Intraventricular haemorrhage in preterm infants: evidence of suppressed fibrinolysis

J P Chen1, V Lorch

  • 1Department of Medical Biology, University of Tennessee Medical Center/Knoxville 37920, USA.

Insights

Premature infants with intraventricular hemorrhage (IVH) show altered levels of plasminogen activator inhibitor-1 (PAI-1) and elevated D-dimer crosslinked fibrin degradation products (XDP), indicating a hypercoagulable state. This suggests PAI-1 and XDP may be key risk factors for IVH in preterm infants.

Area of Science:

  • Neonatology
  • Hematology
  • Pediatric Neurology

Background:

  • Intraventricular hemorrhage (IVH) is a significant concern in premature infants, potentially linked to immature germinal matrix vasculature.
  • Hemostatic alterations may represent an additional risk factor for IVH in preterm neonates.

Purpose of the Study:

  • To investigate alterations in six hemostatic parameters as potential risk factors for IVH in preterm infants.
  • To identify specific hemostatic markers associated with IVH development in neonates.

Main Methods:

  • Measurement of six hemostatic parameters in full-term and preterm infants (with and without IVH) on postnatal day 1.
  • Assessed plasma concentrations of fibrinogen, plasminogen, von Willebrand factor, antithrombin III, platelet counts, plasminogen activator inhibitor-1 (PAI-1) activity and antigen.
  • Utilized the SimpliRED D-dimer test to determine crosslinked fibrin degradation products (XDP).

Main Results:

  • Significant differences in PAI-1 activity and antigen were observed between preterm infants with and without IVH, and between preterm and full-term infants.
  • Elevated D-dimer XDP levels correlated with IVH diagnosis in 4 out of 5 preterm infants.
  • No significant differences were found in fibrinogen, plasminogen, von Willebrand factor, or platelet counts between preterm infants with and without IVH.

Conclusions:

  • A hypercoagulable state, indicated by elevated D-dimer XDP, may contribute to IVH in preterm infants, possibly triggered by vascular trauma.
  • Increased PAI-1 release further exacerbates hypercoagulability by suppressing fibrinolysis, highlighting its role in IVH pathogenesis.

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