Non-steroidal anti-inflammatory drugs have bacteriostatic and bactericidal activity against Helicobacter pylori

Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) are each associated with gastrointestinal mucosal damage, but the extent and direction of their interactions remain controversial. Therefore, the purpose of the present paper was to examine whether specific NSAIDs inhibit the growth of Helicobacter pylori in vitro.

Sodium salicylate, ibuprofen, indomethacin, the selective cyclooxygenase-2 inhibitor NS-398 and two derivatives of sulindac sulfoxide were tested against two laboratory strains of H. pylori, the mouse-adapted Sydney strain, and against seven fresh clinical isolates of Helicobacter pylori. Possible effects on Campylobacter jejuni, Staphyloccoccus aureus, Escherichia coli, Salmonella typhimurium, and Shigella boydii were also examined.

Certain NSAIDs possess antibacterial activity against Helicobacter pylori at therapeutically achievable doses; an effect that appears to be independent of cyclooxygenase enzymes inhibition. For Helicobacter pylori, >90% growth inhibition and bactericidal activity were observed consistently for sulindac sulfide at < or =70 microg/mL and sulindac sulfone at < or =175 microg/mL. The minimal inhibitory concentration against Helicobacter pylori was 125 microg/mL for ibuprofen, 100 microg/mL for indomethacin and 300 microg/mL for NS-398 but much higher concentration of sodium salicylate (4000 microg/mL) and sulindac sulfoxide (> or =1250 microg/mL) were required to inhibit the growth of Helicobacter pylori.

The decreased prevalence of Helicobacter pylori in specimens from some NSAID users and the chemopreventive effects of NSAIDs in gastric cancer may be related to inhibition of Helicobacter pylori growth.