Thromb Haemost 1998; 79(02): 291-295
DOI: 10.1055/s-0037-1614980
Letters to the Editor
Schattauer GmbH

Patterns of Hepatitis G Viraemia and Liver Disease in Haemophiliacs Previously Exposed to Non-virus Inactivated Coagulation Factor Concentrates

John P. Hanley
1   From the Department of Haematology, Royal Infirmary of Edinburgh
,
Lisa M. Jarvis
2   From the Department of Medical Microbiology, University of Edinburgh
,
Peter C. Hayes
3   From the Department of Medicine, University of Edinburgh
,
Amanda J. Lee
4   From the Medical Statistics Unit, University of Edinburgh, Scotland, UK
,
Peter Simmonds
2   From the Department of Medical Microbiology, University of Edinburgh
,
Christopher A. Ludlam
1   From the Department of Haematology, Royal Infirmary of Edinburgh
› Author Affiliations
Further Information

Publication History

Received 26 May 1997

Accepted after revision 12 September 1997

Publication Date:
08 December 2017 (online)

Summary

Hepatitis G virus (HGV), a novel flavivirus, has been implicated as a cause of posttransfusion hepatitis. We have performed a longitudinal study in a cohort of haemophiliacs (n = 68) who previously received non-virus inactivated coagulation factor concentrates to assess both patterns of HGV viraemia and any associated liver disease. Hepatitis C virus (HCV) RNA was present in 58/68 and co-infection with human immunodeficiency virus (HIV) was present in 15/68.

HGV RNA was detected in 17/68 (25%) samples from the mid-1980s. There was no association between either HIV infection (p = 0.74) or co-infection with a particular HCV genotype (p = 0.62). However, there was a relationship between HGV viraemia and the severity of haemophilia (p = 0.0004) with HGV RNA detected in 5/19, 9/16 and 3/32 patients with mild, moderate and severe haemophilia respectively.

A longitudinal study was performed in 15/17 haemophiliacs with HGV viraemia using stored serum samples from the 1980s and 1990s. HGV viraemia persisted in 8/15 and cleared in 7/15 over a variable period of time. A Weibull model was constructed to estimate the duration of HGV viraemia in the study group. The 75th and 90th percentiles for the duration of HGV were estimated to be 8.7 years (95%, confidence interval 4.8-15.7) and 23.6 years (95% confidence interval 11.8-47.1) respectively. Laparoscopic liver inspection/biopsy was performed in 25/68. There was no association between severity of liver disease and HGV viraemia (p = 0.43). This study demonstrates considerable variation in patterns of HGV viraemia in haemophiliacs. We found little evidence to implicate HGV as a major cause of chronic liver disease in haemophiliacs.

 
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