INTERFERENCE ON HELICOBACTER-PYLORI GROWTH AND ADHESION BY OMEPRAZOLEAND OTHER DRUGS

Helicobacter pylori Is the causative agent of gastritis and a co-agent in other gastroduodenal diseases. Gastroduodenal ulcer and MALT-lymph oma in particular, regress when patients are administered antimicrobia l agents to eradicate infection. Sometimes eradication is not definiti ve and is difficult to check. The aim of our study was to test the ant imicrobial activity of omeprazole on H. pylori in comparison with ampi cillin and other anti-H, drugs (ranitidine and famotidine), and to eva luate their interference with bacterial adhesion of H. pylori. We also compared results of the agar dilution antibacterial sensitivity test on H. pylori to those obtained using a bacteria adherence to cell mono layers model, to see if drug activity was different against adhered ba cteria. We evaluated omeprazole and ampicillin MIC90s (minimum inhibit ory concentrations) against 20 H. pylori isolates by traditional agar dilution method and by exposing previously adhered bacteria to an Hep- 2 monolayer to different drug concentrations. The activity. against ba cteria adhered to cell lines was evaluated by counting viable adhered bacteria after 1, 6, 12 hours of contact with drug. Interference with adherence to Hep-2 cells was also tested. Omeprazole and ampicillin MI Cs were comparable to other findings (omeprazole MIC90 was 12.5 mu g/m l and ampicillin MIC90 was 0.016 mu g/ml), while higher concentrations were necessary (4 x MIC90) against adhered bacteria. These findings s uggest that MICs evaluated with traditional assays can have different predictivity than tests on adhered H. pylori.