The pathogenesis of accelerated fibrinolysis in liver cirrhosis: a critical
role for tissue plasminogen activator inhibitor
SL Hersch, T Kunelis and RB Francis
The pathogenesis of accelerated fibrinolysis in liver cirrhosis was
investigated by comparing the results of specific assays for tissue
plasminogen activator (tpa) antigen, tpa activity, tpa inhibitor, and
alpha-2 plasmin inhibitor (a2PI) in 12 patients with cirrhosis and markedly
accelerated fibrinolysis (dilute whole blood clot lysis time (DWBCLT) less
than two hours), in nine patients with cirrhosis and moderately accelerated
fibrinolysis (DWBCLT two to four hours), and in nine patients with
cirrhosis and normal fibrinolysis (DWBCLT greater than four hours). Mean
tpa antigen was markedly increased in all three groups, but no correlation
was observed between overall fibrinolytic activity as measured by the
DWBCLT and the level of tpa antigen. In contrast, there was a significant
correlation between overall fibrinolytic activity and tpa activity and an
equally significant correlation between fibrinolytic activity and decreased
tpa inhibition. Mean a2PI activity was significantly lower than normal in
groups 1 and 2 but was normal in group 3. The pathogenesis of accelerated
fibrinolysis in liver cirrhosis thus appears to depend critically on the
capacity of plasma inhibitors to inhibit increased circulating tpa antigen.
Reduced a2PI also appears to play a role.
Volume 69,
Issue 5,
pp. 1315-1319,
05/01/1987
Copyright © 1987 by The American Society of Hematology
