Thrombomodulin, von Willebrand factor and E-selectin as plasma markers of endothelial damage/dysfunction and activation in pregnancy induced hypertension

Sunil K. Nadar, Eman Al Yemeni, Andrew D. Blann, Gregory Y H Lip*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

48 Citations (Scopus)

Abstract

Objective: Endothelial disturbance (whether activation, dysfunction or damage) is a likely pathogenic mechanism in pre-eclampsia and pregnancy-induced hypertension (PIH). We set out to determine which of three plasma markers of endothelial disturbance, indicating endothelial activation (E-selectin) or damage/dysfunction (von Willebrand factor (vWf), soluble thrombomodulin), would provide the best discriminator of PIH compared to normotensive pregnancy. Study design: Cross-sectional study of 36 consecutive women with PIH (age 31±6 years) and 36 consecutive women with normotensive pregnancies (age 29±5 years) of similar parity. Plasma levels of vWf, E-selectin and thrombomodulin were measured using ELISA. Results: As expected, women with PIH had significantly higher levels of plasma vWf (by 19%, p=0.003), E-selectin (by 40%, p<0.001) and thrombomodulin (by 61%, p=0.01) than normotensive women. However, on stepwise multiple regression analysis, only thrombomodulin was an independent significant predictor of the presence of PIH (p=0.023). Conclusions: We conclude that although vWf, E-selectin and thrombomodulin are all raised in PIH, only thrombomodulin was independently associated with PIH. This molecule could potentially be useful in monitoring and in providing clues in aetiology and pathophysiology, and may have implications for the clinical complications associated with PIH.

Original languageEnglish
Pages (from-to)123-128
Number of pages6
JournalThrombosis Research
Volume113
Issue number2
DOIs
Publication statusPublished - 2004

Keywords

  • E selectin
  • Pregnancy induced hypertension
  • Thrombomodulin
  • von Willebrand factor

ASJC Scopus subject areas

  • Hematology

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