ACTIVATION OF THE PLASMA CLOTTING, FIBRINOLYTIC, AND KININ KALLIKREINSYSTEM IN PRETERM INFANTS WITH SEVERE IDIOPATHIC RESPIRATORY-DISTRESSSYNDROME

We studied the activation pattern of clotting, fibrinolysis, and kinin -kallikrein during the first 5 d of life in 10 preterm infants with si gns of severe idiopathic respiratory distress syndrome (IRDS) after bi rth (IRDS group) and in 12 healthy preterm infants (reference group). We found systemic activation of clotting, fibrinolysis, and kinin-kall ikrein in the IRDS infants within 12 to 24 h of birth, represented by increased median thrombin-antithrombin III complex formation (90 ng/mL versus 10 ng/mL in the reference group, p < 0.05), increased mean tis sue-type plasminogen activator plasma concentrations (11.8 ng/mL versu s 3.5 ng/mL in the reference group, p < 0.05), and increased mean plas ma kallikrein activity (182.6% versus 162.0% of maximal activated huma n plasma in the reference group,p < 0.05), respectively. Clotting acti vation was accompanied by a significant decrease of the platelet count . Clotting and fibrinolytic activity decreased in the IRDS group durin g the first 2 to 3 d of life. Kinin-kallikrein activation was accompan ied by decreased plasma kallikrein inhibitor activity values and did n ot change throughout the study period. Plasma factor XII activity was not significantly increased in the IRDS infants during the first 2 d o f life but did significantly increase thereafter. The cause of simulta neous activation of clotting, fibrinolysis, and kinin-kallikrein in ou r IRDS infants has not yet been clarified. However, this activation pr ocess may contribute to lung injury such as that described in the adul t respiratory distress syndrome.