title: Clinical perspectives of drugs inhibiting acid secretion--H+K+-ATPase inhibitors.
abstract: The H+K+-ATPase is supposed to be the terminal step in the acid-secreting pathway in the parietal cell. Omeprazole blocks this enzyme, resulting in a marked inhibition of basal and stimulated acid secretion. With omeprazole 20 mg daily, 24-hour intragastric acidity is decreased by about 90%. Several clinical studies have now been published in which omeprazole has been compared with the H2-receptor antagonists cimetidine and ranitidine. Omeprazole in doses between 20 and 40 mg daily resulted in healing rates between 65% and 82% after treatment for 2 weeks and between 90% and 100% after treatment for 4 weeks. Treatment with omeprazole also gave faster and more pronounced pain relief. One comparative study in gastric ulcer has also been published showing healing rates equal to those with ranitidine. Placebo-controlled trials have also shown very pronounced therapeutic effect in reflux esophagitis. Omeprazole seems to be the drug of choice in Zollinger-Ellison syndrome, giving beneficial clinical effects and pronounced and long-lasting reduction in gastric acid secretion.
mesh_terms: D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors*; D004066:Digestive System Diseases / Q000188:drug therapy*; D004381:Duodenal Ulcer / Q000188:drug therapy; D004942:Esophagitis, Peptic / Q000188:drug therapy; D005744:Gastric Acid / Q000378:metabolism*; D017506:H(+)-K(+)-Exchanging ATPase; D006801:Humans; D009853:Omeprazole / Q000627:therapeutic use*; D013276:Stomach Ulcer / Q000188:drug therapy; D015043:Zollinger-Ellison Syndrome / Q000188:drug therapy
chemical_list: D000251:Adenosine Triphosphatases; D017506:H(+)-K(+)-Exchanging ATPase; D009853:Omeprazole