Interferon and prednisone therapy in chronic hepatitis C with non-organ-specific antibodies.
OBJECTIVE
The relationship between hepatitis C virus and autoimmunity is controversial. The issue is particularly relevant in those patients with hepatitis C virus infection and serum autoantibodies in whom steroids can exacerbate viral replication and interferon can lead to decompensated liver disease. The aim of this study was to evaluate the response to a course of prednisone or interferon-alpha 2b.


RESULTS
The 12 study patients had biopsy-proven chronic hepatitis, serum HCV-RNA (by nested polymerase chain reaction) and non-organ-specific antibodies (eight with liver and kidney microsomal antibodies and four with antinuclear antibodies). Eight of these 12 patients received a 4-month course of prednisone (0.5 mg/kg per day), which increased alanine aminotransferase (mean +/- SE) (174 +/- 31 vs 252 +/- 18 U/l, p < 0.05) and bilirubin levels (0.96 +/- 0.17 vs 1.42 +/- 0.18 mg/dl, p = 0.09), without changing liver histology (Knodell index, 13.6 +/- 0.4 vs 13.1 +/- 0.3). Subsequent treatment with interferon in the 12 patients reduced serum alanine aminotransferase levels (170 +/- 20 vs 41 +/- 7 U/l, p < 0.0001) and portal and lobular inflammation (Knodell index, 13.8 +/- 0.5 vs 8.4 +/- 0.2, p < 0.001). A complete response to interferon was observed in ten of these patients (83%), eight of whom had previously been treated with prednisone. Serum HCV-RNA level decreased in interferon responders. A sustained response 1 year after withdrawal of interferon was seen in only five patients (41%).


CONCLUSIONS
Patients with chronic hepatitis C and autoantibodies show a favorable response to interferon, but not to prednisone. The latter regimen can exacerbate liver necrosis in these subjects. The presence of autoantibodies in hepatitis C patients does not modify the response to interferon.
Calleja
J L
JL
Department of Gastroenterology, Clínica Puerta de Hierro, Madrid, Spain.
Albillos
A
A
Cacho
G
G
Iborra
J
J
Abreu
L
L
Escartín
P
P
D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000974:Antibodies, Antinuclear / Q000276:immunology*; D000998:Antiviral Agents / Q000627:therapeutic use*; D001323:Autoantibodies / Q000276:immunology*; D015551:Autoimmunity / Q000276:immunology; D001663:Bilirubin / Q000097:blood; D001706:Biopsy; D002908:Chronic Disease; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology; D006526:Hepatitis C / Q000276:immunology / Q000628:therapy*; D018937:Hepatitis C Antibodies / Q000032:analysis; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011241:Prednisone / Q000627:therapeutic use*; D012367:RNA, Viral / Q000032:analysis; D011994:Recombinant Proteins
D000974:Antibodies, Antinuclear; D000998:Antiviral Agents; D001323:Autoantibodies; D005938:Glucocorticoids; D018937:Hepatitis C Antibodies; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; C060729:anti-liver kidney microsome antibody; D000410:Alanine Transaminase; D001663:Bilirubin; D011241:Prednisone