Hepatitis G virus infection in fulminant hepatic failure

Background—RNA sequences of the recently identified hepatitis GB virus C (HGBV-C), also named hepatitis G virus (HGV), have been detected in patients with idiopathic fulminant hepatic failure (FHF) but the role of this agent in the disease remains controversial. Aims—To investigate the presence and...

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Veröffentlicht in:Gut 1997-11, Vol.41 (5), p.696-699
Hauptverfasser: Sáiz, J C, Sans, M, Mas, A, Olmedo, E, Forns, X, López-Labrador, F X, Restrepo, J C, Costa, J, Salmerón, J M, Guilera, M, Ampurdanés, S, Sánchez-Tapias, J M, de Anta, M T Jiménez, Rodés, J
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container_end_page 699
container_issue 5
container_start_page 696
container_title Gut
container_volume 41
creator Sáiz, J C
Sans, M
Mas, A
Olmedo, E
Forns, X
López-Labrador, F X
Restrepo, J C
Costa, J
Salmerón, J M
Guilera, M
Ampurdanés, S
Sánchez-Tapias, J M
de Anta, M T Jiménez
Rodés, J
description Background—RNA sequences of the recently identified hepatitis GB virus C (HGBV-C), also named hepatitis G virus (HGV), have been detected in patients with idiopathic fulminant hepatic failure (FHF) but the role of this agent in the disease remains controversial. Aims—To investigate the presence and implications of HGV infection in a large series of Spanish patients with FHF. Patients—Sixty eight patients with FHF, including 19 with idiopathic disease, were studied. In 28 cases, studies were performed before and after liver transplantation. For comparison 200 volunteer blood donors and 22 patients transplanted for chronic liver disease were also studied. Methods—HGV RNA was measured in serum by reverse transcriptase polymerase chain reaction of the 5′ non-coding region. Results—Evidence of HGV infection was found in 3% (6/200) of blood donors and in 19% (13/68) of patients with FHF. HGV infection was more frequent in patients with hepatitis B (24%, 6/25) or hepatitis D (42%, 5/12), than in patients with idiopathic disease (11%, 2/19). Half of the patients with HGV infection used illicit intravenous drugs. Specific clinical features associated with HGV infection were not identified. A very high rate of infection with HGV was observed in patients who underwent liver transplantation, either for FHF (60%, 15/24) or chronic liver disease (45%, 9/20). Conclusions—In our geographical area, HGV infection is relatively frequent in FHF, but it does not seem to play a major role in idiopathic cases.
doi_str_mv 10.1136/gut.41.5.696
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Aims—To investigate the presence and implications of HGV infection in a large series of Spanish patients with FHF. Patients—Sixty eight patients with FHF, including 19 with idiopathic disease, were studied. In 28 cases, studies were performed before and after liver transplantation. For comparison 200 volunteer blood donors and 22 patients transplanted for chronic liver disease were also studied. Methods—HGV RNA was measured in serum by reverse transcriptase polymerase chain reaction of the 5′ non-coding region. Results—Evidence of HGV infection was found in 3% (6/200) of blood donors and in 19% (13/68) of patients with FHF. HGV infection was more frequent in patients with hepatitis B (24%, 6/25) or hepatitis D (42%, 5/12), than in patients with idiopathic disease (11%, 2/19). Half of the patients with HGV infection used illicit intravenous drugs. Specific clinical features associated with HGV infection were not identified. A very high rate of infection with HGV was observed in patients who underwent liver transplantation, either for FHF (60%, 15/24) or chronic liver disease (45%, 9/20). 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Aims—To investigate the presence and implications of HGV infection in a large series of Spanish patients with FHF. Patients—Sixty eight patients with FHF, including 19 with idiopathic disease, were studied. In 28 cases, studies were performed before and after liver transplantation. For comparison 200 volunteer blood donors and 22 patients transplanted for chronic liver disease were also studied. Methods—HGV RNA was measured in serum by reverse transcriptase polymerase chain reaction of the 5′ non-coding region. Results—Evidence of HGV infection was found in 3% (6/200) of blood donors and in 19% (13/68) of patients with FHF. HGV infection was more frequent in patients with hepatitis B (24%, 6/25) or hepatitis D (42%, 5/12), than in patients with idiopathic disease (11%, 2/19). Half of the patients with HGV infection used illicit intravenous drugs. Specific clinical features associated with HGV infection were not identified. A very high rate of infection with HGV was observed in patients who underwent liver transplantation, either for FHF (60%, 15/24) or chronic liver disease (45%, 9/20). 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subjects Adult
Biological and medical sciences
Blood & organ donations
Blood products
Chronic Disease
Female
Flaviviridae - genetics
fulminant hepatic failure
GB virus C
Genomes
Hepatic Encephalopathy - virology
Hepatitis
Hepatitis B - virology
Hepatitis D - virology
Hepatitis G
hepatitis G virus
Hepatitis, Viral, Human - complications
Human viral diseases
Humans
Infections
Infectious diseases
Laboratories
Liver
Liver diseases
Liver Diseases - virology
Liver Transplantation
Male
Medical sciences
Middle Aged
Polymerase Chain Reaction
RNA, Viral - blood
Studies
Transplants & implants
Tropical medicine
Viral diseases
Viral hepatitis
Viral infections
Virus GB C
Viruses
title Hepatitis G virus infection in fulminant hepatic failure
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