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Hepatitis C virus replication in 'autoimmune' chronic hepatitis
Insights
Hepatitis C virus (HCV) can cause chronic active hepatitis in patients with autoantibodies. Early diagnosis and alpha-interferon treatment are crucial for managing this specific subgroup of autoimmune hepatitis.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Autoimmune chronic active hepatitis (ACAH) diagnosis can be complicated by varying anti-hepatitis C virus antibody (anti-HCV) prevalence.
- Distinguishing HCV-related liver disease from primary autoimmune hepatitis is critical for appropriate treatment.
Purpose of the Study:
- To confirm ELISA specificity for anti-HCV in autoantibody-positive chronic active hepatitis patients.
- To evaluate hepatitis C virus replication using serum HCV-RNA.
- To assess treatment response to prednisone and alpha-interferon.
Main Methods:
- Study included 15 HBsAg-negative, ELISA anti-HCV-positive, autoantibody-positive patients with biopsy-proven chronic active hepatitis.
- ELISA results were confirmed by immunoblot test (RIBA-HCV).
- Serum HCV-RNA was quantified to assess viral replication.
Main Results:
- RIBA-HCV confirmed ELISA anti-HCV positivity in all patients.
- HCV-RNA was detected in 10 out of 15 patients.
- Prednisone treatment showed poor response, while alpha-interferon led to prompt normalization of transaminases in non-responsive patients.
Conclusions:
- A distinct subgroup of autoantibody-positive chronic active hepatitis is associated with HCV infection.
- This HCV-related subgroup requires differentiation from primary autoimmune chronic active hepatitis.
- Alpha-interferon therapy is a promising treatment option for steroid non-responsive cases.
Abstract:
Both high and low anti-hepatitis C virus antibody (anti-HCV) prevalence has been reported in autoimmune chronic active hepatitis. Therefore, we studied 15 consecutive HBsAg-negative, ELISA anti-HCV-positive, autoantibody-positive patients with biopsy proven chronic active hepatitis in order to confirm ELISA specificity by immunoblot test (RIBA-HCV), and to evaluate HCV replication by serum HCV-RNA. Nine patients were anti-nuclear, three type 1 anti-liver-kidney microsomal and three anti-smooth muscle antibody positive. None had associated autoimmune disease. All cases showed mild clinical disease and only moderate necroinflammatory activity. Response to prednisone was poor. RIBA-HCV confirmed ELISA results in all patients. HCV-RNA was found in the serum from 10 patients. Institution of alpha-interferon treatment in three steroid non-responsive patients was followed by prompt normalization of transaminases. Thus, a subgroup of autoantibody-positive chronic active hepatitis can be recognized as HCV-related and should be clinically and etiologically distinguished from autoimmune chronic active hepatitis. Trials of alpha-interferon treatment are worthwhile in this condition.