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Pathogenesis of pre- eclampsia
Review ofLiterature
The exact nature ofthe primary event causing pre-eclampsia is not
known. However, one of the initial events in this disease is abnormal
placentation, in which the main feature is inadequate trophoblastic
invasion ofthe maternal spiral arterioles. In normal pregnancy the wall of
the spiral arteries is invaded by trophoblastic cells and transformed into
large, tortuous channels that carry a large amount of blood to the
intervillous space and are resistant to the effects of vasmotor agents.
These physiologic changes are restricted in-patients with pre-eclampsia
(Brosens, 1977).
The anatomic and physiologic disruption ofnormal placentation is
thought to lead to altered endothelial cell function and multiple organ
damage (Shankil and Sibai ,1989). .
The majority of pregnant women with chronic hypertension have
essential hypertension. Rarely, the hypertension results from chronic
renal disease, renal artery stenosis, pheochromocytoma,
hyperaldosteronism, or other casuses (Lindheimer and Katz, 1985).
In pre-eclampsia, absence of normal stimulation of the renin­
angiotensin system, despite hypovolaemia, and increased vasucular
sensitivity to angiotensin II and norepinephrine can be explained by a
biologic dominance of TxA2 over prostacyclin. A reduction in urinary
excretion of prostacyclin metabolites precedes the development of
clinical disease, whereas TXA2 biosynthesis is increased in pre-eclampsia.
Increased TxA2 production in pre-eclampsia is largely derived from
platelets and the placenta. Placental prostacyclin production is reduced.
(Dekker and Sibai, 1998).
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