抄録
By an enzyme-linked immunosorbent assay (ELISA), plasmin-α2 plasmin inhibitor (Plm-α2PI) complex, an indicator of in vivo plasmin generation, was measured in plasma from 48 patients with disseminated intravascular coagulation (DIC), 10 patients with thrombotic thrombocytopenic purpura (TTP), one patient with primary fibrinolysis and 11 patients (15 episodes) with thromboembolic disorders during fibrinolytic therapy with urokinase. Urokinase was infused at an initial dose of 60, 000-960, 000 units, mostly by a bolus infusion followed by a drip infusion for 1-2 hours. In DIC, Plm-α2PI complex was markedly elevated to 7.9±4.26mg/l (mean±SD), normal values being less than 0.8mg/l. Its level changed in parallel with the course of DIC, but remained high (1.9±1.49mg/l) in remission when FDP values became less than 10mg/l with normalization of fibrinogen concentration. Among various underlying disorders, DIC patients with acute promyelocytic leukemia had the highest levels (mean 10.8mg/l) and septic patients had the lowest (mean 3.4mg/l). In TTP, the elevation of Plm-α2PI complex was modest (1.8±0.95mg/l). Plm-α2PI complex was also elevated in a patient with primary fibrinolysis, and its level decreased following the administration of t-AMCHA. Following urokinase infusion, Plm-α2PI complex increased in all patients except in one case who received a low dose of urokinase (60, 000 units). However, changes in cross-linked fibrin derivatives (XDP) were variable among the patients and were independent of the increase in Plm-α2PI complex. These results indicate that the quantitative assay of Plm-α2PI complex would be valuable for the assessment of hyperfibrinolysis in selected disease states. Simultaneous measurements of XDP and Plm-α2PI complex would be useful to monitor the thrombolysis during fibrinolytic therapy.
