AMERICAN JOURNAL OF HEMATOLOGY, cilt.83, ss.50-53, 2008 (SCI İndekslerine Giren Dergi)
Intraalveolar fibrin deposition found in neonates with respiratory distress syndrome (RDS) is explained by the activation of the coagulation system and inefficient fibrinolysis. However, thrombin activatable, fibrinolysis inhibitor activity (TAFla), an inhibitor of fibrinolysis, and the ratio of D-dimer to thrombin-antithrombin complex (D-dimer/TAT), an index of fibrinolytic activity, have not been reported previously in neonatal RDS. Aim of this study is to evaluate the influence of plasma TAFla levels on the fibrinolytic state in neonatal RDS. The RDS group (Group 1) consisted of 29 neonates, and 18 neonates served as the control group (Group 2). Plasma TAFla levels and D-dimer/TAT ratios were evaluated in all neonates in the first 6 hr of life. Neonates in the RDS group were further divided into two subgroups; Group la consisted of 12 neonates with evidence of mild asphyxia (Apgar score at 5 min < 7 and cord pH < 7.26), and Group 1b consisted of 17 nonasphyxiated neonates. No significant difference was found in TAFla levels and D-dimer/TAT ratios between Groups 1 and 2 [214% (56.2-361%) and 124.3 (4.4-3,921) in Group 1 and 201% (60.3-381%) and 147 (5.9-1,426) in Group 2]. There were negative correlations between cord pH and TAFla levels in both groups. Increased TAFla levels and decreased D-dimer/TAT ratios and platelet counts were detected in mildly asphyxiated neonates when compared with nonasphyxiated ones. TAFla is not responsible for the hypofibrinolytic state reported in RDS. However, asphyxia influences TAFla levels and increased TAFla levels depress fibrinolysis.