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11 - Dyslipidemia and pre-eclampsia

from Part I - Basic science

Published online by Cambridge University Press:  03 September 2009

Fiona Lyall
Affiliation:
University of Glasgow
Michael Belfort
Affiliation:
University of Utah
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Summary

Introduction

The causes of the pregnancy syndrome pre-eclampsia are multifactorial and poorly understood. According to current concepts, the disorder has two principal stages (Redman et al., 1999; Roberts and Hubel, 1999). The first stage is reduced placental perfusion, frequently secondary to abnormal implantation and insufficient remodeling of spiral arteries feeding the intervillous space. The second stage is the maternal response to this condition, modulated by maternal constitution and heredity, and characterized by widespread inflammation and endothelial cell dysfunction. The link between the two stages is an area of intense investigation. It is clear that placental factors are not solely accountable for the maternal manifestations of pre-eclampsia. Intrauterine growth restriction and preterm birth are commonly associated with abnormalities in Stage 1 but without the occurrence of a maternal syndrome. Maternal factors, including pre-pregnancy obesity and insulin resistance, predispose to development of pre-eclampsia. Evidence is accumulating that maternal constitutional predisposition to cardiovascular disease, unmasked or accentuated during the stress of pregnancy, is a key component in the development of pre-eclampsia. Data also suggest that women with a history of pre-eclampsia are at increased risk of cardiovascular disease in later life. Dyslipidemia may play an important role in these interrelationships. This chapter reviews the changes in lipid metabolism that occur with normal pregnancy and pre-eclampsia, and develops the hypothesis that dyslipidemia contributes to both the pathogenesis of preeclampsia and risk of later-life cardiovascular disease.

Pregnancy-induced changes in lipid metabolism

The diverse effects of pregnancy include a profound impact upon lipid metabolism.

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