Serum inhibin levels increase during normal pregnancy, but are significantl
y higher in patients with pre-eclampsia. The aim of this study was to demon
strate possible increased expression of inhibin within the placentas of wom
en with preeclampsia compared with non-prl-eclamptic controls. Cellular exp
ression of inhibin alpha and beta(A) subunits was studied using immunohisto
chemistry on formalin-fixed, paraffin-embedded placental sections from case
s of pre-eclampsia (n = 23) and gestational age-matched non-pre-eclamptic c
ontrols (n = 16). Immunohistochemistry was per formed using monoclonal anti
bodies against inhibin alpha and beta(A) subunits by the indirect immunoper
oxidase technique. intensity of staining was graded by a semiquantitative s
coring method. Differences in distribution and intensity of staining betwee
n control and pre-eclamptic placentas were analyzed using a nonparametric M
ann-Whitney U test. Staining for both inhibin alpha and beta(A) was predomi
nantly confined to the cytoplasm of syncytiotrophoblast, with weak expressi
on within intermediate trophoblast. The intensity of staining for inhibin a
: was significantly greater in the syncytiotrophoblast of pre-eclamptic pat
ients (mean staining intensity controls = 0.97, disease = 1.87; p < 0.001).
inhibin beta(A) staining was generally stronger than for the a: subunit, a
nd was also significantly increased in pre-eclamptic patients compared with
controls (mean controls = 1.72, disease 2.19; p < 0.05). This: is the firs
t evidence for increased placental inhibin presence in pre-eclampsia, sugge
sting increased inhibin production within the placenta, a finding that coul
d account for increased serum inhibin levels in pre-eclampsia.