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Pre-eclampsia is associated with significant maternal and fetal morbidity and mortality worldwide. While provision of adequate antenatal care would significantly reduce morbidity and mortality in third-world countries, in first-world countries efforts are being focused on identification of at-risk patients and on targeted therapies. Pre-eclampsia can be distinguished as early (<34 weeks gestation) and late (>34 weeks) onset phenotypes. While these have been thought traditionally to be synonymous with severe and mild disease phenotypes, respectively, recent analyses show that an appreciable amount of severe disease is also late onset. There is evolving evidence that there are different underlying etiologies that ultimately lead to this syndrome defined by hypertension, proteinuria and edema. It is unlikely that one single biomarker will identify all individuals destined to develop pre-eclampsia. Rather, panels of biomarkers specific for the different phenotypes may identify those at risk for pre-eclampsia prior to the appearance of overt disease. Importantly, these measurements may also provide different (biochemical) definitions of disease. In order to have a significant impact on clinical or economic outcome it is vital to identify women who will develop early onset disease or severe disease, as these phenotypes are those associated with significant morbidity and mortality. Similarly, therapies must be targeted at these same outcomes and not just the appearance of hypertension and proteinuria at term. While there is abundant evidence in the literature for changes in expression or concentration of many biomarkers in established disease, there is still a dearth of prospective studies with well-defined clinical outcomes in which prospective measurement of biomarkers have been made.
The placenta plays a unique role in supporting the fetal allograft throughout gestation, protecting against immune rejection whilst also serving to supply oxygen and nutrients to, and remove carbon dioxide and waste products from, the fetus. As the nutrient interface between mother and fetus, the placenta may passively or actively transfer nutrients to the fetus or metabolise them en route. In addition the placenta produces a variety of peptide and steroid hormones that affect placental, maternal and fetal metabolism and development. The developmental origins of health and adult disease hypothesis proposes that alterations in fetal development, or adaptations of the fetus to alterations in the normal amount or pattern of substrate supply across the placenta, lead somehow to cardiovascular and metabolic disease in adult life. There is now abundant evidence both from human epidemiological studies and from animal studies that maternal nutrition may ‘programme’ the offspring for adult disease. This effect may be direct but it is more likely to be mediated in some manner by placental structure and/or function regulating the amount or composition of nutrients transferred. Does the placenta therefore play an active or a passive role in programming? Reduced fetal and placental weights are both associated with fetal programming. However, it is argued that, rather than reduced placental weight (and function) being linked to reduced fetal weight in a cause-and-effect relationship, reduced weight(s) might be a surrogate marker for an adverse intrauterine experience.
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