Complement and contact activation in term neonates after fetal acidosis
Department of Neonatology
Virchow-Klinikum, Humboldt-University
Augustenburger Platz 1, 13 353 Berlin,
Germany
Correspondence to: Dr Josef Sonntag.
Accepted 18 September
AIMS
To evaluate complement and contact activation
after fetal acidosis.
METHODSFifteen 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.
RESULTSMedian complement function (46 vs 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 (5.0 vs 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.
CONCLUSIONSComplement and contact activation
occurred in the newborns with hypoxic-ischaemic encephalopathy.
Activation of these systems generates mediators which can trigger
inflammation and tissue injury.
© 1998 by Archives of Disease in Childhood
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