploratory laparotomy revealed several small nonresectable masses at the root of the mesentery, which were identified histologically as a neuroendocrine neoplasm. Immunohistochemical staining of the neoplasm was positive for gastrin and negative for insulin, glucagon, pancreatic polypeptide, and vasoactive intestinal polypeptide. Fasting serum gastrin concentrations were high. Zollinger-Ellison syndrome was diagnosed, and the dog was treated with omeprazole, an H+,K(+)-ATPase inhibitor. All clinical signs resolved, and the dog remains asymptomatic 2 years later. Omeprazole may be the gastric acid antisecretory drug of choice for dogs with gastrinoma.
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PMID:Omeprazole in a dog with gastrinoma. 947 Jan 66

Sphincter of Oddi dysfunction is caused by stenosis or dyskinesia of the sphincter of Oddi, leading to blockage of bile drainage from the common bile duct. We present the case of a 16-year-old female with chronic abdominal pain who underwent laparoscopic cholecystectomy for cholelithiasis but continued to experience abdominal pain, nausea, and vomiting along with persistently elevated ALT and AST levels. Postoperative abdominal ultrasound was nondiagnostic. Esophagogastroduodenoscopy showed mild reflux esophagitis and mild chronic Helicobacter pylori-negative gastritis. Omeprazole was started, but it did not decrease the frequency and severity of the abdominal symptoms. Magnetic resonance cholangiopancreatography did not reveal any pathology. Endoscopic retrograde cholangiopancreatography with manometry confirmed an elevated biliary sphincter pressure. Biliary sphincterotomy was performed, and the symptoms improved.
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PMID:Sphincter of Oddi Dysfunction: A Perplexing Presentation. 2810 Sep 91