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III. Lp (a) ill P.LH:
Review ofLiterature
Wang et al, (1998) demonstrated an increased plasma Lp(a) levels
in pregnant women with Preeclampisa and eclampsia in comparison to
normal pregnancy. While its level was significantly higher in severe than
in mild Preeclampisa. They concluded that Lp(a) level was associated
with the severity ofdisease and may serve as a marker ofthe pathogenic
process.
A further study was done investigating women with a history of
severe Preeclampisa and controls with a history ofnormal pregnancies
only All were tested at least 10 weeks after delivery in the second halfof
a normal menstrual cycle. None ofthe controls or patients were pregnant
or used oral contraceptives. There was no statistically significant
difference of Lp(a) level between the two groups (Van pampus et al.,
1998).
The data ofWang et al, 1998 in addition to those ofVanPampus
et a1.1998 suggest that in Preeclampisa, levels of Lp(a) increase in
relation with the severity of disease. After delivery, Lp(a) normalizes.
This suggests a specific alteration of Lp(a) level in relation to
Preeclampisa.
Hypothesis suggesting the mechanism of action of Lp(a) in
Preeclampisa (whether elevated Lp(a) is causative factor for
P reeclampisa,
In Preeclampisa, endothelial cell injury and altered endothelial cell
function appear to play a pivotal role in the genesis ofall aspects ofthe
multisystem damage, including renal and liver functions seen in
Preeclampisa (Rodgers et al., 1998). Lp(a) has been shown to induce
endothelial cell dysfunction (Hajjar et al., 1989).
A recent hypothesis was laid suggesting that genetically
determined elevated Lp(a) and its deposition in endothelial cells ofthe
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