Treatment of Acid-Related Disorders with Gastric Acid Inhibitors: The State of the Art

Abstract

Since their introduction in 1976, and until recently, the H₂-receptor antagonists have been the ‘state-of-the-art’ gastric acid inhibitors, but the advent of omeprazole, the acid pump inhibitor, has necessitated a reassessment of therapy for acid-related diseases. In making this reassessment, the following therapeutic goals should be considered: rapid and reliable therapeutic effect, safety, simple treatment regimen, resolution of recurrence, and cost-effectiveness. Extensive clinical evidence indicates that omeprazole offers an advance over the H₂-receptor antagonists in achieving these goals. A series of meta-analyses shows that omeprazole gives more rapid symptom relief and more reliable healing than the H₂-receptor antagonist, ranitidine, in uncomplicated duodenal ulcer (DU), in uncomplicated gastric ulcer (GU) and in reflux oesophagitis (RO). By contrast with the H₂-receptor antagonists, refractoriness leading to failure to heal is virtually unknown with omeprazole. Omeprazole also fulfils the goal of therapeutic safety, and this has been documented in extensive short- and long-term clinical and laboratory studies. Omeprazole has a simple treatment regimen: 20 mg once daily is recommended in the routine treatment of DU, GU and RO. As a result of its high therapeutic success rate, omeprazole is also cost-effective. Taking all these factors into account, it is concluded that omeprazole approaches the therapeutic targets set for the treatment of acid-related disorders.

Risk-Benefit Assessment of Omeprazole in the Treatment of Gastrointestinal Disorders

“…The greatest advantage for omeprazole over H2-antagonists has been found by all authors in patients with reflux oesophagitis: after 4 and 8 weeks' treatment there was a 30 to 40% advantage in healing rate for omeprazole 20mg and a greater than 40% advantage for omeprazole 40mg (Arens & Dent 1993;Blum 1990;Holt & Howden 1991;Maton 1991). The advantage of omeprazole regarding relief from heartburn was 40 to 50%.…”

“…Excellent summaries and meta-analyses of the numerous comparative studies against different H2-receptor antagonists have been published in the last 3 years (Arens & Dent 1993;Blum 1990;Holt & Howden 1991a;Maton 1991).…”

“…The therapeutic advantage for omeprazole over H2-antagonists was greatest in the first 2 weeks of treatment and was less marked after 4 weeks, although still significant in most studies. Comprehensive tables and graphs, summarising the results and references of the different comparative trials can be found in recent reviews (Arens & Dent 1993;Blum 1990;Holt & Howden 1991;Maton 1991). Comparison is sometimes difficult because of different dosage regimens (omeprazole 20 and 40mg once daily vs cimetidine 800, 1200 or 1600 mg/day in divided doses; ranitidine 150mg twice daily or 300mg once daily; famotidine 20mg twice daily or 40mg once daily).…”

Optimisation of chiral separation of omeprazole and one of its metabolites on immobilized α1-acid glycoprotein using chemometricsglycoprotein using chemometrics

“…Both enantiomers of omeprazole have this inhibitory effect, performed by a different mechanism than e.g. H2-receptor blockers [13]. Omeprazole is transformed to intermediary products that selectively inhibit H § K+-ATPase.…”

Gastric Fundic Mucous Epithelial Cells Isolated from Omeprazole-Treated Guinea Pigs Have Increased Basal and Hormone-Stimulated Growth Rates

“…Omeprazole is known to be a potent in hibitor of gastric acid secretion [1] and has been shown to be more effective than some H2 blockers in promoting the healing of gas tric ulcers [2][3][4], It has also been suggested that omeprazole may promote healing in ways other than through the suppression of acid secretion [5], For example, Hakanson et al [6] have shown that omeprazole has spe cific trophic effects on the gastric mucosa in hamsters, guinea pigs, and chickens, but not on pancreas or intestine. This growth effect on the stomach by omeprazole has been pos tulated to be a combination of effects caused by hypergastrinemia [7][8][9] which also in creases the enterochromaffinlike cell popula tion [10][11][12][13], Without any omeprazole treat ment.…”