High prevalence of hepatitis G virus after liver transplantation without apparent influence on long-term graft function

Haagsma, EB; Cuypers, H. T. M.; Gouw, A. S. H.; Sjerps, M; Huizenga, [No Value]; Slooff, Mjh; Jansen, Plm

doi:10.1016/s0168-8278(97)80261-9

Cited by 21 publications

(7 citation statements)

References 9 publications

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“…5,6 Although prevalence of HGV infection was not assessed in this study, a number of studies have now cast doubt on the relevance of HGV infection in both the pretransplantation and posttransplantation setting. 5,6,[27][28][29][30] Because steatosis has been implicated in the etiology of NASH and CC, 2 and because recurrent NASH has been reported in liver graft recipients, 31 we evaluated liver biopsy specimens for these features. Steatosis and steatohepatitis were identified in 4% of patients who had undergone transplantation for CC and in 11% of patients who underwent transplantation for alcoholrelated cirrhosis.…”

Section: Discussionmentioning

confidence: 95%

“…Although hepatitis G virus (HGV) and a novel DNA virus, TT-virus, have been suggested as potential causes of CC, their relevance is questionable. [5][6][7][8] As an indication for orthotopic liver transplantation (OLT), CC is currently the fourth most common indication for liver transplantation in the United States. 9 Few series, however, have reported on long-term patient and graft survival after liver transplantation for cryptogenic cirrhosis.…”

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confidence: 99%

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An evaluation of long-term outcomes after liver transplantation for cryptogenic cirrhosis

Heneghan

2003

Liver Transplantation

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Patients with cryptogenic cirrhosis (CC) comprise a significant proportion of liver transplant recipients. Poor outcome after transplantation has been reported by some centers, with fibrosis occurring in a significant proportion of patients. Outcome of 46 patients with CC who underwent transplantation between 1989 and 1999 at King's College Hospital London were compared with timematched recipients who underwent transplantation for hepatitis C virus (HCV) cirrhosis (n ‫؍‬ 58) and patients with alcohol-related cirrhosis (AC, n ‫؍‬ 53) during the same time period. Mean follow-up was 46 ؎ 37 months for CC patients, 41 ؎ 31 months for AC patients, and 49 ؎ 31 months for HCV patients. No protocol liver biopsy specimens were obtained, and biopsies were performed only for investigation of biochemical abnormalities. Acute cellular rejection occurred in 30% of CC, 26% of AC, and 37% of HCV patients (P ‫؍‬ NS). Overall patient and graft survival at 1 year was 85% and 80% for CC patients, 87% and 81% for AC patients, and 91% and 82% for patients with HCV (P ‫؍‬ NS). Five-year patient and graft survival was 81% and 77% for CC patients, 60% and 48% for AC patients, and 79% and 57% for HCV patients (Log rank; P ‫؍‬ .369). Twenty-two percent of CC patients had inflammation on last evaluable liver biopsy, compared with 25% of patients who underwent transplantation for AC and 68% of patients who underwent transplantation for HCV. No patient who underwent transplantation for CC had histologic evidence of cirrhosis on last evaluable biopsy, compared with 2% of patients who underwent transplantation for AC and 16% of patients who underwent transplantation for HCV (Chisquared ‫؍‬ 13.053, P ‫؍‬ .0015). These results suggest that CC is a favorable indication for OLT and that although a proportion of patients develop inflammation in the liver allograft, this does not result in significant graft dysfunction or loss. (Liver Transpl 2003;9:921-928.)

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Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

An evaluation of long-term outcomes after liver transplantation for cryptogenic cirrhosis

Heneghan

2003

Liver Transplantation

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“…1997). In the absence of HBV or HCV in liver transplant recipients, the prevalence of GBV‐C/HGV infection has no influence on the graft (Haagsma et al . 1997).…”

Section: Detection Of Gbv‐c/hgvmentioning

confidence: 99%

“…During OLT, pre-transplant GBV-C/HGV has been reported to be associated with post-transplant viraemia (Fried et al 1997;Feucht et al 1997;Haagsma et al 1997). In the absence of HBV or HCV in liver transplant recipients, the prevalence of GBV-C/HGV infection has no influence on the graft (Haagsma et al 1997). Berg et al (Berg et al 1996 found a significantly higher percentage of hepatocellular carcinoma in patients with pre-OLT GBV-C/HGV co-infection compared with patients with HCV infection alone (5/6 vs. 16/68; P , 0.01).…”

Section: Current Status Reviewmentioning

confidence: 99%

GB Virus C/Hepatitis G Virus (GBV‐C/HGV): still looking for a disease

Sathar

Soni²,

York

2000

Int J Experimental Path

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GB Virus C and Hepatitis G Virus (GBV-C/HGV) are positive, single-stranded flaviviruses. GBV-C and HGV are independent isolates of the same virus. Transmission via the blood-borne route is the commonest mode, although vertical and sexual transmission is well documented. GBV-C/HGV is distributed globally; its prevalence in the general population is 10 fold higher in African countries than in non-African countries. High prevalences of GBV-C/HGV have been found in subjects with frequent parenteral exposure and in groups at high risk of exposure to blood and blood products. The clinical significance of human infection with GBV-C/HGV is currently unclear. The virus can establish both acute and chronic infection and appears to be sensitive to interferon. Only some 12-15% of chronic Non-A, B, C hepatitis cases are infected with GBV-C/HGV. A direct association with liver pathology is still lacking and it is not yet clear as to whether GBV-C/HGV is indeed a hepatotropic virus. Current evidence suggests that the spectrum of association of GBV-C/HGV infection with extrahepatic diseases ranges from haematalogical diseases, aplastic anaemia, human immunodeficiency virus (HIV)-positive idiopathic thrombocytopenia and thalassemia, through to common variable immune deficiency and cryoglobunemia.

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“…GBV-C/ HGV itself appears to respond well to interferon alpha treatment although the response appears to be of a transient nature, particularly in individuals with a high GBV-C/HGV viral load [49,50,62]. GBV-C/HGV RNA has been found at a high prevalence in liver transplant recipients both pre-and post-operatively [63,64]. In particular, the high GBV-C/HGV prevalence after transplantation (44±53%) has been attributed to blood transfusions administered during transplantation procedures, in conjunction with the high-dose immunosuppression the patients were under at the time they received infected blood [63,64].…”

Section: Clinical Manifestations Of Gbv-c/hgv Infectionmentioning

confidence: 99%