Thromb Haemost 1985; 54(03): 693-696
DOI: 10.1055/s-0038-1660099
Original Article
Schattauer GmbH Stuttgart

Increased Factor VIII Complex in Fulminant Hepatic Failure

P G Langley
The Liver Unit, King’s College Hospital and School of Medicine and Dentistry, London, UK
,
R D Hughes
The Liver Unit, King’s College Hospital and School of Medicine and Dentistry, London, UK
,
Roger Williams
The Liver Unit, King’s College Hospital and School of Medicine and Dentistry, London, UK
› Author Affiliations
Further Information

Publication History

Received 03 May 1985

Accepted 21 August 1985

Publication Date:
19 July 2018 (online)

Summary

In 30 patients with fulminant hepatic failure (FHF) all three components of the factor VIII complex were significantly increased (VIIIC = 6.43 ± 1.12 u/ml; VIIIRAg = 3.91 ± 0.25 u/ ml; VIIIvWF = 3.89 ± 0.29 u/ml). There was good correlation between all three parameters in control subjects, but only between VIIIRAg and VIIIvWF (r= 0.67; p <0.001) in patients with FHF. VIIIC was significantly higher than VIIIRAg and VIIIvWF. These results suggest that VIIIC and VIIIRAg are increased by different mechanisms in FHF. These processes may include endothelial cell damage, reduced reticuloendothelial system function and lack of production of inactivating substances by the damaged liver.

Platelet adhesion to glass beads was increased in FHF (36.4 ± 5.9% compared to 16.6 ± 2.1%, p <0.01). There was no significant correlation between platelet adhesion and any of the parameters of the factor VIII complex. Thus the increase in platelet adhesion cannot be due to the increase in VIIIvWF in FHF.

 
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