BACKGROUND: Various environmental factors have been shown to hasten cirrhosis and hepatocellular carcinoma in patients with genetic haemochromatosis. AIM: To assess the prevalence and the role of the recently identified hepatitis G virus in 70 patients with genetic haemochromatosis in comparison with 40 patients with cryptogenic chronic hepatitis and 200 regular blood donors. PATIENTS: Six patients with genetic haemochromatosis (9%) had serum hepatitis B surface antigen, 14 (20%) had serum hepatitis C virus RNA. A liver biopsy was available in 66 patients with genetic haemochromatosis (43 with cirrhosis) and 40 with cryptogenic hepatitis (4 with cirrhosis). METHODS: Serum HGV-RNA was detected by a reverse transcriptase polymerase chain reaction using primers derived from the 5'-non-coding and non-structural-5A regions of the viral genome. Serum IgG antibodies against HGV were detected by enzyme-linked immunosorbent assay using a recombinant E2 protein of the virus envelope. RESULTS: The prevalence of serum HGV-RNA was higher in patients with cryptogenic hepatitis (n = 6, 15%) and genetic haemochromatosis (n = 6, 9%) than in donors (n = 3, 1.5%) (p = 0.0008 and p = 0.01, respectively). The corresponding figures for serum anti-HGV were 4 (10%), 16 (23%) and 10 (5%). The six haemochromatotic patients with serum HGV-RNA more often had parenteral exposure to blood (50% vs 5%, p < 0.001), and persistently elevated serum aminotransferases (100% vs 31%, p < 0.001) than the 64 non-viraemic patients. The six HGV-RNA seropositive patients with cryptogenic hepatitis were older than the 34 non-viraemic patients (56 vs 34 years, p < 0.05). CONCLUSIONS: The prevalence of serum markers of HGV infection in patients with genetic haemochromatosis is higher than in blood donors, but similar to that of patients with cryptogenic chronic hepatitis. However, HGV is not a cofactor of morbidity in patients with genetic haemochromatosis.
BACKGROUND: Various environmental factors have been shown to hasten cirrhosis and hepatocellular carcinoma in patients with genetic haemochromatosis. AIM: To assess the prevalence and the role of the recently identified hepatitis G virus in 70 patients with genetic haemochromatosis in comparison with 40 patients with cryptogenic chronic hepatitis and 200 regular blood donors. PATIENTS: Six patients with genetic haemochromatosis (9%) had serum hepatitis B surface antigen, 14 (20%) had serum hepatitis C virus RNA. A liver biopsy was available in 66 patients with genetic haemochromatosis (43 with cirrhosis) and 40 with cryptogenic hepatitis (4 with cirrhosis). METHODS: Serum HGV-RNA was detected by a reverse transcriptase polymerase chain reaction using primers derived from the 5'-non-coding and non-structural-5A regions of the viral genome. Serum IgG antibodies against HGV were detected by enzyme-linked immunosorbent assay using a recombinant E2 protein of the virus envelope. RESULTS: The prevalence of serum HGV-RNA was higher in patients with cryptogenic hepatitis (n = 6, 15%) and genetic haemochromatosis (n = 6, 9%) than in donors (n = 3, 1.5%) (p = 0.0008 and p = 0.01, respectively). The corresponding figures for serum anti-HGV were 4 (10%), 16 (23%) and 10 (5%). The six haemochromatotic patients with serum HGV-RNA more often had parenteral exposure to blood (50% vs 5%, p < 0.001), and persistently elevated serum aminotransferases (100% vs 31%, p < 0.001) than the 64 non-viraemic patients. The six HGV-RNA seropositive patients with cryptogenic hepatitis were older than the 34 non-viraemic patients (56 vs 34 years, p < 0.05). CONCLUSIONS: The prevalence of serum markers of HGV infection in patients with genetic haemochromatosis is higher than in blood donors, but similar to that of patients with cryptogenic chronic hepatitis. However, HGV is not a cofactor of morbidity in patients with genetic haemochromatosis.