Maternal serum endostatin at gestational weeks 16–20 is elevated in subsequent pre‐eclampsia but not in intrauterine growth retardation

Objective . Endostatin, an important anti‐angiogenic factor produced by endothelial cells, is elevated in established pre‐eclampsia. We measured maternal serum endostatin concentrations in early pregnancy associated with later pre‐eclampsia and intrauterine growth retardation (IUGR). Design . Retrospective case–control study. Setting . University Central Hospital. Sample . Serum samples were collected at 12–15 and 16–20 gestational weeks from a total of 124 pregnant women of whom 49 developed pre‐eclampsia, 16 gave birth to infants with IUGR without pre‐eclampsia, and 59 remained normotensive giving birth to healthy, normal‐weight infants. Methods . Enzyme‐linked immunosorbent assay. Main outcome measures . Endostatin concentrations in serum. Results . At 12–15 gestational weeks, there was no difference in median endostatin concentrations between the groups. At 16–20 gestational weeks, the median endostatin concentration was higher in the women with subsequent pre‐eclampsia ( p = 0.026), especially preceding a later severe form of the disease ( p = 0.041), than in the controls. The results were further confirmed by receiver operating characteristic (ROC) analysis showing an area under the curve (AUC) of 0.64 (95% confidence interval: 0.50–0.81) for endostatin to identify subsequent pre‐eclampsia, and 0.71 (0.53–0.89) in cases of severe pre‐eclampsia. Optimal cut‐off values were determined and used for calculations of sensitivity and specificity, which were 80 and 52% (cut‐off value = 58.0 μg/L) in pre‐eclampsia, and 80 and 65% (cut‐off value = 65.5 μg/L) in the severe form of the disease. Conclusions . The concentrations of endostatin in maternal serum at 16–20 weeks’ of gestation are associated with an increased risk of pre‐eclampsia but not IUGR.