PT  - JOURNAL ARTICLE
AU  - Sonntag, Josef
AU  - Wagner, Mathias H
AU  - Strauss, Evelyn
AU  - Obladen, Michael
TI  - Complement and contact activation in term neonates after fetal acidosis
AID  - 10.1136/fn.78.2.F125
DP  - 1998 Mar 01
TA  - Archives of Disease in Childhood - Fetal and Neonatal Edition
PG  - F125--F128
VI  - 78
IP  - 2
4099  - http://fn.bmj.com/content/78/2/F125.short
4100  - http://fn.bmj.com/content/78/2/F125.full
SO  - Arch Dis Child Fetal Neonatal Ed1998 Mar 01; 78
AB  - 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.