THE CHEMOTHERAPEUTIC EFFECTS OF H+ K+ INHIBITORS ON HELICOBACTER-PYLORI INFECTION/

Helicobacter pylori's powerful urease enzyme is essential for colonisa tion and adaptation to the acid milieu of the stomach. Eradication of infection with ''standard triple therapy'' abolishes the chronic immun ological and inflammatory responses to H. pylori and, thus, cures gast ritis and peptic ulcer. In vitro, proton pump inhibitors (PPI) are act ive against H. pylori with minimum inhibitory concentrations that comp are favourably with bismuth salts. PPIs are also potent urease inhibit ors, but because PPIs are also active against urease negative mutant H elicobacter spp., it is unlikely that urease inhibition alone accounts for their anti-H. pylori activity. Early reports suggested that omepr azole monotherapy was able to eradicate H. pylori. This has not been c onfirmed by more comprehensive studies, which have shown that treatmen t with omeprazole is associated with a shift of infection from the ant rum to the corpus. The explanation for this observation is unclear, bu t does not appear to be due to bacterial overgrowth. Raising the intra gastric pH with a PPI lowers the minimum inhibitory concentration of t he many antimicrobials, while decreasing the acid storage pool increas es the intramucosal concentration. Dual therapy (omeprazole with eithe r amoxycillin or clarithromycin) is a more logical and highly effectiv e alternative to standard triple therapy, with fewer side effects and better patient compliance. However, H. pylori eradication regimens bas ed on a PPI and two antimicrobials will be the first line treatment fo r H. pylori gastritis and peptic ulcer in the future.