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Complement and contact activation in term neonates after fetal acidosis
  1. Josef Sonntag,
  2. Mathias H Wagner,
  3. Evelyn Strauss,
  4. Michael Obladen
  1. Department of Neonatology Virchow-Klinikum, Humboldt-University Augustenburger Platz 1, 13 353 Berlin, Germany
  1. Dr Josef Sonntag.


AIMS To evaluate complement and contact activation after fetal acidosis.

METHODS Fifteen term neonates with hypoxic–ischaemic encephalopathy after umbilical arterial pH < 7.10 were compared with 15 healthy neonates with umbilical arterial pH > 7.20. Determinations of the complement function and C1-inhibitor activity were performed as kinetic tests 22–28 hours after birth. C1q, C1-inhibitor, and factor B concentrations were determined by radial immunodiffusion and those of C3a, C5a, and factor XIIa by enzyme immunoabsorbent assay.

RESULTS Median complement function (46vs 73 %), C1q (4.3 vs 9.1 mg/dl), and factor B (5.2 vs 7.7 mg/dl) decreased after fetal acidosis. The activated split products C3a (260 vs 185 μg/l), C5a (5.0vs 0.6 μg/l), and factor XIIa (3.2 vs 1.3 μg/l) increased in the neonates after fetal acidosis. No differences were found in the concentration and activity of C1-inhibitor.

CONCLUSIONS Complement and contact activation occurred in the newborns with hypoxic–ischaemic encephalopathy. Activation of these systems generates mediators which can trigger inflammation and tissue injury.

  • birth asphyxia
  • complement activation
  • contact activation
  • fetal acidosis

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