786 IMMUNO-IDENTIFICATION OF HUMAN FETAL FIBRINOGEN

Samples of plasma were obtained from the umbilical cords (UP) of uncomplicated pregnancies at term, from neonates with ‘reactive’ hyperfibrinogenemia (NP) and from normal adults (AP). Fibrinogen was measured as thrombin-clottable protein (TCF) by the methods of Clauss and Astrup, and as immunoassayable material (IAF) by radial diffusion and nephelometry. Functional and structural characterization were pursued respectively by studies of fibrin monomer polymerization (FMP) and by cross-over immuno-electrophoresis (CIE). IAF-UP exceeded TCF-UP (n = 40, p < 0.001). No such difference existed in NP or AP and the observation could not be explained by partial proteolysis nor by inhibition of thrombin. Prolonged incubation (24 hours) with thrombin resulted in higher values for TCF-UP but not for TCF-AP. FMP was delayed in UP - median 12 minutes - by comparison with AP - median 9 minutes (n = 17, p < 0.005). CIE revealed disproportionate anodal migration in UP fibrinogen in all samples investigated (n = 13) with mobility ratios of 1.10 - 1.86 to pooled AP fibrinogen. The TCF-IAF difference in UP may represent fetal fibrinogen. Furthermore, the lack of an inverse relationship between ‘fetal fibrinogen’ levels and gestational age, and the previously reported rise in the concentration of TCF within a few days of delivery, suggest that the stimulus to change from the synthesis of fetal to that of adult fibrinogen is provided by the event of birth or its immediate sequelae.