Complement and contact activation in term neonates after fetal acidosis
J Sonntag, MH Wagner, E Strauss… - Archives of Disease in …, 1998 - fn.bmj.com
J Sonntag, MH Wagner, E Strauss, M Obladen
Archives of Disease in Childhood-Fetal and Neonatal Edition, 1998•fn.bmj.comAIMS 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 …
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 …
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.
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