Impaired Fibrin Formation in Advanced Cirrhosis

Abstract

The process of fibrin formation was systematically investigated in 25 patients with severe alcoholic cirrhosis. Results of functional tests are reported. A significant lengthening of the thrombin time was found which could not be completely attributed either to hypofibrinogenaemia or to an increase in physiological anticoagulants or to the presence of pathological antithrombins. A defect in fibrin polymerization was seen in the absence of significant levels of antipolymerizing agents. Indirect evidence pointed to an abnormal fibrinogen function. This was mainly suggested by the ‘polymerization curves’ of mixtures of normal and pathological plasmas and the changes in physico-chemical properties of the clot (optical and elastic properties; tensile strength). Altered synthesis in hepatocytes may lead to an ‘acquired dysfibrinogenaemia’ in the late stages of liver cirrhosis, although alteration of a normal fibrinogen molecule after secretion cannot be definitely excluded.

Haemostatic abnormalities in liver disease: could some haemostatic tests be useful as liver function tests?

“…In the current study, significant prolongation of the TT was noted only in patients with HCC, which is in agreement with many earlier studies [3,22,23]. This prolongation was ascribed to a defect in the polymerization of an abnormally produced fibrinogen molecule (i.e.…”

“…dysfibrinogenaemia) [24]. The normal TT in liver cirrhosis in the present study is in line with some reports [25] and disagrees with others [15,23,[26][27][28][29][30]. This discrepancy can be due to differences in the TT assay technique.…”