background. Pre-eclampsia might result from a less effective invasion of trophoblast cells in the myometrium, caused by attenuated immunosuppression in the spiral arteries, resulting from inhibition of plasmin-mediated activation of transforming growth factor-β-like substances. In vitro evidence indicates that lipoprotein(a) is capable of inhibiting plasmin-mediated activation of transforming growth factor-β. Thus, high plasma levels of lipoprotein(a) might result in increased incidence of preeclampsia.
Methods. The patient group consisted of 39 patients with a history of pre-eclampsia in a previous pregnancy: Forty-seven women without pre-eclampsia in their history and matched for age were the control group. All participants gave their informed consent. In both the patient and control group blood pressure, CRP, urinalysis, cholesterol, HDL-cholesteroI, triglycerides, lipoprotein(a) level and apolipoprotein(a) phenotype were determined.
Results. None of the participants had elevated CRP levels, excluding acute phase related elevations of lipoprotein(a). Proteinuria was present in 33% of patients and in 11% of controls (p=0.01). However, no relation was observed between proteinuria and Lp(a) level. Median Lipoprotein(a) levels in both groups were equal (300 mg/1 vs. 275 mg/1; p=0.48), as well as the apo(a) phenotype distribution in both groups.
Conclusions. Lipoprotein(a) and apolipoprotein(a) phenotype do not contribute significantly to the pathogenesis of pre-eclampsia.