Helicobacter pylori infection causes persistent platelet activation in vivo through enhanced lipid peroxidation

Objective - We aimed at investigating the relationship between Helicobacter pylori infection and in vivo lipid peroxidation and platelet activation, as reflected by urinary 8-iso-prostaglandin (PG)F-2alpha and 11-dehydro-thromboxane (TX)B-2, respectively, in otherwise healthy dyspeptic subjects. Methods and Results - We measured urinary 8-iso-PGF(2alpha) and 11-dehydro-TXB2 excretion in 40 dyspeptic subjects with a positive C-13-urea breath test and 38 dyspeptic individuals with a negative test. Moreover, we investigated the effects of H pylori eradication on prostanoid metabolite excretion in 23 H pylori-positive subjects. We also measured prostanoid metabolite excretion before and after selective cyclooxygenase-2 inhibition with rofecoxib in 4 H pylori-positive subjects. Urinary 8-iso-PGF(2alpha) and 11-dehydro-TXB2 excretion was significantly higher in the H pylori - positive individuals than in controls. A significant direct correlation was found between the degree of positivity to the C-13-urea breath test and urinary 8-iso-PGF(2alpha) excretion. The latter was linearly correlated with urinary 11-dehydro-TXB2. Successful eradication of H pylori infection led to a significant reduction in both 8-iso-PGF(2alpha) and 11-dehydro-TXB2. Furthermore, their levels were unaffected after treatment with rofecoxib. Conclusions - Our study provides evidence of enhanced in vivo lipid peroxidation and platelet activation in association with H pylori infection and suggests a novel mechanism by which an infectious agent could contribute to atherothrombosis.