fibrin and Budd-Chiari-Syndrome

Fibrin formation and removal occurs continuously during the development of malignancy. Moreover, plasma D-dimer is indicative of ongoing fibrinolysis, and soluble fibrin polymer (Thrombus precursor protein, TpP) represents thrombogenic activity. We evaluated the relationship between the levels of plasma D-dimer and TpP and tumor thrombosis in patients with hepatocellular carcinoma (HCC), and examined these markers as possible predictors of tumor thrombus in the portal or the hepatic vein.. Plasma levels of D-dimer and TpP were measured in 66 HCC patients (38 without tumor thrombosis, 28 with tumor thrombosis) and 29 healthy controls, by enzyme immunoassay using an Asserachrom D-Di kit (Diagnostica Stago, France) and a TpP kit (American Biogenetic Sciences, USA).. The plasma levels of D-dimer and TpP in HCC patients were found to be significantly higher than those in healthy controls, and these values were also significantly higher in patients with tumor thrombosis than those without tumor thrombosis. Positive D-dimer (>367 ng/ml) correlated weakly with the presence of tumor thrombosis, whereas positive TpP (>5.4 microg/ml) correlated strongly with the presence of tumor thrombosis. By multivariant logistic analysis, positive TpP level was found to be a significant predictor of the presence of tumor thrombosis. In contrast, positive D-dimer level was not found to be a significant predictor for predicting tumor thrombosis.. Increased D-dimer and TpP levels in HCC may suggest that fibrinolysis and coagulation occur continuously during tumor progression. This study shows that a positive TpP level is a predictor of tumor thrombosis in HCC, which suggests that TpP may be useful for identifying tumor thrombus in the portal and hepatic veins.

Topics: Biomarkers; Budd-Chiari Syndrome; Carcinoma, Hepatocellular; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Humans; Liver Neoplasms; Male; Middle Aged

Radiation-induced liver disease is characterized structurally by progressive fibrous obliteration of central veins (veno-occlusive disease [VOD]). The pathogenesis is unknown. Samples of liver from 11 patients with radiation-induced VOD were studied by light and electron microscopy for evidence of central vein thrombosis. The patients had received fractionated radiation with total doses of 1,850 to 4,050 rads, or single doses of 1,000 rads. In addition, six patients had received chemotherapy. Although usually undetectable by light microscopy, fibrin was found in all samples, sometimes in large amounts, within central veins, and also often in the adjacent sinusoids. One sample had a small platelet aggregate. In two patients, portal veins also showed occlusive lesions. We postulate that ionizing radiation injures preferentially the endothelial cells of central veins, which leads to focal deposition of fibrin. The resulting fibrin network is eventually replaced by collagen, causing fibrous occlusion. In several patients, this type of liver injury occurred at radiation doses conventionally considered safe even in the absence of chemotherapy.

Topics: Adolescent; Adult; Aged; Budd-Chiari Syndrome; Female; Fibrin; Hepatic Veins; Humans; Liver; Male; Middle Aged; Neoplasms; Radiation Injuries; Radiotherapy

Topics: Animals; Benzopyrans; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Platelet Disorders; Budd-Chiari Syndrome; Coronary Disease; Female; Fibrin; Fibrinogen; Fibrinolysis; Heparin; Mice; Microscopy; Microscopy, Electron; Placenta; Placenta Diseases; Pregnancy; Pregnancy Complications; Pulmonary Embolism; Renal Veins; Thrombosis; Veins

Topics: Animals; Budd-Chiari Syndrome; Dogs; Femoral Artery; Fibrin; Humans; Portal Vein; Pulmonary Embolism; Rabbits; Thrombin; Thromboembolism; Thrombosis; Veins