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P624 Impaired intestinal barrier function promotes procoagulatory state in Inflammatory Bowel Diseases

L. Pastorelli*1, 2, E. Dozio2, L.F. Pisani1, M. Boscolo-Anzoletti3, E. Vianello2, N. Munizio1, L. Spina1, G.E. Tontini1, F. Peyvandi3, 4, M.M. Corsi Romanelli2, 5, M. Vecchi1, 2

1IRCCS Policlinico San Donato, Gastroenterology and Gastrointestinal Endoscopy Unit, San Donato Milanese, Italy, 2University of Milan, Department of Biomedical Sciences for Health, Milan, Italy, 3IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Angelo Bianchi Bonomi Hemophilia and Thrombosis Centre, Milan, Italy, 4University of Milan, Department of Medical and Surgical Pathophisiology and Transplantations, Milan, Italy, 5IRCCS Policlinico San Donato, Operative Unit of Laboratory Medicine, San Donato Milanese, Italy


Inflammatory and immune mediated disorders are risk factors for arterial and venous thromboembolism. Inflammatory Bowel Diseases (IBD), namely Crohn's disease (CD) and ulcerative colitis (UC) confer an even greater risk of thromboembolic events than other inflammatory conditions. It has been shown that IBD patients display defective intestinal barrier functions. Thus, pathogen-associated molecular patterns (PAMPs) coming from the intestinal bacterial burden might reach systemic circulation and activate innate immunity receptors on endothelial cells and platelets, promoting a procoagulative state.

Aim of the study was to test this hypothesis, correlating the presence of circulating PAMPs with the activation of innate immune system and the activation of the coagulatory cascade in IBD patients


Lipopolysaccharide (LPS), Toll-like receptor (TLR) 2, TLR4 and markers of activated coagulation (i.e. D-Dimer and prothrombin fragment F1+2) in the serum and plasma of IBD patients (N=35 CD and 25 UC) and controls (CONT) (N=20) were measured using commercially available immunoassays.


LPS levels were more elevated in CD (0.400 [0.333-0.540] EU/ml) and UC (0.410 [0.275-0.659] EU/ml) patients vs. CONT (0.325 [0.264-0.411] EU/ml; P=0.048 and P=0.253, respectively). TLR2 was more abundant in CD (517.21 [412.07-890.73] pg/ml) and UC (438.43 [286.63-699.98] pg/ml) sera vs. CONT (281.15 [122.23-412.05] pg/ml; P=0.002 and P=0.055, respectively). LPS and TLR4 levels significantly correlated in IBD patients (r=0.408, P=0.001) with a more robust correlation for UC (r=0.512, P=0.008), than for CD (r=0.332, P=0.054). Only a weak correlation between circulating LPS and CRP concentrations (r=0.274, P=0.046) was found, whereas, no correlations were observed between Harvey-Bradshaw and CAI scores and circulating LPS and TLR4. Interestingly, LPS levels significantly correlated with both D-Dimer (r=0.398, P=0.002) and F1+2 concentrations (r=0.395, P=0.002).


Taken together, our data support the role of an impairment of intestinal barrier in triggering the activation of the coagulatory cascade in IBD.