Kivonat:
The purpose of this study was to explore the role of the
complement system in normal human pregnancy and preeclampsia in
a comprehensive manner, measuring circulating levels of
complement proteins, their activation fragments and regulatory
factors, as well as those of C-reactive protein (CRP). Sixty
preeclamptic patients, 60 healthy pregnant women and 59 healthy
non-pregnant women were involved in this case-control study.
Circulating levels of complement components and CRP were
determined with ELISA, radial immunodiffusion and particle
enhanced immunoturbidimetric assay. Levels of CRP, C4d, C3a,
SC5b9, C3, C9 and factor H antigen were significantly higher,
while those of C1-inhibitor were significantly lower in healthy
pregnant than non-pregnant women. In addition, preeclamptic
patients had significantly higher CRP, C4d, C3a, SC5b9 levels
and significantly lower C3 concentrations as compared to healthy
pregnant women. Their CRP, C4d, C3a, SC5b9, C4, C3, C9 and
factor H antigen levels were significantly higher, while C1-
inhibitor concentrations were significantly lower compared with
healthy non-pregnant women. However, no significant difference
was found in Bb and C4b-binding protein levels among the three
study groups. Preeclamptic patients with fetal growth
restriction had significantly higher plasma SC5b9 levels than
those without IUGR. There was a relative deficiency of C1-
inhibitor and C4b-binding protein, and a relative abundance of
factor H both in normal pregnancy and preeclampsia. Activation
of the classical or lectin pathway (C4d) showed significant
positive correlation to C3 activation (C3a) both in healthy
pregnant women and preeclamptic patients. However, the
correlation between C3 and terminal pathway activation was
dominating only in patients with preeclampsia, but not in
healthy pregnant women. In conclusion, the complement system is
activated through the classical and/or lectin pathways with
increased terminal complex formation in the third trimester of
normal human pregnancy, and further in preeclampsia, as shown
by the elevated amounts of activation markers in the systemic
circulation. Excessive activation of the terminal pathway is
associated with fetal growth restriction in preeclamptic women.
However, additional studies are required to determine the cause
and consequence of systemic complement activation in this
pregnancy-specific disorder.
