The role of lipoprotein (a) in pregnancies complicated by pre-eclampsia

被引:23
作者
Manten, GTR [1 ]
van der Hoek, YY [1 ]
Sikkema, JM [1 ]
Voorbij, HAM [1 ]
Hameeteman, TM [1 ]
Visser, GHA [1 ]
Franx, A [1 ]
机构
[1] Univ Utrecht, Ctr Med, Dept Perinatol & Gynaecol, NL-3508 AB Utrecht, Netherlands
关键词
D O I
10.1016/j.mehy.2004.04.026
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:162 / 169
页数:8
相关论文
共 38 条
  • [1] The elevated plasma lipoprotein(a) concentrations in preeclampsia do not precede the development of the disorder
    Bar, J
    Harell, D
    Bardin, R
    Pardo, J
    Chen, R
    Hod, M
    Sullivan, M
    [J]. THROMBOSIS RESEARCH, 2002, 105 (01) : 19 - 23
  • [2] LP(A) LIPOPROTEIN - AN OVERVIEW
    BERG, K
    [J]. CHEMISTRY AND PHYSICS OF LIPIDS, 1994, 67-8 : 9 - 16
  • [3] Lipoprotein metabolism during normal pregnancy
    Brizzi, P
    Tonolo, G
    Esposito, F
    Puddu, L
    Dessole, S
    Maioli, M
    Milia, S
    [J]. AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1999, 181 (02) : 430 - 434
  • [4] Dyslipidemia in early second trimester is mainly a feature of women with early onset pre-eclampsia
    Clausen, T
    Djurovic, S
    Henriksen, T
    [J]. BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY, 2001, 108 (10): : 1081 - 1087
  • [5] LP(A) LIPOPROTEIN IN CARDIOVASCULAR-DISEASE
    DAHLEN, GH
    [J]. ATHEROSCLEROSIS, 1994, 108 (02) : 111 - 126
  • [6] THE CLASSIFICATION AND DEFINITION OF THE HYPERTENSIVE DISORDERS OF PREGNANCY
    DAVEY, DA
    MACGILLIVRAY, I
    [J]. AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1988, 158 (04) : 892 - 898
  • [7] Djurovic S, 1997, CLIN GENET, V52, P371
  • [8] He S, 1999, THROMB HAEMOSTASIS, V81, P538
  • [9] Long term mortality of mothers and fathers after pre-eclampsia:: population based cohort study
    Irgens, HU
    Reisæter, L
    Irgens, LM
    Lie, RT
    [J]. BRITISH MEDICAL JOURNAL, 2001, 323 (7323): : 1213 - 1216
  • [10] KAMBOH MI, 1991, AM J HUM GENET, V49, P1063