title: Changes in plasma levels of protease and fibrinolytic inhibitors induced by treatment in acute myeloid leukemia.
abstract: We have studied the main protease inhibitors of leukocytes, alpha-1-protease (alpha 1-PI), alpha-1-antichymotrypsin (alpha 1-Achy) and alpha-2-macroglobulin (alpha 2-M), as well as different parameters of coagulation and fibrinolysis in 21 cases of acute nonlymphoblastic leukemia (ANLL) before, during and after therapy. Nine of the patients presented signs of DIC, 8 of whom belonged to subtype M3 and to subtype 1 M1. The initial alpha 1-PI and alpha 1-Achy levels, which were elevated, increased during the treatment period. There was no significant difference between patients with and without DIC. However, those leukemic patients with DIC showed a significant decrease in plasminogen (p less than 0.005) and fast antiplasmin (p less than 0.01) only during the treatment compared with DIC free patients. All DIC cases demonstrated circulating plasmin-antiplasmin complex (P-AP) both before and during treatment. Independent of a possible proteolytic action of leukocyte enzymes on clotting factors in the clinical course of ANLL (mainly M3 subtype), our results suggest an activation of plasmin-mediated fibrinolysis related to the activation of plasminogen by leukocytes, reactive DIC or both.
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000933:Antifibrinolytic Agents / Q000097:blood*; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D002648:Child; D004211:Disseminated Intravascular Coagulation / Q000097:blood / Q000150:complications; D005260:Female; D005341:Fibrinolysin / Q000378:metabolism; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D011480:Protease Inhibitors / Q000097:blood*; D000979:alpha-2-Antiplasmin / Q000378:metabolism
chemical_list: D000933:Antifibrinolytic Agents; D011480:Protease Inhibitors; D000979:alpha-2-Antiplasmin; D005341:Fibrinolysin