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)B2, respectively, in otherwise healthy dyspeptic subjects.


RESULTS
We measured urinary 8-iso-PGF2alpha 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-PGF2alpha 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 13C-urea breath test and urinary 8-iso-PGF2alpha 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.
Center of Excellence on Aging, Fondazione Università G. d'Annunzio, Chieti, Italy.
Giovanni
G
Davì
Matteo
M
Neri
Angela
A
Falco
Davide
D
Festi
Tea
T
Taraborelli
Giovanni
G
Ciabattoni
Stefania
S
Basili
Franco
F
Cuccurullo
Carlo
C
Patrono
D000328:Adult; D000368:Aged; D003430:Cross-Sectional Studies; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015237:Dinoprost / Q000031:analogs & derivatives* / Q000378:metabolism / Q000652:urine; D005215:Fasting / Q000502:physiology / Q000652:urine; D016481:Helicobacter Infections / Q000188:drug therapy / Q000473:pathology* / Q000652:urine; D016480:Helicobacter pylori / Q000187:drug effects / Q000302:isolation & purification; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D015539:Platelet Activation / Q000502:physiology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D013929:Thromboxane B2 / Q000031:analogs & derivatives* / Q000378:metabolism / Q000652:urine
D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D008565:Membrane Proteins; C075750:8-epi-prostaglandin F2alpha; D013929:Thromboxane B2; C049235:11-dehydro-thromboxane B2; D015237:Dinoprost; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases