Detection of hepatitis C virus antibodies and hepatitis C virus RNA in patients with alcoholic liver disease

The relationship between alcoholic liver disease and hepatitis C virus was studied in 80 patients by searching for hepatitis C virus RNA with the polymerase chain reaction and by measuring hepatitis C virus antibodies. By C-100 enzyme-linked immunosorbent assay, hepatitis C virus antibodies were found in 2 of 10 patients with fibrosteatosis, 8 of 20 patients with alcoholic hepatitis, 14 of 19 patients with chronic hepatitis and 19 of 31 patients with cirrhosis. Percentages of patients with antibodies found by C-100 radioimmunoassay and by enzyme-linked immunosorbent assay based on sequence peptide 42 were lower; of the 16 patients with a low titer by C-100 enzyme-linked immunosorbent assay, 10 were negative by radioimmunoassay and 6 were negative by sequence peptide 42. By a second-generation recombinant immunoblot assay, hepatitis C virus antibodies were found in 1 of 10 patients with fibrosteatosis, 2 of 20 patients with alcoholic hepatitis, 15 of 19 patients with chronic hepatitis and 18 of 31 patients with cirrhosis. Hepatitis C virus RNA was found in 1 of 10 patients with fibrosteatosis, 3 of 20 patients with alcoholic hepatitis, 13 of 19 patients with chronic hepatitis and 20 of 31 patients with cirrhosis. Of the 37 patients with hepatitis C virus RNA, 31 had antibodies by C-100 enzyme-linked immunosorbent assay (25 patients at a high titer [cut-off index >6]), and 31 had antibodies by second-generation recombinant immunoblot assay. Patients with cirrhosis and hepatitis C virus RNA had higher ALT activity than such patients without hepatitis C virus RNA (p < 0.05). Of the 80 patients, 25 patients stopped drinking, 11 of these patients had hepatitis C virus RNA. The ALT of the 11 patients tended to decrease during hospitalization but increased in 7 of 11 after discharge. Of the 14 patients without hepatitis C virus RNA who stopped drinking, ALT decreased significantly (p < 0.01) during hospitalization and increased only in 3 of the 14 after discharge. The histological activity index of Knodell for patients with fibrosis, chronic hepatitis or cirrhosis with hepatitis C virus RNA was 11.8 ± 4.2, but without hepatitis C virus RNA it was 8.4 ± 4.3 (p < 0.01). Patients with hepatitis C virus RNA had worse periportal and bridging necrosis, intralobular degeneration, focal necrosis and portal inflammation than patients without hepatitis C virus RNA. (HEPATOLOGY 1991;14:985–989.)