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

作者：van Paassen Judith; Bauer Martijn P; Arbous M Sesmu; Visser Leo G; Schmidt Chanasit Jonas; Schilling Stefan; Oelschlaeger Stephan; Rieger Toni; Emmerich Petra; Schmetz Christel; van de Berkmortel Franchette; van Hoek Bart; van Burgel Nathalie D; Osterhaus Albert D; Vossen Ann C T M; Guenther Stephan; van Dissel Jaap T^*

来源：Lancet Infectious Diseases, 2012, 12(8): 635-642.

DOI：10.1016/S1473-3099(12)70018-X

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%26apos;s condition.

• 出版日期2012-8