Tissue factor-dependent pathway in severe preeclampsia revisited

Abstract

Previously we investigated the tissue factor (TF)-dependent coagulation pathway and key haemostatic cofactors in white women with preeclampsia (P-EC) and suggested that plasma factor VII (FVII) levels can differentiate women with P-EC from healthy nonpregnant women or normal pregnant women, at the same trimester, with high sensitivity, specificity, positive and negative predictive values. Here we re-examine the TF-dependent pathway in a large cohort of Brazilian women. A total of 240 women were studied. These included healthy nonpregnant women (n = 79), normotensive pregnant women (n = 80) and women with severe P-EC (n = 81). Commercially available enzyme-linked immunosorbent assays were used to measure plasma FVII, activated factor VII (FVIIa), TF and tissue factor pathway inhibitor (TFPI). All study participants were matched for age. Pregnant women (with/without P-EC) were matched for gestational age and parity. Plasma levels of FVII, FVIIa and TFPI were significantly increased in women with severe P-EC compared with healthy nonpregnant women (P < 0.01) or normotensive pregnant women (P < 0.01). FVIIa was also higher in normotensive pregnant women compared with nonpregnant women (P < 0.01). However, no such significant trends were observed for plasma TF levels (P = 0.074). In conclusion, circulating FVII, FVIIa and TFPI were significantly elevated in women with severe P-EC in the absence of comparable changes in plasma TF levels. The present work is in agreement with our previous report on FVII levels in white women with P-EC. Thus, this lends further support to the notion that plasma FVII levels are potentially valuable diagnostic marker for P-EC, irrespective of ethnicity.

Serum proteins differentially expressed in early- and late-onset preeclampsia assessed using iTRAQ proteomics and bioinformatics analyses

“…These results are consistent with those of many previous trials (discussed below). The level of plasma FVII in patients with severe PE is significantly higher than that in healthy pregnant women; therefore plasma FVII levels may show high sensitivity and specificity in differentiating between PE and normal pregnancy (Dusse et al, 2016). The coagulation factor vWF is a specific marker that reflects damage of endothelial cells; thus, damaged microvascular endothelial cells in PE promote the expression of vWF.…”

Increased contact activated endogenous thrombin potential in pregnant women with preeclampsia

“…Predisposition to endothelial dysfunction is thought to play a central role [4] and can lead to inflammation and hemostatic abnormalities. Women with preeclampsia are in a hyper-coagulable state compared with normal pregnant women [5], and clinical features of the disease are associated with intravascular coagulation [6], which can also complicate preeclampsia. Furthermore, women with a history of preeclampsia have an increased risk of future cardiovascular disease such as ischemic heart disease, stroke, and venous thromboembolism [1,4].…”

Pathophysiology of the Venous Thromboembolism Risk in Preeclampsia

“…While the pattern of these haemostatic derangements appears to be heterogeneous and dependent on the severity of disease and the stage of pregnancy, preeclampsia appears to exacerbate pregnancy-associated hypercoagulability leading to an overall increased risk of venous thromboembolism (VTE). 2,3,31,32 The interplay between haemostatic derangements and severity of preeclampsia does not appear to represent a one-way process and increased coagulation activation, coagulation protease signalling and intra-vascular fibrin deposition likely worsen underlying vascular dysfunction and placental hypoxia thereby contributing to disease progression. 33 Among women presenting with preeclampsia, the clinical features are frequently heterogeneous with a more severe phenotype usually observed among women presenting with early-onset preeclampsia (EOP; onset before 34 weeks of gestation) in contrast to women presenting with late-onset preeclampsia (LOP; onset at 34 weeks of gestation or later).…”