INCREASED RELEASE OF TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-6 INWOMEN WITH THE SYNDROME OF HEMOLYSIS, ELEVATED LIVER-ENZYMES, AND LOWPLATELET COUNT
M. Haeger et al., INCREASED RELEASE OF TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-6 INWOMEN WITH THE SYNDROME OF HEMOLYSIS, ELEVATED LIVER-ENZYMES, AND LOWPLATELET COUNT, Acta obstetricia et gynecologica Scandinavica, 75(8), 1996, pp. 695-701
Background. Complement is activated in preeclampsia and complement pro
ducts are known to activate macrophages. The aim of this study was to
determine whether the macrophage derived cytokines, interleukin-1 beta
, interleukin-6 and tumor necrosis factor-alpha, are released in patie
nts with a form of severe preeclampsia characterized by the syndrome o
f hemolysis, elevated liver enzymes, and low platelet count (HELLP syn
drome). Methods. Complement activation and plasma levels of cytokines
were studied in 11 women with HELLP syndrome and in 11 controls with u
ncomplicated pregnancies. To further evaluate the connection between c
omplement activation and cytokine release an in vitro study on heparin
ized whole blood incubated with recombinant C5a was performed. Results
. In the HELLP group, complement anaphylatoxin C5a was increased in pl
asma at delivery (p<0.01) and one day after delivery (p<0.05), termina
l C5b-9 complement complex was elevated in plasma at delivery (p<0.001
) and one day after (p<0.01), plasma levels of interleukin-6 were incr
eased one day after delivery (p<0.01), and plasma concentrations of tu
mor necrosis factor-alpha were elevated at delivery (p<0.01), compared
with corresponding levels in controls. All parameters normalized with
in one week. Interleukin-1 beta did not differ between the groups. In
vitro, recombinant C5a incubated in whole blood gave a dose-dependent
release of interleukin-6. No increased release of interleukin-1 or tum
or necrosis factor-alpha was seen after incubation. Conclusions. Since
cytokine release occurs in severe preeclampsia, inflammatory mechanis
ms may participate in the pathophysiology of severe preeclampsia.