Increased thrombin generation and circulating levels of tumour necrosis factor- a in patients with chronic Helicobacter pylori -positive gastritis A. CONSOLAZIO*, M. C. BORGIA*, D. FERRO  , F. IACOPINI*, O. A. PAOLUZI*, P. CRISPINO*, F. NARDI à , M. RIVERA* & P. PAOLUZI* *Department of Clinical Sciences, Gastroenterology Unit, Rome;  Institute of Clinical Medicine I and àDepartment of Pathology, University ‘La Sapienza’ of Rome, Italy; àDepartment of Pathology Accepted for publication 19 May 2004 SUMMARY Background: Conflicting data have been reported con- cerning the relationship between Helicobacter pylori infection and coronary heart disease. Aim: To evaluate clotting system activation and plasma levels of tumour necrosis factor-a, a procoagulant cytokine, in patients with H. pylori-positive and - negative gastritis. Methods: Three groups of patients were identified: 38 with H. pylori-positive gastritis, 18 with H. pylori- negative gastritis, and 40 H. pylori-negative controls with normal gastric mucosa. Plasma levels of pro- thrombin fragment 1 + 2 (F1 + 2) and tumour necrosis factor-a were assayed. Patients were also controlled after 2 and 6 months following standard H. pylori eradication treatment. Results: At baseline, fragment 1+2 and tumour necrosis factor-a levels in H. pylori-positive patients were significantly higher than those in H. pylori- negative patients with gastritis (P < 0.05 and P < 0.01, respectively). After H. pylori eradication, fragment 1 + 2 and tumour necrosis factor-a levels showed a significant decrease at 2 months (P ¼ 0.03 and P ¼ 0.02, respectively) and a further reduction at 6 months, reaching levels observed in H. pylori-negative patients and controls. Conclusions: The increase thrombin generation rate and the correlation of plasma fragment 1 + 2 and tumour necrosis factor-a levels in H. pylori-positive patients suggest a role for inflammation in mediating the relationship between H. pylori infection and activation of the clotting system. INTRODUCTION One century ago, infections and related inflammation were included in the causes of coronary heart disease and, in 1994 Mendall et al. suggested that chronic Helicobacter pylori infection is an independent risk factor for acute myocardial infarction. 1 Many epidemiological and clinical studies later reported contradictory results, related to different study designs and several confound- ing factors, such as age and social class. 2–4 Atherosclerotic lesions were shown to share many characteristics with a chronic inflammatory process, which can be activated by various harmful stimuli, such as hypercholesterolaemia, hypertension and smoking habit. 5 Inflammatory cytokines interferon (INF)-c, interleukin (IL)-1 and tumour necrosis factor (TNF)-a were found in atherosclerotic plaques of the vascular walls, where they activate T-lymphocytes and macrophages, stimu- Correspondence to: Dr A. Consolazio, Dipartimento di Scienze Cliniche, Policlinico Umberto I, Viale del Policlinico 155, 00161, Rome, Italy. E-mail: adriana.consolazio@uniroma1.it Aliment Pharmacol Ther 2004; 20: 289–294. doi: 10.1111/j.1365-2036.2004.02074.x Ó 2004 Blackwell Publishing Ltd 289