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Antithrombin-III (AT-III )/heparin cofactor is now recognized as a major inhibitor of thrombin and other serine proteases in coagulation. Since the reaction between AT-III and serine proteases is irreversable.AT-III consumption should be expected in pathological intravascular coagulation and attendent generation of thrombin and other serine proteases. Using a new AT-III assay system, unaffected by heparin or fibrino(geno)lytic degradation products, AT-III was monitored in 17 patients with DIC, It was found that early and significant decreases occured in all pts. It was further noted that monitoring of AT-III during therapy for DIC reflected a cessation of AT-III consumption and, thus, appeared to reflect efficacy of therapy in stopping the clotting process. Only 1 of 17 patients failed to show an increase in AT-III with initiation of therapy. In this group of patients, mini-heparin therapy appeared to be as efficacious as large doses of heparin in correcting AT-III consumption and other laboratory abnormalities of acute DIC, and in controlling hemorrhage of acute DIC. Four patients had chronic DIC with malignancy; the use of ASA and dipyridamole corrected AT-III consumption and clinical manifestations in these patients, although the response required more time than with heparin or mini-heparin. These findings suggest that the monitoring of DIC with AT-III levels may be useful in both confirming the diagnosis and, more importantly, in monitoring efficacy of therapy. Significant rises in AT-III were noted in all but 1 patient after initiating therapy, presumably reflecting cessation of consumption. In addition, mini-heparin appeared to be as efficacious as large heparin doses in stopping acute DIC and antiplatelet therapy appeared to stop AT-III consumption and clinical manifestations in patients with chronic DIC associated with malignancy.

Antithrombin-III as a Diagnostic AID in Disseminated Intravascular Coagulation