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Published on: November 20, 2015
Intraventricular haemorrhage in preterm infants: evidence of suppressed fibrinolysis
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.
Abstract:
Intraventricular hemorrhage (IVH) in premature infants may be related to the immaturity of the vascular bed in the germinal matrix. We measured six hemostatic parameters whose alterations may represent an additional risk factor for IVH in preterm infants. On postnatal day 1 there were differences between plasminogen activator inhibitor-1 (PAI-1) activity and antigen, of both full-term and preterm infants with and without IVH (P < 0.05). Preterms with IVH were different to both full-terms and preterms without IVH. No difference was observed in plasma concentrations of fibrinogen, plasminogen and von Willebrand factor. Plasma concentrations of antithrombin III were significantly higher in full-term infants than in preterm infants. The difference between the platelet counts of preterm infants with and without IVH was not significant (P > 0.05). Elevation of crosslinked fibrin degradation products (XDP), determined by the SimpliRED D-dimer test, correlated in four out of five premature infants with the diagnosis of IVH by ultrasonography. No elevation of D-dimer XDP was observed in premature infants without IVH (11/12) and full-term infants (6/6). In conclusion, a hypercoagulable state, indicated by a rise in D-dimer XDP, may be initiated by some types of trauma to fragile blood vessels of the preterm infants who develop IVH. This hypercoagulability is further exacerbated by the increased release of PAI-1 leading to suppressed fibrinolysis.
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