Placenta derived factors involved in the pathogenesis of the liver in the syndrome of haemolysis, elevated liver enzymes and low platelets (HELLP): A review

L. C. E. W. van Lieshout*, G. H. Koek, M. A. Spaanderman, P. J. van Runnard Heimel

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

5 Citations (Web of Science)

Abstract

Aim: With this review we try to unravel if placenta-derived factors are able to initiate liver sinusoidal endothelial cells (LSEC) decay in HELLP syndrome and eventually cause the development of sinusoidal obstruction syndrome (SOS).

Background: Haemolysis, Elevated Liver enzymes and Low Platelets (HELLP) syndrome is a severe complication of pregnancy. It is characterized by elevated liver enzymes, low platelet count and haemolytic anaemia. The risk of developing HELLP syndrome within a pregnancy is 0.1-0.8%. The mortality rate among women with HELLP syndrome is 0-24% and the perinatal death goes up to 37%. The aetiology of HELLP syndrome is not fully understood but the pathogenesis of the liver pathology in the HELLP syndrome resembles that of a SOS with endothelial damage of the LSECs which ultimately leads to liver failure.

Objectives: We hypothesize that placenta derived factors cause LSEC damage and thereby liver dysfunction.

Methods: We searched in the PubMed database for relevant articles about placenta derived factors involved in endothelial activation especially in the liver. We yielded eventually 55 relevant articles.

Results: Based on this literature search we associate that in HELLP syndrome there is an increase of soluble fmslike tyrosine kinase (sFlt1), vascular endothelial growth factor (VEGFR), soluble endoglin (sEng), galectin-1 (Gall), endothelin-1 (ET-1), Angiopoietin 2 (Angs-2), Asymmetric dimethylarginine (ADMA), activin B, inhibin A, Fas ligand (FasL) and heat shock protein 70 (Hsp70).

Conclusion: We assume that these eleven increased placenta derived factors are responsible for LSEC damage which eventually leads to liver failure. This concept shows a possible design of the complicated pathophysiology in HELLP syndrome. However further research is required.

Original languageEnglish
Pages (from-to)42-48
Number of pages7
JournalPregnancy Hypertension: an international journal of women's cardiovascular health
Volume18
DOIs
Publication statusPublished - Oct 2019

Keywords

  • HELLP syndrome
  • Haemolysis elevated liver enzymes and low platelets syndrome
  • Etiology
  • Pathophysiology
  • Pathogenesis
  • SOS
  • Sinusoidal obstruction syndrome
  • Placenta derived factors
  • Liver function
  • LSEC
  • Liver sinusoidal endothelial cells
  • Endothelial activation
  • FAS LIGAND
  • ACTIVIN-A
  • BETA-B
  • EXPRESSION
  • PREECLAMPSIA
  • GALECTIN-1
  • ANGIOGENESIS
  • BIOLOGY
  • HEAT-SHOCK-PROTEIN-70
  • DIMETHYLARGININE

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