Giuseppe
Emeritus
[Source: The Lancet Infect Dis., abstract, full text: (LINK). Edited.]
The Lancet Infectious Diseases, Volume 12, Issue 8, Pages 635 - 642, August 2012
doi:10.1016/S1473-3099(12)70018-X
Published Online: 05 March 2012
Acute liver failure, multiorgan failure, cerebral oedema, and activation of proangiogenic and antiangiogenic factors in a case of Marburg haemorrhagic fever
Original Text
Judith van Paassen MD, Martijn P Bauer MD, M Sesmu Arbous MD, Leo G Visser MD, Jonas Schmidt-Chanasit MD, Stefan Schilling MD, Stephan ?lschl?ger MSc, Toni Rieger MSc, Petra Emmerich PhD, Christel Schmetz MSc, Franchette van de Berkmortel MD, Prof Bart van Hoek MD, Nathalie D van Burgel MD, Prof Albert D Osterhaus PhD, Ann CTM Vossen MD, Prof Stephan G?nther MD, Prof Jaap T van Dissel MD
Summary
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
lGF 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.
- -------doi:10.1016/S1473-3099(12)70018-X
Published Online: 05 March 2012
Acute liver failure, multiorgan failure, cerebral oedema, and activation of proangiogenic and antiangiogenic factors in a case of Marburg haemorrhagic fever
Original Text
Judith van Paassen MD, Martijn P Bauer MD, M Sesmu Arbous MD, Leo G Visser MD, Jonas Schmidt-Chanasit MD, Stefan Schilling MD, Stephan ?lschl?ger MSc, Toni Rieger MSc, Petra Emmerich PhD, Christel Schmetz MSc, Franchette van de Berkmortel MD, Prof Bart van Hoek MD, Nathalie D van Burgel MD, Prof Albert D Osterhaus PhD, Ann CTM Vossen MD, Prof Stephan G?nther MD, Prof Jaap T van Dissel MD
Summary
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
lGF 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.