PATHOGENESIS OF THE COAGULATION DEFECT DEVELOPING DURING PATHOLOGICAL PLASMA PROTEOLYTIC (“FIBRINOLYTIC”) STATES. II. THE SIGNIFICANCE, MECHANISM AND CONSEQUENCES OF DEFECTIVE FIBRIN POLYMERIZATION*

Norma Alkjærsig, Anthony P. Fletcher, Sol Sherry

Journal of Clinical Investigation · 1962 · 171 citations · 28 references

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Abstract

A clinical syndrome characterized by a coagulation defect, hypofibrinogenemia, often an associated hemorrhagic diathesis and manifestations of whole blood or plasma fibrinolysis (spontaneous lysis of whole blood or plasma clots), has long been recognized. Usually developing acutely after the trauma of surgery or in association with certain obstetric complications, it may also present as a chronic syndrome complicating the course of long-term medical disease (reviews noted in References 1, 2). Moreover, the iatrogenic induction of the syndrome, usually in a mild form, frequently accompanies the treatment of the acute thromboembolic complications of vascular disease by enzymatic means (3-6).

References

28