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Serial blood coagulation studies in two patients with acute promyelocytic leukemia (APL) showed them to have disseminated intravascular coagulation (DIC) as evidenced by hypofibrinogenemia, positive plasma protamine sulfate paracoagulation tests and elevated fibrin degradation products. Serial samples were assayed for functional antithrombin- II I (AT-III) and anti-factor Xa (anti-Xa) activity before, during, and after heparin therapy. Heparin was detected by a modified thrombin time. AT-III was determined by fluorometric measurement of residual thrombin activity on a synthetic substrate (“Protopath” System, Dade Corporation, Florida, U.S.A.). Anti-Xa was determined by coagulation assay of residual Xa after prolonged incubation of prepared Xa with the test plasma. Patient #1 showed normal AT-III levels before and during heparin therapy, which fell to lower levels after the heparin was stopped. Anti-Xa was normal initially and then rose to very high levels during heparin therapy. There was an abrupt fall on cessation of heparin. Patient #2 showed normal AT-III levels at all times, but anti-Xa levels were initially low, rising to normal or high levels only when heparin was detectable in the plasma. It is concluded that neither DIC nor heparin necessarily cause a low AT-III activity in APL, and that therapeutic AT-III replacement may not be necessary. The anti-coagulant effect of heparin, as evidenced by a rise in the anti-Xa level, appears to be normal.

thrombosis and haemostasis

Antithrombin III And Anti-Factor Xa Levels In Two Patients With Acute Promyelocytic Leukemia And Diffuse Intravascular Coagulation Treated With Heparin