Abstract

Pre-eclampsia is a syndrome of pregnancy, defined by the gestational-onset of hypertension and proteinuria, which resolves postpartum. This definition does not consider the variable multiorgan involvement of a syndrome that can include seizures, fulminating hepatic necrosis and a consumptive coagulopathy. These disparate clinical features are a consequence of an accelerated but transient metabolic syndrome with widespread maternal endothelial dysfunction and inflammation. A trigger to this maternal state is the relatively ischaemic placenta. As pregnancy progresses, the concentration of vaso-toxic factors released by the relatively ischaemic placenta gradually builds up in the maternal circulation. Those predisposed to endothelial dysfunction, e.g. women with risk factors for cardiovascular disease, are more sensitive to these placental derived factors and will develop pre-eclampsia before natural onset of labour. A woman's vulnerability to pre-eclampsia is therefore composed of a unique balance between her pre-existing maternal endothelial and metabolic health and the concentration of placental derived factors toxic to maternal endothelium. Delivery of the placenta remains the only cure. Years later, women who had pre-eclampsia are at increased risk of chronic hypertension, ischaemic heart disease, cerebrovascular disease, kidney disease, diabetes mellitus, thromboembolism, hypothyroidism and even impaired memory. This article describes how a brief, usually single episode of this acute pregnancy syndrome might both identify those vulnerable to chronic disease in later life and in some cases initiate chronic disease.

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