Metabolism of Fibrinogen in Cirrhosis of the Liver

G. N. Tytgat; D. Collen; M. Verstraete

doi:10.1172/JCI106658

Metabolism of Fibrinogen in Cirrhosis of the Liver

G. N. Tytgat, D. Collen, and M. Verstraete

Published August 1, 1971 - More info

View PDF

Abstract

The metabolism of human fibrinogen labeled with radioactive iodine was studied in 50 patients with documented cirrhosis of the liver and in 35 healthy control subjects. Results in cirrhotic subjects were the following: plasma volume 47 ± 10 ml/kg; plasma fibrinogen concentration 250 ± 102 mg/100 ml; total plasma fibrinogen pool 118 ± 59 mg/kg, representing 0.73 ± 0.10 of the total body pool; fibrinogen half-life 2.99 ± 0.59 days; fractional catabolic rate 0.34 ± 0.09 of the plasma pool per day; absolute catabolic rate 39 ± 20 mg/kg per day; fractional transcapillary efflux rate 0.82 ± 0.30 of the plasma pool per day. Results in the control subjects were the following: plasma volume 42 ± 7 ml/kg; plasma fibrinogen concentration 284 ± 71 mg/100 ml; total plasma fibrinogen pool 119 ± 40 mg/kg, representing 0.72 ± 0.07 of the total body pool; fibrinogen half-life 4.14 ± 0.56 days; fractional catabolic rate 0.24 ± 0.04 of the plasma pool per day; absolute catabolic rate 28 ± 9 mg/kg per day; fractional transcapillary efflux rate 0.60 ± 0.26 of the plasma pool per day.

A significant difference between cirrhotics and controls was observed for plasma volume, fibrinogen half-life, fractional and total catabolic rates, and transcapillary efflux rate. During heparinization of 10 cirrhotic patients the fibrinogen half-life was prolonged from 3.15 ± 0.69 to 4.59 ± 0.79 days. This was associated with a rise in plasma fibrinogen in six out of eight patients. Heparinization did not influence the fibrinogen half-life in five control subjects. Inhibition of the fibrinolytic system in 17 patients resulted in prolongation of the plasma radioactivity half-life of more than 1 day in only three patients, an incidence comparable with that in five control subjects.

These results strongly support the concept of accelerated fibrinogen consumption by a process of disseminated intravascular coagulation in cirrhosis of the liver.