Cm. Salafia et al., PLACENTAL PATHOLOGICAL FEATURES OF PRETERM PREECLAMPSIA, American journal of obstetrics and gynecology, 173(4), 1995, pp. 1097-1105
OBJECTIVE: Our purpose was to compare the incidence and interrelations
hips of uteroplacental vasculopathy and chronic inflammatory and place
ntal vasoocclusive lesions in preeclampsia and spontaneous delivery be
fore 32 weeks' gestation. STUDY DESIGN: Review of singleton live-born
nonanomalous infants born at 22 to 32 weeks' gestation identified 76 c
ases of preeclamspia and 353 cases of spontaneous prematurity (spontan
eous premature membrane rupture [n = 192], preterm labor, intact membr
anes [n = 161]). Histologic lesions were considered as belonging to on
e of five major pathophysiologic groups: (1) uteroplacental vascular l
esions and related villous lesions, (2) chronic inflammatory lesions,
(3) coagulation-related lesions, (4) acute inflammatory lesions, and (
5) unclassified lesions. Contingency table analyses considered p < 0.0
5 significant. Factor analysis extracted combinations of related varia
bles. RESULTS: More frequent in preeclampsia versus spontaneous premat
urity were chronic uteroplacental vasculitis (29% vs 20%, p < 0.05), c
hronic villitis (20% vs 3%, p < 0.001), avascular villi (39% vs 16%, p
< 0.001), and ''hemorrhagic endovasculitis'' (9% vs 2.5%, p < 0.03).
In the preeclampsia cases factor analysis extracted 13 categories of r
elated lesions. Four categories contained uteroplacental vascular lesi
ons. Five categories included lesions related to chronic inflammation,
and eight included lesions related to coagulation. Four categories lo
aded lesions from one major pathophysiologic group only. Three categor
ies loaded lesions from all three pathophysiologic groups. Unclassifie
d lesions loaded into two factor categories that were unrelated to the
other lesions. CONCLUSIONS: Chronic inflammatory and placental vasooc
clusive lesions are more common in preterm preeclampsia than in sponta
neous prematurity. Immunopathologic processes and coagulation may be i
nvolved in the pathophysiologic mechanisms of preterm preeclampsia ind
ependent of uteroplacental vascular pathologic features.