Hemostatic Abnormalities in Cirrhosis and Tumor-Related Portal Vein Thrombosis

Abstract

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.

Pancreatic Carcinoma, Thrombosis and Mean Platelet Volume: Single Center Experience from the Southeast Region of Turkey

“…Pancreatic carcinomas frequently invade or metastasize the liver. In a study done by Alkim H et al, it was shown that abnormalities of coagulation and fibrinolysis systems have some role in provoking thrombosis of portal veins in HCC (Alkim et al, 2012). There is no study suggesting this finding regarding pancreatic cancer.…”

Nomogram for Preoperative Estimation of Microvascular Invasion Risk in Hepatitis B Virus–Related Hepatocellular Carcinoma Within the Milan Criteria

“…Because cirrhosis leads to hypersplenism with a low platelet count, and as portal blood flow to the liver slows, formation of MVI is facilitated. Studies 22 have suggested that an increased serum level of von Willebrand factor and decreased levels of anticoagulants (especially antithrombin) in patients with cirrhosis played a significant role in provoking thrombosis and vascular invasion. In addition, a typical dynamic pattern of HCC suggested that there was sufficient tumor blood supply and good vascular connection between tumor vessels and branches of portal venous system, which facilitates cancer cell invasion and MVI formation.…”

Decreased Activity of the Protein C Anticoagulant Pathway in the Early Hours of Paroxysmal Atrial Fibrillation

“…31 Therefore, they are a good indicator of its evaluation. 32,33 In this sense, the high levels of protein C in PAF could be interpreted as indicative of enhanced liver function and, respectively, enhanced protein C biosynthesis and secretion in the early hours of the rhythm disorder. The formation of ''pure'' groups in terms of comorbidities and medications affecting hemostasis is an important prerequisite for this claim (see Table 1).…”