Helicobacter Pylori Infection Causes Persistent Platelet Activation In Vivo Through Enhanced Lipid Peroxidation

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Abstract
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 2α and 11-dehydro-thromboxane (TX)B 2 , respectively, in otherwise healthy dyspeptic subjects. Methods and Results— We measured urinary 8-iso-PGF 2α and 11-dehydro-TXB 2 excretion in 40 dyspeptic subjects with a positive 13 C-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 2α and 11-dehydro-TXB 2 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 13 C-urea breath test and urinary 8-iso-PGF 2α excretion. The latter was linearly correlated with urinary 11-dehydro-TXB 2 . Successful eradication of H pylori infection led to a significant reduction in both 8-iso-PGF 2α and 11-dehydro-TXB 2 . 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.