Reply

Abstract

To the Editors:We thank van Pampus et al for the interest in our article. In our report we suggested that prospective studies of lipoprotein(a) levels in pregnant women and in vitro experiments of the effects of lipoprotein(a) on placental vessel formation and “atherosis” changes are needed to establish the existence of a causal relationship between elevated lipoprotein(a) and pre-eclampsia. Panteghini and Pagani1Panteghini M Pagani F Serum concentrations of lipoprotein(a) during normal pregnancy and postpartum.Clin Chem. 1991; 37: 2009-2010PubMed Google Scholar reported that lipoprotein(a) levels gradually increased until the end of pregnancy. This increase was parallel to those well known for plasma triglycerides, cholesterol, and apolipoprotein B. They have further shown that the serum lipoprotein(a) concentrations in the postpartum period (median 84 mg/L [range 2 to 646 mg/L]) is still much higher than in nonpregnant controls (61 mg/L [2 to 702 mg/L]). A study of 1-year follow-up of lipoprotein metabolism after pregnancy showed that pregnancy-related changes in lipid metabolism did not wane within 3 months after delivery and lactation also affected lipid metabolism.2Erkkola R Viikari J Irjala K Solakivi-Jaakola T One-year follow-up of lipoprotein metabolism after pregnancy.Biol Res Pregnancy Perinatol. 1986; 7: 47-51PubMed Google Scholar It is therefore possible that the study of van Pampus et al does not prove that the lipoprotein(a) levels are restored to the levels before pregnancy within 3 months. A prospective study of lipoprotein(a) levels in pregnant women is required to investigate whether elevated lipoprotein(a) is a causative factor for pre-eclampsia occurring before the clinical disorder. One-year follow-up of lipoprotein(a) levels after delivery is also needed.In pre-eclampsia endothelial cell injury and altered endothelial cell function appear to play a pivotal role in the genesis of all aspects of the multisystem damage, including renal and liver functions seen in pre-eclampsia. Lipoprotein(a) has been shown to induce endothelial cell dysfunction. We hypothesize that genetically determined elevated lipoprotein(a) and its deposition in endothelial cells of the small vessels of placenta bed initiates “acute atherosis” and related thrombosis in maternal uterine spiral arteries leading to insufficient perfusion of the placental bed and the clinical symptoms of pre-eclampsia. An alternative explanation is that impaired renal function in pre-eclampsia could result in elevated lipoprotein(a) levels. This in turn would promote and extend endothelial cell damage and dysfunction. In vitro studies are needed to complement population studies as to whether lipoprotein(a) is a causative factor for pre-eclampsia. To the Editors:We thank van Pampus et al for the interest in our article. In our report we suggested that prospective studies of lipoprotein(a) levels in pregnant women and in vitro experiments of the effects of lipoprotein(a) on placental vessel formation and “atherosis” changes are needed to establish the existence of a causal relationship between elevated lipoprotein(a) and pre-eclampsia. Panteghini and Pagani1Panteghini M Pagani F Serum concentrations of lipoprotein(a) during normal pregnancy and postpartum.Clin Chem. 1991; 37: 2009-2010PubMed Google Scholar reported that lipoprotein(a) levels gradually increased until the end of pregnancy. This increase was parallel to those well known for plasma triglycerides, cholesterol, and apolipoprotein B. They have further shown that the serum lipoprotein(a) concentrations in the postpartum period (median 84 mg/L [range 2 to 646 mg/L]) is still much higher than in nonpregnant controls (61 mg/L [2 to 702 mg/L]). A study of 1-year follow-up of lipoprotein metabolism after pregnancy showed that pregnancy-related changes in lipid metabolism did not wane within 3 months after delivery and lactation also affected lipid metabolism.2Erkkola R Viikari J Irjala K Solakivi-Jaakola T One-year follow-up of lipoprotein metabolism after pregnancy.Biol Res Pregnancy Perinatol. 1986; 7: 47-51PubMed Google Scholar It is therefore possible that the study of van Pampus et al does not prove that the lipoprotein(a) levels are restored to the levels before pregnancy within 3 months. A prospective study of lipoprotein(a) levels in pregnant women is required to investigate whether elevated lipoprotein(a) is a causative factor for pre-eclampsia occurring before the clinical disorder. One-year follow-up of lipoprotein(a) levels after delivery is also needed.In pre-eclampsia endothelial cell injury and altered endothelial cell function appear to play a pivotal role in the genesis of all aspects of the multisystem damage, including renal and liver functions seen in pre-eclampsia. Lipoprotein(a) has been shown to induce endothelial cell dysfunction. We hypothesize that genetically determined elevated lipoprotein(a) and its deposition in endothelial cells of the small vessels of placenta bed initiates “acute atherosis” and related thrombosis in maternal uterine spiral arteries leading to insufficient perfusion of the placental bed and the clinical symptoms of pre-eclampsia. An alternative explanation is that impaired renal function in pre-eclampsia could result in elevated lipoprotein(a) levels. This in turn would promote and extend endothelial cell damage and dysfunction. In vitro studies are needed to complement population studies as to whether lipoprotein(a) is a causative factor for pre-eclampsia. We thank van Pampus et al for the interest in our article. In our report we suggested that prospective studies of lipoprotein(a) levels in pregnant women and in vitro experiments of the effects of lipoprotein(a) on placental vessel formation and “atherosis” changes are needed to establish the existence of a causal relationship between elevated lipoprotein(a) and pre-eclampsia. Panteghini and Pagani1Panteghini M Pagani F Serum concentrations of lipoprotein(a) during normal pregnancy and postpartum.Clin Chem. 1991; 37: 2009-2010PubMed Google Scholar reported that lipoprotein(a) levels gradually increased until the end of pregnancy. This increase was parallel to those well known for plasma triglycerides, cholesterol, and apolipoprotein B. They have further shown that the serum lipoprotein(a) concentrations in the postpartum period (median 84 mg/L [range 2 to 646 mg/L]) is still much higher than in nonpregnant controls (61 mg/L [2 to 702 mg/L]). A study of 1-year follow-up of lipoprotein metabolism after pregnancy showed that pregnancy-related changes in lipid metabolism did not wane within 3 months after delivery and lactation also affected lipid metabolism.2Erkkola R Viikari J Irjala K Solakivi-Jaakola T One-year follow-up of lipoprotein metabolism after pregnancy.Biol Res Pregnancy Perinatol. 1986; 7: 47-51PubMed Google Scholar It is therefore possible that the study of van Pampus et al does not prove that the lipoprotein(a) levels are restored to the levels before pregnancy within 3 months. A prospective study of lipoprotein(a) levels in pregnant women is required to investigate whether elevated lipoprotein(a) is a causative factor for pre-eclampsia occurring before the clinical disorder. One-year follow-up of lipoprotein(a) levels after delivery is also needed. In pre-eclampsia endothelial cell injury and altered endothelial cell function appear to play a pivotal role in the genesis of all aspects of the multisystem damage, including renal and liver functions seen in pre-eclampsia. Lipoprotein(a) has been shown to induce endothelial cell dysfunction. We hypothesize that genetically determined elevated lipoprotein(a) and its deposition in endothelial cells of the small vessels of placenta bed initiates “acute atherosis” and related thrombosis in maternal uterine spiral arteries leading to insufficient perfusion of the placental bed and the clinical symptoms of pre-eclampsia. An alternative explanation is that impaired renal function in pre-eclampsia could result in elevated lipoprotein(a) levels. This in turn would promote and extend endothelial cell damage and dysfunction. In vitro studies are needed to complement population studies as to whether lipoprotein(a) is a causative factor for pre-eclampsia.