Angiogenic factors and uterine Doppler velocimetry in early‐ and late‐onset preeclampsia

Abstract

Preeclamptic patients have increased soluble fms-like tyrosine kinase-1 and soluble endoglin serum levels and this increase is directly correlated with uterine artery resistance, especially in those with early-onset preeclampsia.

Sequential plasma angiogenic factors levels in women with suspected preeclampsia

“…Finally, our data is consistent with prior work showing a positive correlation of uterine artery flow abnormalities with abnormalities in angiogenic factors, particularly more evident in patients who had early onset preeclampsia diagnosed <34 weeks. 26,27 Our data does not allow us to claim that alterations in angiogenic factors can lead to uterine artery flow abnormalities, however the temporal relationship between changes in circulating angiogenic factors and uterine artery flow abnormalities is consistent with this hypothesis. Original Research OBSTETRICS ajog.org…”

Predictive accuracy of the first trimester Doppler scan: a meta-study

“…The first trimester UAD has elusive or limited diagnostic accuracy in predicting preeclampsia and FGR [3,11,12,[57][58][59][60][61][62][63][64][65][66][67][68][69][70] IV 9…”

“…(1) the first trimester UAD indices are highly predictive of both preeclampsia and FGR [5,7,9,10,; (2) the first trimester UAD is highly predictive of preeclampsia and fairly predictive or not predictive of the FGR [1,2,8,; (3) the first trimester UAD has elusive or limited diagnostic accuracy in preeclampsia and FGR [3,11,12,[57][58][59][60][61][62][63][64][65][66][67][68][69][70]; and (4) the first trimester UAD indices are not predictive of preeclampsia or FGR [6,[71][72][73][74][75][76][77][78].…”

Placental Growth Factor, Soluble fms-Like Tyrosine Kinase 1, Soluble Endoglin, IL-6, and IL-16 as Biomarkers in Preeclampsia

“…It is an important cause of maternal and perinatal morbidity and mortality [ 2 , 3 ]. PE affects 2–8% of all pregnancies [ 4 , 5 ], accounting for over 60,000 maternal deaths annually worldwide [ 6 ] The pathogenesis of PE is not completely understood. It is thought to involve defective placentation [ 6 , 7 ], inadequate trophoblast invasion of maternal spiral arteries during gestation [ 5 , 8 – 16 ], placental ischemia [ 5 , 9 , 10 , 12 , 14 , 16 ], increased oxidative stress [ 9 , 10 , 16 ], release of antiangiogenic proteins into maternal plasma [ 5 , 8 – 14 , 16 ], excessive maternal inflammatory response [ 6 , 8 – 13 , 15 ], endothelial injury [ 8 – 10 ], generalized endothelial dysfunction [ 5 , 8 – 10 , 13 , 16 ], hypertension [ 8 – 14 , 16 ], and multiorganic manifestation [ 10 , 13 , 16 , 17 ].…”