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Link to original content: https://pubmed.ncbi.nlm.nih.gov/22394985/
Acute liver failure, multiorgan failure, cerebral oedema, and activation of proangiogenic and antiangiogenic factors in a case of Marburg haemorrhagic fever - PubMed Skip to main page content
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Case Reports
. 2012 Aug;12(8):635-42.
doi: 10.1016/S1473-3099(12)70018-X. Epub 2012 Mar 5.

Acute liver failure, multiorgan failure, cerebral oedema, and activation of proangiogenic and antiangiogenic factors in a case of Marburg haemorrhagic fever

Judith van Paassen  1 , Martijn P Bauer, M Sesmu Arbous, Leo G Visser, Jonas Schmidt-Chanasit, Stefan Schilling, Stephan Ölschläger, Toni Rieger, Petra Emmerich, Christel Schmetz, Franchette van de Berkmortel, Bart van Hoek, Nathalie D van Burgel, Albert D Osterhaus, Ann Ctm Vossen, Stephan Günther, Jaap T van Dissel
Affiliations
Case Reports

Acute liver failure, multiorgan failure, cerebral oedema, and activation of proangiogenic and antiangiogenic factors in a case of Marburg haemorrhagic fever

Judith van Paassen et al. Lancet Infect Dis. 2012 Aug.

Abstract

A woman developed Marburg haemorrhagic fever in the Netherlands, most likely as a consequence of being exposed to virus-infected bats in the python cave in Maramagambo Forest during a visit to Uganda. The clinical syndrome was dominated by acute liver failure with secondary coagulopathy, followed by a severe systemic inflammatory response, multiorgan failure, and fatal cerebral oedema. A high blood viral load persisted during the course of the disease. The initial systemic inflammatory response coincided with peaks in interferon-γ and tumour necrosis factor-α concentrations in the blood. A terminal rise in interleukin-6, placental growth factor (PlGF), and soluble vascular endothelial growth factor receptor-1 (sVEGF-R1) seemed to suggest an advanced pathophysiological stage of Marburg haemorrhagic fever associated with vascular endothelial dysfunction and fatal cerebral oedema. The excess of circulating sVEGF-R1 and the high sVEGF-R1:PlGF ratio shortly before death resemble pathophysiological changes thought to play a causative part in pre-eclampsia. Aggressive critical-care treatment with renal replacement therapy and use of the molecular absorbent recirculation system appeared able to stabilise--at least temporarily--the patient's condition.

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