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Interaction of nonsteroidal anti-inflammatory drugs (NSAID) with Helicobacter pylori in the stomach of humans and experimental animals Brzozowski T; Konturek PC; Sliwowski Z; Kwiecien S; Drozdowicz D; Pawlik M; Mach K; Konturek SJ; Pawlik WWJ Physiol Pharmacol 2006[Sep]; 57 Suppl 3 (ä): 67-79Helicobacter pylori (H. pylori) and non-steroidal anti-inflammatory drugs (NSAID) are major pathogenic factors in peptic ulcer disease but whether these two factors exert synergistic or antagonistic action on the gastric mucosa has been a subject of controversy. The classic concept states that there is an increased ulcer occurrence and bleeding in patients with both H. pylori infection and NSAID use. However, the question whether the H. pylori eradication therapy in NSAID users reduces the occurrence of peptic ulcer has not been fully addressed. Studies on secondary prevention of NSAID-associated ulcers in H. pylori patients have indicated that H. pylori eradication results in impaired ulcer healing with an effect on the rate of peptic ulcer occurrence. On the other hand, the treatment of H. pylori in patients with no prior history of chronic NSAID therapy has been shown to decrease the risk of peptic ulcer. Studies in experimental animals revealed for instance, that the H. pylori infection augments the gastric mucosal damage induced by NSAID in Mongolian gerbils. In rats with preexisting chromic gastric ulcers, H. pylori infection attenuated significantly the aspirin-induced inhibition of ulcer healing and accompanying fall in the gastric blood flow at the margin of these ulcers, suggesting negative interaction between aspirin and H. pylori on ulcerogenesis. Accumulated evidence in humans and animals shows that both aspirin and H. pylori upregulate the expression of cyclooxygenase (COX)-2 both at mRNA and protein levels at the ulcer margin, but failed to influence significantly that of COX-1. It was, therefore, proposed that H. pylori may in fact, antagonize, aspirin-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in PGE(2) possibly derived from COX-2 expression and activity and to the overexpression of growth factors such as TGF alpha and VEGF. The present review summarizes and further addresses the issue of the interaction between these two major ulcer risk factors determined in the stomach of humans and experimental animals.|*Helicobacter Infections/complications/drug therapy[MESH]|Animals[MESH]|Anti-Bacterial Agents/therapeutic use[MESH]|Anti-Inflammatory Agents, Non-Steroidal/*adverse effects[MESH]|Anti-Ulcer Agents/therapeutic use[MESH]|Gastric Mucosa/drug effects/microbiology[MESH]|Helicobacter pylori/drug effects[MESH]|Humans[MESH]|Peptic Ulcer/drug therapy/*etiology[MESH]|Stomach/drug effects/microbiology[MESH] |
