Relationship between prothrombin fragment 1+2 and helicobacter pylori associated chronic gastritis

ABSTRACT

Helicohacter pylori [H. pylori] have been suggested to be an independent risk factor for cardiovascular and cerebral stroke; through the activation of clotting system following chronic inflammation. Among proinflammatory cytokines, tumour necrosis factor-alpha [TNF-alpha] and interleukin-8 [TL-8] which have been previously demonstrated to activate the clotting system in human. This study aimed to investigate [i] if there is a difference between the circulating levels of prothromhin fragment 1+2 [F1+2]; a sensitive marker of thrombin generation in patients with chronic gastritis according to N. pylori status, [ii] the relationship between circulating and mucosal levels of TNF-alpha, IL-8 and Fl+2 and [iii] If H. pylori eradication modifies the level of these cytokins and clotting system activation. Forty-two patients with chronic gastritis were diagnosed with upper endoscopy, and enrolled in this study, divided into 2 groups on the basis of histopathological examination of gastric antral biopsies and culture. Group I included 28 H. pylori positive patients, and group H 14 H. pyIori negative patients chronic gastnitis. A triple eradication therapy for H. pylori [omeprazole, amoxacillin and tinidazole] was given for the 28 H. pylori positive patients [Group I] and H. pylori eradication was evaluated after 2 months. Gastric mucosal levels of TNF-alpha and IL-8 as well as plasma levels of TNF-alpha, IL-8 and F1+2 were measured in group II and before and 2 months after H. pylori eradication in group I. Our results showed that patients with H pylori positive gastritis had a significant increase in the mean value of plasma F1+2 mucosal and plasma levels of TNF-alpha and IL-8 compared with group II [P<0.001]. There was a significant positive correlation between plasma level of F1+2 and plasma levels of TNF-alpha and IL-8 [r=0.89, p<0.00, r=0.88, p<0.000] respectively and between the plasma levels of F1+2 and gastric mucosal levels of TNF-alpha and IL-S [r=0.89, P<0.000; r=0.86 P<0.001] respectively. There was a significant reduction in the mean value of plasma levels of TNF-alpha. IL-8 and F1+2 as well as fibrinogen 2 months later after H. pylori eradication. While in-group II [H pylori negative chronic gastrius] there was no significant correlation between the studied parameters. In conclusion, the present study showed a close relationship between plasma levels of prothrombin F1+2, and both plasma and gastric mucosal values of TNF-alpha and IL-8 in cases with H. pylori associated chronic gastritis. These findings suggest that H. pylori may represent a trigger factor for clotting system activation through persistent inflammatory stimulation, cytokines production and consequently H. pylori eradication may reduce the risk of hyper-coagulability state or thrombotic events which may be associated in these patients