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.
Zimmermann AE, Katona BG. Zimmermann AE, et al. Pharmacotherapy. 1997 Mar-Apr;17(2):308-26. Pharmacotherapy. 1997. PMID: 9085323 Review.
Buhl K, Clearfield HR. Buhl K, et al. Am Fam Physician. 1990 Apr;41(4):1225-7. Am Fam Physician. 1990. PMID: 2321497
Massoomi F, Savage J, Destache CJ. Massoomi F, et al. Pharmacotherapy. 1993 Jan-Feb;13(1):46-59. Pharmacotherapy. 1993. PMID: 8437967 Review.
Seifert E. Seifert E. Leber Magen Darm. 1994 Mar;24(2):66-8, 71. Leber Magen Darm. 1994. PMID: 8196467 Review. German.
Baczek J, Laskowiec G. Baczek J, et al. Pol Merkur Lekarski. 1998 Jun;4(24):339-41. Pol Merkur Lekarski. 1998. PMID: 9771021 Review. Polish.
Mohiuddin MA, Pursnani KG, Katzka DA, Gideon RM, Castell JA, Castell DO. Mohiuddin MA, et al. Dig Dis Sci. 1997 Apr;42(4):715-9. doi: 10.1023/a:1018839425118. Dig Dis Sci. 1997. PMID: 9125637 Clinical Trial.
Larson C, Cavuto NJ, Flockhart DA, Weinberg RB. Larson C, et al. Dig Dis Sci. 1996 Mar;41(3):475-9. doi: 10.1007/BF02282321. Dig Dis Sci. 1996. PMID: 8617118 Clinical Trial.
Reid T, Yuen A, Catolico M, Carlson RW. Reid T, et al. Cancer Chemother Pharmacol. 1993;33(1):82-4. doi: 10.1007/BF00686028. Cancer Chemother Pharmacol. 1993. PMID: 8269594
Burger DM, Hekster YA, Hopman WP, Does R. Burger DM, et al. Pharm Weekbl Sci. 1991 Oct 18;13(5):215-9. doi: 10.1007/BF01988878. Pharm Weekbl Sci. 1991. PMID: 1749711