Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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