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A clinical syndrome characterized by hypofibrinogenemia, a coagulation defect, often an associated severe hemorrhagic diathesis, and manifestations of whole blood or plasma "fibrinolysis" (spontaneous lysis of whole blood or plasma clots) has long been recognized (1). The conditions may develop: following surgery (2, 3), particularly thoracic surgery (4, 5); be associated with obstetric complications (6, 7), notably abruptio placenta (8-1 ); develop rarely during the course of neoplastic disease (12), but more commonly if the prostate is involved (13, 14); complicate the course of hepatic cirrhosis (15-18) or certain other medical conditions, most frequently in their terminal stages. Since the syndrome may complicate many disease conditions and is most frequently manifested by rapid whole blood clot lysis, it often has been described as a "pathological fibrinolytic state" or as "'fibrinolysis as a disease state." However, since the phenomenon involves the action of proteolytic rather than strictly fibrinolytic enzymes, descriptive terms involving the word proteolytic rather than fibrinolytic are clearly preferable. Such terms as "excessive plasma proteolytic activity" or "pathological proteolytic state" not only define the condition more accurately, but focus attention on its wider ramifications. Hitherto the study of the syndrome in humans has been difficult for it occurs more frequently as

the journal of clinical investigation/the journal of clinical investigation

PATHOGENESIS OF THE COAGULATION DEFECT DEVELOPING DURING PATHOLOGICAL PLASMA PROTEOLYTIC (“FIBRINOLYTIC”) STATES. I. THE SIGNIFICANCE OF FIBRINOGEN PROTEOLYSIS AND CIRCULATING FIBRINOGEN BREAKDOWN PRODUCTS*