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Review ofLiterature
small vessels of placental bed initiates acute atherosis and related
thrombosis in maternal uterine spiral arteries leading to insufficient
perfusion ofthe placental bed and the clinical symptoms of Preeclampisa
(Wang et al., 1998).
A report of a family with two cases of severe Preeclampisa
/eclampsia in which very high levels ofLp(a) has been found, suggests
that a very high Lp(a) level could be one risk factor for Preeclampisa that
is genetically determined (Husby et al., 1996).
However, Dijurovic et al., (1997) made an examination of 154
women with Preeclampisa (Preeclampisa group) and 76 healthy pregnant
normotensive women (control group) .The Preeclampisa group was
further dvided into the following subgroups: mild Preeclampisa, severe
Preeclampisa and Preeclampisa with fetal growth retardation. They found
that plasma levels ofLp(a) were lower in the total Preeclamptic group as
well as in all ofthe Preeelampisa subgroups than in the control group as
determined by quantitative electroimmunoassay (Dijurovic et al., 1997).
Leerink et al. (1997) in the same year studied levels ofLp(a) and
apolipoprotein (a) phenotype in women with a history ofPreeelampisa in
a previous history (patient group) in comparison with women without
Preeclampisa in their history (control group) . They found median Lp(a)
levels in both groups to be equal as well as the apo (a) phenotype
distribution in both groups concluding. that they do not contribute
significantly to the pathogenesis ofPreeclampisa.
70