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This study was planned for searching possible changes of the total coagulation and fibrinolysis system in inflammatory bowel disease (IBD) in order to obtain some clues for explaining the relation between IBD and hypercoagulability. A total of 24 patients with ulcerative colitis, 12 patients with Crohn disease, and 20 healthy controls were studied. Platelets; prothrombin time (PT); partial thromboplastin time (PTT); fibrinogen; D-dimer; fibrinogen degradation products; protein C; protein S; antithrombin; thrombin time; von Willebrand factor; coagulation factors V, VII, VIII, IX, XI, and XIII; plasminogen; antiplasmin; tissue plasminogen activator; plasminogen activator inhibitor 1; and prothrombin fragments 1 + 2 were studied. Most of the procoagulants (platelets, fibrinogen, von Willebrand factor, coagulation factor IX, and plasminogen activator inhibitor 1) were found increased together with decreases in some anticoagulants (protein S and antithrombin) in IBD. Also the activation markers of coagulation (D-dimer, fibrinogen degradation products, and prothrombin fragments 1 + 2) were all increased. The parameters of the total coagulation-fibrinolysis system were increased in IBD, regardless of the form and the activity of the disease.

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The changes in serum concentrations of cytokines such as interleukin-1 (IL-1) beta, interleukin-6 (IL-6), tumor necrosis factor (TNF) alpha and a soluble-intercellular adhesion molecule (sICAM-1) has been investigated in patients with stable angina and acute myocardial infarction. Thirty-four patients with stable angina (SA), 15 with acute myocardial infarction (AMI), and 20 subjects in the control (C) group were included in the study. The mean serum concentrations of sICAM-1, IL-1-beta, IL-6, and TNF-alpha differed significantly among the three groups. Serum concentrations of IL-1 beta, sICAM-1, and TNF-alpha were comparable in the AMI and SA groups and higher than those found in the C group (p < 0.001). The serum concentration of IL-6 was more than twice as high in the AMI group as compared to the other two groups (p < 0.001). The mean serum concentrations of IL-1 beta, TNF-alpha, and IL-6 were comparable in the AMI and SA groups and higher than in the C group.

In conclusion, we have shown for the first time that patients with isolated CAE have raised levels of plasma P-selectin, beta-TG and PF4 compared with control participants with angiographically normal coronary arteries, suggesting increased platelet activation in patients with CAE.

Thromboembolism is an important cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). The aim of this study was to investigate common thrombophilic markers in patients with IBD and to search for a relation between these predisposing factors and activity of disease. Seventy-four patients with ulcerative colitis, 22 patients with Crohn's disease and 20 healthy volunteers were enrolled into the study. Plasma levels of protein C, protein S, antithrombin III and activated protein C resistance were determined in patients with IBD and healthy controls. Mean values of protein C, protein S and antithrombin III were significantly lower in patients with ulcerative colitis and Crohn's disease compared with the healthy control group. Patients with active ulcerative colitis had lower protein C, protein S and antithrombin III level than patients in remission (P < 0.001, P < 0.001, P < 0.001). Levels of protein C, S and antithrombin III were also decreased in patients with active Crohn's disease compared with those in remission (P < 0.05, P < 0.001, P < 0.05). Differences in all natural anticoagulant levels between patients in remission and healthy individuals in both ulcerative colitis and Crohn's disease groups were not statistically significant (P > 0.05). No significant difference was observed in activated protein C resistance (APCR) between patients with active disease, those in remission and the control group (P > 0.05). Abnormalities in natural anticoagulants are common in patients with IBD during active disease.

In order to investigate the relationship between hemostatic abnormalities and portal vein thrombosis (PVT) in hepatocellular carcinoma (HCC), platelets, prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time, fibrinogen, d-dimer, fibrinogen degradation products (FDPs), protein C, protein S, antithrombin, plasminogen, antiplasmin, coagulation factors (CFs) V, VII, VIII, IX, XI, and XIII, von Willebrand factor (vWF), prothrombin fragment 1 + 2 (PF 1 + 2), tissue-type plasminogen activator (tPA), and plasminogen activator inhibitor 1 (PAI-1) were studied in patients with HCC, cholangiocarcinoma, and metastatic liver tumors and in cirrhosis patients with or without PVT. Platelet, antithrombin, protein C, plasminogen, and CFs V, VII, IX, XI, and XIII levels of HCC group were found lower and PT, aPTT, thrombin time, vWF, FDPs, PF 1 + 2, tPA, and PAI-1 levels were higher than the control group. Our findings suggested that the abnormalities of coagulation and fibrinolysis systems have some role in provoking thrombosis of portal veins in HCC, in addition to the invasion of portal veins by hepatoma cells.

A hypercoagulable state has been reported in patients with mitral stenosis (MS) and sinus rhythm (SR). However it has been suggested that the coagulation activity may be increased only within the left atrium in MS, with normal peripheral blood levels. The aim of the present study was to assess regional left atrial and systemic coagulation activities by measuring PF1+2 in patients with severe mitral stenosis and sinus rhythm, normal blood clotting times, and no left atrial thrombus. The study was conducted in 25 consecutive patients with moderate-to-severe MS and sinus rhythm who underwent percutaneous balloon mitral valvuloplasty. Transesophageal echocardiography was performed before the valvuloplasty procedure in all patients to exclude the presence of left atrial thrombus and left atrial spontaneous echo contrast (LASEC). There were no statistically significant differences between LASEC-positive and LASEC-negative patients with respect to age, gender, fibrinogen levels, prothrombin time, mitral valve area, mean mitral gradient, pulmonary artery pressure (in all p > 0.05). Regional (left atrial) PF1+2 levels of both LASEC-positive and LASEC-negative patients were significantly elevated when compared to control subjects (p < 0.01). Statistically significant elevated systemic level of PF1+2 was observed only in LASEC-positive patients when compared to control subjects (p < 0.01, p > 0.05, respectively). In conclusion patients with severe mitral stenosis and SR have increased regional coagulation activity in both LASEC-negative and LASEC-positive groups. Although this increased regional coagulation activity has been reflected in peripheral blood of LASEC-positive patients, it has not been reflected in peripheral blood of LASEC-negative patients.