Complement and contact activation in term neonates after fetal acidosis

Abstract

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 (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. 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.