Thrombus

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Acute arterial thrombosis in acute promyelocytic leukaemia
Thrombus, Volume 5, Number 3.

Ninety per cent of patients with acute promyelocytic leukaemia (APL) present with a severe haemorrhagic syndrome, out of proportion with the degree of thrombocytopaenia.1 Initially, this phenomenon was ascribed to disseminated intravascular coagulopathy (DIC) due to the release of tissue thromboplastins from blast cells. However, new data favour a fibrinolytic/protolytic process. The plasminogen receptor, annexin 11, is present in abnormally high amounts on the surfaces of leukaemic cells. This receptor is responsible for the linking of plasminogen to tissue plasminogen activator (tPA), activating plasmin and favouring fibrinolysis. Plasmin formation increases by a factor of 60, depleting normal inhibitors, and a haemorrhagic diathesis ensues.2

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