The fact that fibrinolysis in newborn infants is different from fibrinolysis in adults, first suggested by the report of Boisvert1 in 1940, has recently been confirmed by Phillips and Skrodelis.2 Boisvert observed that blood clots from newborn infants, in contrast to those from their mothers, were resistant to lysis in the presence of streptococcal culture supernates. Since placentally transferred antibody to the streptococcal factor could be excluded in many of the neonates, Boisvert postulated the existence of a nonspecific inhibitor of fibrinolysis in newborn blood.
Subsequent expansion of concepts of fibrinolysis has introduced alternative possibilities that might explain the failure of blood clots from newborn infants to lyse in the presence of the streptococcal factor. Milstone3 established that the streptococcal substance (streptokinase) does not lyse fibrin directly but that a lytic factor in serum is necessary. Christensen and MacLeod4 showed that streptokinase acts by conversion of
QUIE PG, WANNAMAKER LW. The Plasminogen-Plasmin System of Newborn Infants: Investigation of the Nature and Persistence of a Deficiency of This System in Human Infants. Am J Dis Child. 1960;100(6):836–843. doi:10.1001/archpedi.1960.04020040838005
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