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Preeclampsia is a multisystem disorder specific to pregnant women. It remains one of the most important causes of maternal and fetal mortality and morbidity in developed countries (1). Although the pathogenesis of this condition is not fully understood, it is now widely accepted that vascular endothelial cell dysfunction is the final common pathway responsible for the maternal syndrome (2)(3). The underlying pathological changes that lead to the endothelial cell dysfunction remain incompletely understood, but poor placentation has been proposed as a major contributory factor (2)(4)(5). As a result of incomplete or failure of trophoblastic invasion of the spiral arteries, placental ischemia results, leading to the release of one or more factors that are responsible for the damage of the maternal vascular endothelium (5)(6). The normal process of trophoblastic invasion is complete by 20 weeks of gestation. Hence, the initiating placental pathology should exist prior to this stage of pregnancy, long before the onset of the clinical syndrome. Therefore, it might be possible to develop new plasma/serum biochemical markers for identifying subjects at increased risk of developing preeclampsia.We previously have shown that women with established preeclampsia have a fivefold increase in circulating fetal DNA concentrations in their plasma compared with control pregnant subjects (7). However, it is unknown whether this is a late phenomenon or whether it precedes the onset of clinical symptoms and signs. In this study, we aimed to test whether the abnormal increase in circulating fetal DNA concentrations can be detected in susceptible subjects before onset of the clinical disease.Pregnant women attending the Department of Obstetrics and Gynecology, Prince of Wales Hospital, Hong Kong were recruited with informed consent. The study was approved by the …

Increased Maternal Plasma Fetal DNA Concentrations in Women Who Eventually Develop Preeclampsia.