Abstract

The investigation of the cause of an accidentally observed prolonged prothrombin time in a patient without a haemorrhagic diathesis led to the discovery of a familial disturbance of the aggregation of fibrin monomers (von Felten, Duckert and Frick, 1965). The observed defect differs from previously reported anomalies in the last phase of coagulation such as congenital afibrinogenaemia or hypofibrinogenaemia (Frick and McQuarrie, 1954), congenital fibrin‐stabilizing‐factor (FSF) deficiency (Duckert, Jung and Shmerling, 1960), and congenital dysfibrinogenaemia (Beck, 1964). It may be similar to the fibrinogen anomaly described by Ménaché (1963).

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