title: Characterizing hereditary and acquired defects of plasminogen.
abstract: Since plasminogen is the proenzyme of plasmin most acquired defects of plasminogen are associated with situations with an increased fibrinolytic activity. Congenital defects also have been described both such associated with thrombotic disease and such that are not. An increased fibrinolytic activity leading to an acquired plasminogen defect is seen 1) in situations complicated with a free proteolytic activity most often involving both the fibrinolytic and the coagulation systems, 2) as a result of locally increased fibrinolytic activity (angiomas), 3) during thrombolytic therapy using plasminogen activators (SK, UK, tPA). A congenital plasminogen defect characterized by 1) a low protein level as well as one with 2) a normal plasminogen protein level in plasma but a defect activation pattern has been reported. Plasminogen can be determined immunochemically, a method which does not differentiate between functionally active plasminogen/plasmin and complexes between these proteins and inhibitors. Plasminogen activity is measured in a chromogenic method using the chromogenic substrate S2251 (Kabi Diagnostica, Stockholm). In this latter method SK is used as a plasminogen activator and the total plasmin formed is measured amidolytically. Using both the immunochemical and the amidolytical methods it has been possible to identify congenital plasminogen defects characterized by a defective activation of plasminogen into plasmin, a defect that has been associated with thromboembolic disease. Another congenital plasminogen defect seems to be caused by a decreased synthesis of a normal plasminogen molecule. Such a defect may not be associated with thrombotic disease. In situations complicated with an increased fibrinolytic activity, decreased plasminogen levels (in both types of assay) are of diagnostic help. Values down to below 50% or even lower may be seen.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Novo Research Institute, Bagsvaerd, Denmark.
authors.forename: U
authors.initials: U
authors.lastname: Hedner
authors.forename: L
authors.initials: L
authors.lastname: Tengborn
mesh_terms: D001778:Blood Coagulation Disorders / Q000097:blood / Q000209:etiology / Q000235:genetics*; D006801:Humans; D010958:Plasminogen / Q000172:deficiency / Q000235:genetics*
chemical_list: D010958:Plasminogen