Preeclampsia is characterized by an imbalance in angiogenic factors, including sEng (soluble endoglin). However, the relationship of sEng with the severity of preeclampsia, clinical, and laboratory parameters, and the occurrence of adverse outcomes are not fully elucidated. We studied 1002 women with preeclampsia. Serum concentrations of sEng were measured by ELISA. Serum sEng levels were significantly different ( P <0.001) in patients with preeclampsia than in healthy pregnancy. In addition, these factors were markedly different in patients with hemolysis, elevated liver enzymes, low platelet count syndrome and eclampsia than in patients with preeclampsia with or without severe features ( P <0.001) and in patients with preeclampsia with severe features than in those without severe features ( P <0.001). sEng correlated positively with blood pressure, proteinuria, and levels of creatinine, uric acid, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase; and inversely with gestational age, infant’s birth weight, and platelets counts ( P <0.001 for all). The risk of combined and specific adverse outcomes (pulmonary edema, acute renal failure, placental abruption, hepatic hematoma or rupture, maternal death, cerebral hemorrhage, thrombocytopenia, elevated liver enzymes, preterm delivery, small for gestational age infant, and need for endotracheal intubation, positive inotropic drug support, and hemodialysis) was higher in patients with sEng values in the highest quartile (odds ratio ≥3.1) compared with the lowest quartile. Patients in the highest quartile of sEng were more likely to deliver early compared with those in the lowest quartile (HR, 2.33; 95% CI, 1.91–2.84). We concluded that circulating concentrations of sEng seem to be a suitable marker to assess the severity of preeclampsia and are associated with increased risk of adverse outcomes.

Preeclampsia is a multisystemic pregnancy-specific disease characterized by endothelial dysfunction.1 This condition develops in 5% to 8% of all pregnant women and remains a major cause of maternal and perinatal morbidity and mortality worldwide. 2,3 Although the cause of this pregnancy-specific syndrome is unclear, accumulating evidence suggests that preeclampsia results from an imbalance between placental proangiogenic and antiangiogenic factors that result in maternal vascular endothelium damage. 4,5 Higher circulating concentrations of soluble vascular endothelial growth factor receptor-1 (also referred as soluble fms-like tyrosine kinase-1 [sFlt-1]) and soluble endoglin (sEng), and lower concentrations of placental growth factor (PlGF), are present at the time of diagnosis of preeclampsia and have been associated with an elevated risk to develop this condition for several weeks before the onset of the clinical manifestations.5-8 On the other hand, prolactin (PRL), which is physiologically elevated during normal pregnancy, has many effects beyond reproduction and lactation, including an eminent role in angiogenesis and antiangiogenesis. 9-11The major circulating PRL isoform is a 23-kDa single-chain polypeptide (monomeric PRL), which comprises up to 90% of total PRL.12 This full-length PRL stimulates angiogenesis. In contrast, 16-and 14-kDa PRL fragments that result from proteolytic cleavage of monomeric PRL have antiangiogenic effects. 9,13 We and others have shown that urinary PRL excretion and its antiangiogenic PRL fragments are elevated in preeclamptic women, increasing with the severity of the disease and the occurrence of adverse outcomes.11,14 Furthermore, the antiangiogenic PRL fragments are also increased in serum, amniotic fluid, and placenta of preeclamptic women.14,15 These data suggest that PRL might contribute to the pathogenesis of preeclampsia and that perturbation of this angiogenesis pathway may have an important impact on the development of clinical manifestations and complications.Despite the establishment of criteria and guidelines for diagnosis of preeclampsia, its severity, and management, these criteria have been unable to predict adverse maternal outcomes.Abstract-Preeclampsia is characterized by an imbalance in angiogenic factors. Urinary prolactin (PRL) levels and its antiangiogenic PRL fragments have been associated with disease severity. In this study, we assessed whether these biomarkers are associated with an increased risk of adverse maternal and perinatal outcomes in preeclamptic women. We studied 501 women with preeclampsia attended at a tertiary care hospital. Serum concentrations of soluble fmslike tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), and soluble endoglin (sEng), as well as urinary PRL levels, were measured by enzymed-linked immunosorbent assay. Antiangiogenic PRL fragments were determined by immunoblotting. The risk for any adverse maternal outcome and for having a small-for-gestational-age infant was higher among women with sFlt-1/PlGF ratios, sEng...

Changes in circulating concentrations of sFlt-1, PlGF, sEng, and the sFlt-1/PlGF ratio precede the onset of preeclampsia in SLE pregnancies. The risk profile of circulating angiogenic factors for developing preeclampsia distinctly evolves depending on whether this condition is manifested earlier or later.

Gestational hypertension (GH) and preeclampsia (PE) are characterized by an imbalance in angiogenic factors. However, the relationship among these factors with the severity of hypertensive disorders of pregnancy (HDP) and adverse outcomes are not fully elucidated. We examined whether these biomarkers are related with the severity of HDP and adverse outcomes.Using a cross-sectional design, serum concentrations of placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), and soluble endoglin were determined in 764 pregnant women: 75 healthy pregnant, 83 with mild GH (mGH), 105 with severe GH (sGH), 122 with mild PE (mPE), and 379 with severe PE (sPE).All angiogenic factors’ concentrations were significantly different (P ≤ 0.041) in HDP than in healthy pregnancy. In addition, these factors were markedly different in sPE than in mPE, sGH, or mGH (P ≤ 0.027) and in patients with sGH that in those with mPE or mGH (P < 0.05). As compared to mGH and mPE, patients with sGH and sPE had higher rates of both preterm delivery at <34 weeks of gestation and small-for-gestational age infants. Moreover, patients with sPE had higher rates of adverse maternal outcomes (P < 0.001) when compared to patients with mGH, sGH, or mPE. In all cases, levels of sFlt-1/PlGF ratio were significantly higher in patients with sGH and sPE who had adverse perinatal and maternal outcomes than in those with sGH and sPE who did not (P ≤ 0.016).Circulating concentrations of angiogenic factors appear to be suitable markers to assess the severity of GH and PE, and adverse outcomes.