Hypercoagulability observed in patients with inflammatory bowel diseases (IBD) may lead to thromboembolic events (TE), which affect the venous and arterial systems alike and are an important factor in patients' morbidity and mortality. The risk of TE in IBD patients has been demonstrated to be approximately three-fold higher as compared to the general population. The pathogenesis of thrombosis in IBD patients is multifactorial and not fully explained. The most commonly listed factors include genetic and immune abnormalities, disequilibrium between procoagulant and anticoagulant factors, although recently, the role of endothelial damage as an IBD-triggering factor is underlined. Several studies report that the levels of some coagulation enzymes, including fibrinogen, factors V, VII, VIII, active factor XI, tissue factor, prothrombin fragment 1 + 2 and the thrombin-antithrombin complex, are altered in IBD patients. It has been demonstrated that there is a significant decrease of tissue plasminogen activator level, a marked increase of plasminogen activator inhibitor type 1 and thrombin-activable fibrinolysis inhibitor, a significantly lower level of antithrombin III and tissue factor pathway inhibitor. IBD patients have been also observed to produce an increased amount of various anticoagulant antibodies. Hyperhomocysteinemia, which is a potential risk factor for TE was also observed in some IBD patients. Further studies are necessary to assess the role of coagulation abnormalities in IBD etiology and to determine indications for thromboprophylactic treatment in patients at high risk of developing TE.
IntroductIon Soluble forms of tumor necrosis factor (TNF) membrane receptors 1 and 2 (sTNFR1 and sTNFR2) are present in body fluids. Their higher concentrations are observed in a number of diseases, including inflammatory bowel diseases (IBDs). sTNFR1 and sTNFR2 are capable of binding TNF-α, acting as an inhibitor that competes with a membrane receptor. The results of the available studies on sTNFR1 and sTNFR2 concentrations in IBDs and their association with disease activity are ambiguous.objectIves The aim of the study was to assess sTNFR1 and sTNFR2 concentrations and their correlation with disease activity in patients with IBD.PAtIents And methods Plasma levels of TNF-α, sTNFR1, and sTNFR2 were measured in 55 consecutive patients with ulcerative colitis (UC), 50 subjects with Crohn's disease (CD), and 41 healthy controls. We assessed the associations of those markers with other inflammatory markers, disease activity and location, type of treatment, and complications.results Positive correlations were observed between CD activity and sTNFR1 and sTNFR2 levels (r = 0.42 for both, P <0.01) as well as between UC activity and sTNFR1 and sTNFR2 levels (r = 0.63, P <0.0001; r = 0.47, P <0.001; respectively). TNF-α levels correlated only with CD activity (r = 0.29, P <0.05). In patients with nonactive UC, higher sTNFR2 levels were observed compared with controls. In patients with CD, higher TNF-α and sTNFR2 levels were demonstrated in patients who developed complications.conclusIons sTNFR1 and sTNFR2 are more sensitive inflammatory markers than TNF-α in the assessment of disease activity in patients with CD and UC. Higher sTNFR2 levels are observed in patients with CD and complications.
Both UC and CD are characterized by formation of dense fibrin networks relatively resistant to lysis. Prothrombotic clot phenotype might represent a novel mechanism increasing thrombotic risk in IBD.
IL28B variation is the strongest host factor not related to insulin resistance that determines outcome of antiviral therapy. Baseline platelet count predicts the outcome of antiviral therapy in CT allele patients.
Anti-inflammatory and anticoagulant properties... 209 INTROduCTION Thromboembolism is an extraintestinal manifestation and an important cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). 1 The pathogenesis of thromboembolic complications in IBD is multifactorial and has not been fully elucidated yet. In patients with IBD, disbalance between procoagulant, anticoagulant, and fibrynolytic factors occurs that predisposes to the development of embolism in IBD. A number of genetic factors have been shown to increase the incidence of thromboembolic complications. Moreover, numerous acquired factors have been confirmed to play a role here, including chronic immobilization, surgical procedures, central venous catheters, steroid therapy, oral contraceptives, cigarette smoking, hyperhomocysteinemia, vitamin deficiency, dehydration, and the inflammatory process itself. 1,2 There are 3 natural anticoagulation mechanisms that control blood clotting: the protein C (PC) anticoagulant pathway, tissue factor pathway inhibitor, and the heparin-antithrombin pathway. The PC pathway is initiated by thrombin attaching
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