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

J van Paassen, MP Bauer, MS (Mendi Sesmu) Arbous, LG Visser, J Schmidt-Chanasit, S Schilling, S Olschlager, T Rieger, P Emmerich, C Schmetz, F van den Berkmortel, B van Hoek, ND van Burgel, Ab Osterhaus, ACTM Vossen, S Gunther, JT van Dissel

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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-gamma and tumour necrosis factor-a 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.
Original languageUndefined/Unknown
Pages (from-to)635-642
Number of pages8
JournalLancet Infectious Diseases
Issue number8
Publication statusPublished - 2012

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