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Complement anaphylatoxin C3a and C5a formation in premature children with respiratory distress
A Enskog1, A Bengtsson, J P Bengtson
1Department of Anaesthesiology and Intensive Care, Sahlgrenska University Hospital, Göteborg, Sweden.
Insights
Respiratory distress (RD) in premature infants is not linked to complement activation unless complications like pneumothorax or hemorrhage occur. These complications correlate with increased anaphylatoxins C3a and C5a levels.
Area of Science:
- Neonatal Medicine
- Immunology
- Pediatric Intensive Care
Background:
- Premature infants often experience respiratory distress (RD).
- Complement activation, specifically anaphylatoxins C3a and C5a, plays a role in inflammatory processes.
- Perinatal complications can exacerbate respiratory distress in neonates.
Purpose of the Study:
- To investigate complement activation in premature infants with respiratory distress.
- To determine the association between perinatal complications and anaphylatoxin levels in preterm infants with RD.
Main Methods:
- Blood samples were collected from 25 premature infants on admission to the NICU.
- Plasma concentrations of anaphylatoxins C3a and C5a were measured.
- Patients were categorized based on the presence or absence of perinatal complications alongside RD.
Main Results:
- Preterm infants with RD and complications (pneumothorax, intracerebral hemorrhage) showed elevated C3a and C5a plasma levels.
- Infants with isolated RD did not exhibit signs of complement activation.
- A positive correlation was observed between C3a and C5a plasma concentrations.
Conclusions:
- Isolated respiratory distress in preterm infants does not typically involve complement activation.
- Complications such as pneumothorax and intracerebral hemorrhage are associated with the release of anaphylatoxins C3a and C5a.
- Complement activation markers may indicate the severity of complications in preterm infants with RD.
Unlabelled:
Premature children (n = 25) with respiratory distress (RD) were studied regarding complement activation and formation of the anaphylatoxins C3a and C5a. Blood samples were drawn on admission to the paediatric intensive care unit. In 18 of the patients RD was accompanied by other perinatal complications like pneumothorax or intracerebral haemorrhages. Seven of the premature children had RD without such complications. Preterm children with RD and with peri- and postnatal complications such as pneumothorax or intracerebral haemorrhage had increased concentrations in plasma of the anaphylatoxins C3a and C5a compared with preterm children with RD without these complications. There was a positive correlation between the plasma C3a and C5a concentrations in the preterm children.
Conclusion:
The present study indicates that isolated RD will appear without signs of complement activation and that complications like pneumothorax or intracerebral haemorrhages are associated with release of the anaphylatoxins C3a and C5a.
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