Summary: There was no significant difference in the levels of factor XII between sick newborns and normal age-matched controls, although the levels of both groups were lower than normal older children. Detailed coagulation studies on 44 sick infants revealed 11 to have disseminated intravascular coagulation (DIC). In those with DIC, the mean Hageman factor was 20% and in those without DIC, 25% (P > 0.05). Rabbits given a constant infusion of lysozyme (which inhibits factor XII) showed laboratory evidence of endotoxin-induced DIC. The data suggest that neither reduced factor XII levels nor Hageman factor inhibition provided protection from DIC. The data further suggest that other coagulation pathways might be involved in order to elicit the DIC.Speculation: Since Hageman factor activation is thought to be involved in initiating the coagulation mechanism and activation of fibrinolytic, kinin, and complement systems and therefore may be involved in basic pathophysiologic reactions, this study was undertaken to determine whether physiologic reductions in this factor might be protective in any way. Although it was found that newborns had lower factor XII levels than older children or adults and that the levels were lower in the younger infants and were therefore thought to be due to a developmental delay, no protection from the development of acquired coagulopathies could be detected. A significant number of sick neonates were found to have a variant form of DIC (reduced plasma factors II, V, VIII, and fibrinogen, but normal platelet counts instead of thrombocytopenia). It is speculated that these infants' platelets were not responsive to the DIC-provoking event due to a developmental platelet dysfunction.
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