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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:246.)
© 2005 American Heart Association, Inc.

Thrombosis

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

Giovanni Davì; Matteo Neri; Angela Falco; Davide Festi; Tea Taraborelli; Giovanni Ciabattoni; Stefania Basili; Franco Cuccurullo; Carlo Patrono

From the Center of Excellence on Aging (G.D., M.N., A.F., D.F., T.T., G.C., F.C.), Fondazione Università "G. d’Annunzio," and Departments of Medicine and Drug Sciences, University of Chieti "G. d’Annunzio" Schools of Medicine and Pharmacy, Italy; and Departments of Medical Therapy (S.B.) and Pharmacology (C.P.), University of Rome "La Sapienza," Italy.

Reprint requests to: Carlo Patrono, MD, Center of Excellence on Aging, Fondazione Università "G. d’Annunzio," Via Colle dell’Ara, 66013, Chieti, Italy. E-mail cpatrono{at}unich.it

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)F₂ and 11-dehydro-thromboxane (TX)B₂, respectively, in otherwise healthy dyspeptic subjects.

Methods and Results— We measured urinary 8-iso-PGF₂ and 11-dehydro-TXB₂ excretion in 40 dyspeptic subjects with a positive ¹³C-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-PGF₂ 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 the¹³C-urea breath test and urinary 8-iso-PGF₂ 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-PGF₂ 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.

Urinary excretion of 8-iso-PGF_2a and 11-dehydro-TXB₂ was significantly higher in Helicobacter pylori–positive individuals than in controls, with direct correlations between the degree of positivity to the ¹³C-urea breath test and urinary 8-iso-PGF₂ and between the 2 metabolites. Successful H pylori eradication led to a reduction in these indexes of lipid peroxidation and platelet activation. We suggest a novel mechanism by which an infectious agent could contribute to atherothrombosis.

Key Words: risk factors • oxidant stress • platelets • infection • inflammation

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