H. R. GRALNICK, M.D.; J. S. FINLAYSON, PH.D.
Despite its molecular heterogeneity (1, 2), a relatively constant set of functional properties has been ascribed to human fibrinogen (3). It is, therefore, of considerable clinical, genetic, and biochemical importance that within the last decade several hereditary functional defects of fibrinogen have been described. These disorders of familial, qualitatively abnormal fibrinogens have been most commonly referred to as congenital dysfibrinogenemias (4).
Congenital variants of fibrinogen are usually first noticed during coagulation tests in which plasma fibrinogen is converted to fibrin—that is, thrombin time, Reptilase time, or prothrombin time. The times are generally prolonged; in some cases no clot forms at
H. R. GRALNICK, J. S. FINLAYSON. Congenital Dysfibrinogenemias. Ann Intern Med. 1972;77:471–473. doi: 10.7326/0003-4819-77-3-471
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Published: Ann Intern Med. 1972;77(3):471-473.
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