Angiogenic Markers in Transition
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See related article, pp 731–738
Preeclampsia is a potentially devastating multisystem disorder affecting 3% to 8% of all pregnancies worldwide. A major contributor to maternal morbidity and mortality, as well as to premature delivery and its resulting neonatal consequences, preeclampsia imposes a substantial economic burden on society and an intense emotional strain on families. Newly diagnosed hypertension and proteinuria >300 mg/d or other signs of end-organ dysfunction after the 20th week of gestation have historically defined the condition. Although preeclampsia has been recognized since the ancient times,1 research performed in the last 2 decades has advanced our understanding of the potential mechanisms underlying its pathogenesis. Along with the contribution by Sovio et al2 in this issue, this new knowledge has allowed new diagnostic criteria to be established and opened doors for novel treatment strategies.
In preeclamptic pregnancies, antiangiogenic soluble VEGF receptor 1 (vascular endothelial growth factor, also known as sFlt-1 [soluble fms-like tyrosine kinase-1]) is pathologically overexpressed by the placenta and excessively secreted into the bloodstream.3 The excess circulating sFlt-1 scavenges VEGF and other proangiogenic factors, such as PlGF (placental growth factor), thereby opposing the otherwise natural trophic signal of VEGF on endothelial cells and consequently producing endothelial damage and dysfunction.
The utility of using sFlt-1 and PlGF plasma levels as diagnostic tools in patients with suspected preeclampsia was suggested over a decade ago, when the rise in sFlt-1 and decline in PlGF plasma levels was shown to antedate clinical symptoms by ≈4 weeks.4,5 Several case-controlled studies have suggested that measurement of angiogenic factors in combination with either ultrasound studies or clinical characteristics in patients with suspected preeclampsia may be used to predict, diagnose, and prognosticate preeclampsia.6–8