Abstract
We assessed the pattern of hepatitis C viremia in chronic liver disease by studying 100 hepatitis C virus antibody–positive patients: 48 with chronic hepatitis, 21 with cirrhosis and 31 with hepatocellular carcinoma and cirrhosis. Serum hepatitis C virus RNA was detected by means of both the conventional nested polymerase chain reaction and a newly developed assay based on branched DNA that can also quantify viremia. Hepatitis C virus RNA was found in 94 of 100 patients with polymerase chain reaction and in 71 of 100 patients with branched-DNA (p < 0.001). Mean viremia level (× 103 genome equivalents/ml ± S.D.), as assessed with the branched-DNA test, was 5,700 ± 7,618 in the 48 patients with chronic hepatitis, 3,340 ± 3,633 in the 21 patients with cirrhosis and 1,768 ± 2,770 in the 31 patients with hepatocellular carcinoma (p < 0.02). We also analyzed retrospectively the relationship between viremia and treatment. Fifty-five patients (41 chronic hepatitis, 14 cirrhosis) underwent interferon-α treatment. Mean viremia level was comparable among the 30 responders (5,644 ± 8,207) and the 25 nonresponders (5,519 ± 6,208) to interferon, but it was significantly lower (1,841 ± 1,864) in the 12 of 30 responders (11 chronic hepatitis, 1 cirrhosis) who maintained remission up to 1 yr after cessation of interferon treatment. Fourteen patients (7 chronic hepatitis, 7 cirrhosis) with autoantibodies (12 antinuclear, 2 anti–liver-kidney microsomal) were treated with prednisone. The mean viremia level significantly increased after 3 mo of treatment, even in face of ALT decrease. In conclusion, serum hepatitis C virus RNA is detectable in almost all patients with hepatitis C virus antibody–positive chronic liver disease, polymerase chain reaction being more sensitive than the branched-DNA test. Hepatitis C viremia is lowest in patients with advanced liver disease. A low pretreatment value of viremia could identify patients with chronic hepatitis who will derive long-term benefit from interferon. Corticosteroids generally increase viremia in hepatitis C virus antibody–positive, autoantibody-positive chronic hepatitis, independent of ALT response. (Hepatology 1994;19:273–279).
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