Abstract
The plasminogen-plasmin system involves proteolytic enzymes which are primarily responsible
for the degradation of fibrin deposits in blood vessels. Through intricate interactions
between the various components and inhibitors, a balance is maintained between profibrinolysis
and impaired fibrinolytic activity. Several hereditary defects have been described
affecting functional plasminogen concentrations, plasminogen activator levels, and
plasminogen activator inhibitor activity. These defects have been implicated as risk
factors for thrombosis based on a multitude of case reports associating impaired fibrinolysis
with thrombosis. However, under close scrutiny, the role of decreased fibrinolysis
as an etiologic factor in thrombosis has not been firmly established. Rather, dysfibrinolysis
may manifest itself through an accentuation of an underlying thrombophilic state such
as recurrent thrombotic episodes. Further evaluation of impaired fibrinolytic activity
in conjunction with an underlying thrombophilic condition is warranted.
Keywords:
Plasminogen - congenital plasminogen deficiency - plasminogen activator - plasminogen
activator inhibitor - impaired fibrinolysis
