Abstract

The Benzimidazole derivative lansoprazole, which has antisecretory and antiulcer properties, lowers the acid secretion of parietal cells. Because of the acidic environment in these cells, lansoprazole is changed into active metabolites. It is quickly absorbed from a formulation resistant to stomach acid, and human plasma has about 97% of it bound. Lansoprazole’s single dose pharmacokinetics seems to follow a linear pattern from 15 to 60 mg. Although food and the time of administration have an impact on absorption after single doses, they have no impact on the antisecretory action of successive doses. The cytochrome P450 enzymes CYP3A4 and CYP2C18 significantly metabolise lansoprazole into sulphone and 5-hydroxylated metabolites after oral treatment. Plasma contains two more compounds that have been identified sulphide and hydroxylated sulphone. The average plasma elimination half-life (t1/2) in healthy individuals ranges from 1.3 to 2.1 hours. Unchanged lansoprazole is not detectable in urine, however free and conjugated hydroxylated metabolites accounting for 15 to 23% of the total dose are. In comparison to H2-receptor antagonists, lansoprazole showed quicker symptom relief and better healing rates in individuals with stomach or duodenal ulcers or reflux esophagitis. In patients with Zollinger-Ellison syndrome, lansoprazole was more efficacious than H2-receptor antagonists and gave a similar therapeutic outcome to omeprazole. Like omeprazole or H2-receptor antagonists, lansoprazole is well tolerated and has a low frequency of side effects.