Real-world data on the clinical use of angiogenic factors in pregnancies with placental dysfunction

Abstract

BACKGROUND: In routine clinical practice, angiogenic factor measurement can facilitate prediction and diagnosis of preeclampsia and other manifestations of placental dysfunction (eg, intrauterine growth restriction). OBJECTIVE: This real-world data analysis investigated the utility of soluble fms-like tyrosine kinase-1 and placental growth factor for preeclampsia and placental dysfunction. STUDY DESIGN: Blood serum soluble fms-like tyrosine kinase-1 and placental growth factor were measured using Elecsys soluble fmslike tyrosine kinase-1 and placental growth factor immunoassays (cobas e analyzer; Roche Diagnostics). Overall, 283 unselected singleton pregnancies with !1 determination of soluble fms-like tyrosine kinase-1etoeplacental growth factor ratio were included. Distribution of the ratio at admission was normal (<38 [58.7%]), intermediate (38À85/110 [19.1%]), or pathologic (>85/110 [22.3%]). Overall, 15.5% had preeclampsia or hemolysis, elevated liver enzyme levels, and low platelet count, and 15.5% of women had intrauterine growth restriction. RESULTS: Increasing soluble fms-like tyrosine kinase-1etoe placental growth factor ratio was associated with an increase in priority of delivery (r¼0.38; P<.001). The percentage of patients who developed preeclampsia by soluble fms-like tyrosine kinase-1etoeplacental growth factor ratio at admission was 5.4% (normal), 7.4% (intermediate), and 49.2% (pathologic). The greatest difference in soluble fms-like tyrosine kinase-1etoe placental growth factor ratio from admission to birth occurred in pathologic pregnancies (171.12 vs 39.84 for normal pregnancies). Soluble fms-like tyrosine kinase-1etoeplacental growth factor ratio correlated inversely with gestational age at delivery, birthweight, and prolongation time. There was no significant relation between the prolongation period or the gestational age at first determination to the increase of soluble fms-like tyrosine kinase-1 and placental growth factor between admission and delivery (DQ). This analysis used a real-world approach to investigate the clinical utility of the soluble fms-like tyrosine kinase-1etoeplacental growth factor ratio in placental dysfunction. CONCLUSIONS: Confirming the results of prospective studies, we observed a positive correlation between soluble fms-like tyrosine kinase-1etoeplacental growth factor ratio and severity of placental dysfunction and a negative association with time to delivery. In a real-world setting, the soluble fms-like tyrosine kinase-1eplacental growth factor ratio stratifies patients with normal outcome and outcome complicated by placental dysfunction.

Comparison of the Soluble fms-Like Tyrosine Kinase 1/Placental Growth Factor Ratio Alone versus a Multi-Marker Regression Model for the Prediction of Preeclampsia-Related Adverse Outcomes after 34 Weeks of Gestation

“…Multi-marker regression models, including the combination of risk factors, assessment of the sFlt-1/PlGF ratio, and other clinical tests to predict PE-related AOs, have been investigated in a multitude of studies [22][23][24][25][26][27][28][29][30][31][32]. In a prospective study of n = 616 women, Rana et al reported that a cutoff value of the sFlt-1/PlGF ratio of 85 shows an AUC of 89% when predicting maternal and perinatal AOs within 2 weeks.…”

Novel therapeutic and diagnostic approaches for preeclampsia

“…The previous studies (although some pragmatic) have been controlled in a research setting. Importantly, recent evidence shows that these factors also perform well in real world conditions [16 ▪▪ ,26 ▪ ].…”

Hsa_circ_0001326 inhibited the proliferation, migration, and invasion of trophoblast cells via miR‐145‐5p/TGFB2 axis

“…There have been several hypotheses trying to explain the origins of preeclampsia, such as placental function disorder, abnormal immunity, and oxidative stress 4–7 . Among them, long‐term placental dysfunction and abnormal molecular expression are important factors in the pathogenesis of PE 8,9 …”

“…[4][5][6][7] Among them, long-term placental dysfunction and abnormal molecular expression are important factors in the pathogenesis of PE. 8,9 The proper function of the placenta depends on the normal proliferation/differentiation of the trophoblast cells in the placenta. These cells are involved not only in the transport of nutrients and oxygen but also in the secretion of pregnancy hormones and communication with maternal cells.…”