Abstract
During the past decade a new hypothesis has been formulated that explains many of
the disparate findings associated with the pregnancy syndrome preeclampsia. With an
increased awareness of the physiological significance of vascular endothelial cell
function, the seemingly unrelated signs of hypertension, proteinuria, edema, and hypercoagulability
have converged to provide clinical evidence of a unifying pathophysiological mechanism:
systemic, maternal endothelial cell dysfunction. Investigators have attempted to test
this hypothesis through two approaches. The first approach involves the identification
of in vivo markers of vascular endothelial cell injury in women with clinically evident
preeclampsia. The second approach focuses on the ability of circulating factors derived
from the serum or plasma of patients afflicted with preeclampsia to perturb endothelial
cell function in vitro. In this review we summarize the increasingly compelling evidence
that maternal vascular endothelial cells are a critical target for toxic humoral activities
that precipitate the multifaceted preeclampsia syndrome.
Keywords:
Preeclampsia - endothelial cell dysfunction
