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The influence of l ‐asparaginase therapy on the fibrinolytic system
Author(s) -
Vellenga E.,
Kluft C.,
Mulder N. H.,
Wijngaards G.,
Nieweg H. O.
Publication year - 1984
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1984.tb02893.x
Subject(s) - fibrinolytic therapy , medicine , asparaginase , pharmacology , fibrinolysis , intensive care medicine , leukemia , lymphoblastic leukemia
S ummary. Fibrinolytic factors were assessed during L‐asparaginase administration, to study whether their changes may predispose to a haemorrhagic or thrombotic diathesis. The total level of α 2 ‐antiplasmin declined, as well as the ratio of the plasminogen‐binding form of α 2 ‐antiplasmin to the non‐plasminogen‐binding form. After cessation of L‐asparaginase administration, the ratio increased to 1.6 times that of the pretreatment value. These data indicate that the plasminogen‐binding form of α 2 ‐antiplasmin is the form primarily synthesized in vivo . L‐Asparaginase therapy reduced plasma levels of plasminogen and histidine‐rich glycoprotein (HRG) and influenced the equilibrium between HRG, plasminogen and HRG‐plasminogen complex, with a more pronounced decrease of plasminogen (62%±8) and HRG (76%±11) in comparison to the free‐plasminogen levels (51%±6). α 2 ‐Macroglobulin was only slightly influenced by L‐asparaginase and may consequently play a more pronounced role in inhibition. This is suggested by moderate declines in functional tests of plasmin, urokinase and tissue activator inhibition by patients plasma, and by the ratio of inhibition of these enzymes over α 2 ‐antiplasmin. Thus the bleeding tendency described during L‐asparaginase therapy can be ascribed not only to a temporary deficiency of coagulation factors but also to temporary α 2 ‐antiplasmin deficiency.