Summary
Treatment of acute lymphoblastic leukaemia (ALL) with L-asparaginase (L-asp) may be
associated with thrombotic complications, but the pathogenetic mechanisms of thrombus
formation and persistence remain unclear. We studied the procoagulant activity (PCA)
of peripheral blood mononuclear cells and some components of the plasma fibrinolytic
system in L0 children with ALL undergoing remission induction therapy which includes
L-asp. Mononuclear cells obtained 14 days after starting L-asp treatment generated
significantly higher amounts of PCA (identified as tissue factor) than cells isolated
before the first dose of L-asp and 7 days after the cessation of L-asp administration
(p <0.01). Augmented PCA coincided with an increase in the plasma D-dimer. The plasma
levels of type 1- plasminogen activator inhibitor were found signiticantly elevated
during L-asp therapy (p <0.05), whereas plasminogen levels were markedly decreased
(p <0.05). These findings suggest that, during the course of L-asp treatment, the
coagulation-fibrinolysis balance is shifted towards promotion of fibrin formation
and deposition. Although it remains to be conclusively established whether Lasp per
se or the concurrent administration of multiple chemotherapeutic agents is responsible
for these changes, the latter could contribute to the thrombotic complications associated
with remission induction therapy for ALL.
