RESUMO
Helicobacter pylori [H.pylori] infection is now recognized to be of major etiological importance in peptic ulcer disease and gastric cancer. More recently, interest in the possible association be- tween H pylori infection and thrombotic events has developed. This study aimed to evaluate the relationship between plasma levels and gastric mucosal concentrations of tumor nemesis factor-a [TNF-alpha] and interleukin-8 [IL-8] as pro-inflammatory cytokines and plasma levels of prothrombin fragments 1+2 [PF1+2] and fib- rinogen in H. pylori positive patients before and after successful eradication therapy. Forty-two patients proven to have chronic gastritis were enrolled in this study. They were divided into 2 groups based on histopathological examination of gastric antral biopsies. Group I: included 28 H. pylori positive patients, and group II: 14 H. pylori negative patients' chronic gastritis. Plasma levels and antral mucosal concentrations of TNF-alpha and IL- 8 as well as plasma levels of fibrinogen and PF1+2 were assessed in all patients. A triple eradication therapy for H. pylori was given for Group I. Eradication was histopathologically evaluated 2 months post-therapy together with estimation of plasma levels of fibrinogen, PF1+2, TNF-alpha and IL-8. The results showed that, group I of patients had significantly increased plasma fibrinogen and PF1+2 as well as mucosal and plasma levels of TNF-alpha and IL-8 compared with group II. Furthermore, in-group I, positive correlations were found between plasma level of PF1+2 and gastric mucosal concentrations of TNF-alpha and IL-8. While in-group II [H pylori negative chronic gastritis], no significant correlations were detected between the studied parameters. A significant reduction in the mean value of plasma levels of TNF-alpha IL-8 and PF1+2 were observed in those with infection eradication. In conclusion, the present study showed a close relationship between plasma levels of PF1+2, plasma and mucosal levels of TNF-alpha and IL-8 in H. pylori associated chronic gastritis patients. These findings suggest that H. pylori may represent a trigger factor for clotting system activation through persistent inflammatory stimulation, cytokine production. Therefore, H. pylori eradication may reduce the risk of hypercoagulable state and thrombotic events in those patients