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Glass-contacted human serum infused into animals induces stasis thrombi similar to red thrombi observed in man (1). The activity in glass-contacted human serum initiating these thrombi has been termed serum thrombotic accelerator (STA) activity (2). It can be measured by a rabbit assay (3) and is distinct from tissue thromboplastin, platelets, and thrombin (4, 5). Silicone-processed ("intact") serum from normal subjects and glasscontacted serum from patients deficient in coagulation Factors XII (Hageman), XI (PTA), or IX (PTC) develop little, if any, STA activity (2, 5). In contrast, glass-contacted serum from patients with other clotting defects develops normal STA activity (2). These observations led to the hypothesis that elaboration of STA activity was mediated through activation of the initial three procoagulants (Factors XII, XI, and IX) involved in the in vitro formation of intrinsic, or blood, thromboplastin (1). The role of Factor IX in the elaboration of STA activity has been recently brought under fresh scrutiny. Preparations rich in activated Factor XI (activation product, AP) and essentially devoid of other known clotting factors, have been found to be thrombogenic (6). This is true whether the AP is isolated from normal or Factor IX-deficient plasma or serum (6). As a result of these studies, it has been suggested that the thrombogenic activity originally described as STA activity is attributable to AP and that STA activity, in fact, represents the in vivo manifestation of AP (6). To examine the validity of this thesis, the thrombogenic activity of serum obtained from patients with established heredofamilial defects of Factor

Activation Product, Factor IX, Serum Thrombotic Accelerator Activity, and Serum-induced Thrombosis*