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Complement and contact activation related to surfactant response in respiratory distress syndrome
M H Wagner1, J Sonntag, E Strauss
1Department of Neonatology, Charité-Virchow-Hospital, Humboldt-University, Berlin, Germany.
Insights
Inflammation and coagulation pathways are implicated in infant respiratory distress syndrome (RDS). This study found that complement and contact system activation were higher in infants with severe RDS, particularly those who responded poorly to surfactant therapy.
Area of Science:
- Neonatal medicine
- Immunology
- Pulmonology
Background:
- The pathogenesis of respiratory distress syndrome (RDS) involves inflammation and coagulation.
- Previous research shows contact activation in preterm infants with RDS, but complement activation findings are inconsistent.
Purpose of the Study:
- To investigate complement and contact system activation in preterm infants with severe RDS.
- To correlate these activations with surfactant therapy response.
Main Methods:
- Studied 30 preterm infants with severe RDS and 18 healthy controls.
- Analyzed blood samples for complement (C1q, C4, factor B, C3a, C5a) and contact system (factor XIIa, C1-inhibitor) markers.
- Grouped RDS infants into responders and poor responders based on surfactant therapy efficacy.
Main Results:
- Infants with severe RDS showed altered complement and contact system markers compared to controls.
- Higher levels of activated complement (C3a, C5a) and contact factors (factor XIIa) were observed in poor responders to surfactant.
- Lower levels of complement precursors (C1q, C4) were found in poor responders.
Conclusions:
- Both complement and contact systems are activated in preterm infants with severe RDS.
- This activation is more pronounced in infants who respond poorly to exogenous surfactant treatment.
Abstract:
The activation of inflammation and coagulation cascades is part of the pathogenesis of adult respiratory distress syndrome (RDS). Previous studies have demonstrated contact activation in preterm infants with RDS, whereas no concordant results have been found with complement activation. In this study, both systems were investigated in preterm infants with severe RDS and related to surfactant response. Thirty preterm newborns with severe respiratory distress (FiO2 > 0.5), but with no evidence of infection or fetal acidosis, were studied. Eighteen healthy preterm newborns of similar gestational age and birth weight served as controls. The study group was divided into two subgroups, according to their response to a porcine natural surfactant 6 h after administration: responders (FiO2 reduction > 50%) and poor responders (FiO2 reduction < or = 50%). C1q, C4, factor B, C3a, C5a, complement, and C1-inhibitor activity, as well as factor XIIa, were determined in blood samples, drawn 24 h after birth. Except for C1-inhibitor concentration and C1-inhibitor activity, all parameters for infants with severe RDS were different from controls. Complement precursor proteins were lower, and activated split products of the complement and contact system were higher. Infants with a poor response after application of surfactant showed higher amounts of C3a, C5a, and factor XIIa but lower C1q and C4 levels compared with infants with a good response to surfactant. Activation of the complement and the contact system was demonstrated in all respiratory distress patients. This activation was more pronounced in poor responders to exogenous surfactant.