How does Acute Promyelocytic Leukaemia (APML) cause Disseminated Intravascular Clotting (DIC)?
Actually, APML is associated with fibrinolysis and a disorder similar to but *not* identical to DIC (despite what an eMedicine article on AML states). EDIT: The IL-1 secretion mechanism proposed by Cozzolino et al in which vascular endothelial cells respond by synthesizing procoagulants does not explain why APL is more commonly associated with this coagulopathy than other forms of AML. It would seem to me that if promyelocytes contain sufficient plasminogen activators to generate plasmin, then fibrinolysis might be the salient coagulopathy in APML that initiates a cascade that generates a DIC-like clotting profile through feedback mechanisms and upregulation of clotting factors, but I don’t know whether there have been temporal analyses that would back up such speculation. I could not find much literature on the topic. If the question arises, you may want to re-direct it to the audience, suggesting some theories. P.S. I wasn’t suggesting you were simply browsing eMedicine articles (sor
