No abstract

SummaryWe measured levels of protein C inhibitor in patients with disseminated intravascular coagulation (DIC) and liver disease using a functional assay. Levels in 24 normal subjects averaged 93% of the amount in normal pooled plasma, giving a normal range of 65 to 121%. Levels were below normal in 8 of 17 patients with DIC, in 4 of 19 patients with liver cirrhosis, and in 3 patients with acute hepatic necrosis. Levels were normal or elevated in 9 of 10 patients with cirrhosis and accelerated fibrinolysis, and in 6 patients receiving warfarin. We conclude that protein C inhibitor may be involved in regulation of protein C activity during pathologic activation of the hemostatic system (DIC). Decreased protein C inhibitor does not appear to contribute to the pathogenesis of accelerated fibrinolysis in liver disease. The liver may be the site of synthesis of protein C inhibitor.

Venous and arterial thromboembolism frequently complicate the nephrotic syndrome. Increased platelet aggregation, high levels of fibrinogen and other procoagulants, and depressed levels of antithrombin III and plasminogen are commonly cited as reasons. Less attention has been paid to changes in the hemostatic system which might protect against thrombosis. We found a high frequency of reduced α₂-antiplasmin levels in 40 patients with nephrotic syndrome, correlating with serum albumin and with antithrombin III levels. Since α₂-antiplasmin is a major determinant of the sensitivity of fibrin thrombi to lysis, and since reduced levels would be expected to promote fibrinolysis, we conclude that in many patients with nephrotic syndrome depressed antiplasmin levels may help reduce the risk of thrombosis posed by diminished antithrombin III levels.