Endothelial cell dysfunction is a key feature of the pathogenesis of
pre-eclampsia. The cause of the endothelial cell injury is probably multifactorial, but poor placenta perfusion plays a major role. In
pre-eclampsia, characteristic pathological lesions in the placenta are
fibrin deposits, acute atherosis and
thrombosis. The similarity between the lesions of
pre-eclampsia and
atherosclerosis has led to speculations of a common pathophysiological pathway. An abnormal
lipid profile is known to be strongly associated with atherosclerotic
cardiovascular disease and has a direct effect on endothelial function. Abnormal lipid metabolism seems important in the pathogenesis of
pre-eclampsia too. An elevated plasma
lipoprotein (a) concentration is a known risk factor for atherosclerotic
cardiovascular disease. In this paper, we discuss three hypotheses about the mechanisms by which
lipoprotein (a) may be associated with
pre-eclampsia: 1. Lp(a), as an
acute-phase reactant, transporting
cholesterol to sites of endothelial damage for reparation, temporarily increases during pregnancy and increases more during a pregnancy complicated by mild to moderate
pre-eclampsia as compared to an uncomplicated pregnancy, in response to a greater extend of endothelial injury in
pre-eclampsia. After delivery,
pre-eclampsia subsides and Lp(a) concentrations return to baseline levels. 2. In cases of severe
pre-eclampsia, there is even more extensive endothelial damage and consequently a higher consumption of Lp(a) in reparation of this vascular damage. These women will have lower concentrations of Lp(a). 3. High baseline concentrations of Lp(a), which are genetically determined, may induce or contribute to the development of
pre-eclampsia by promoting endothelial dysfunction. In this line of reasoning one would expect to find higher concentrations of Lp(a) in women at risk for developing
pre-eclampsia in a future pregnancy or with a history of
pre-eclampsia. As discussed above, these women are also at increased risk for future
cardiovascular disease as compared to women with a history of normal pregnancy. The pathophysiologic changes associated with
cardiovascular disease may also be responsible for the increased incidence of
pre-eclampsia in these women.