THYROID DYSFUNCTION IN CHRONIC HEPATITIS C PATIENTS TREATED WITH PEG INTERFERON AND RIBAVIRIN

Abstract

Introduction Hepatitis C virus (HCV)-RNA can be detected in the serum of most patients with chronic hepatitis C using the reverse transcription polymerase chain reaction. During therapy with interferon-a, levels of HCV-RNA tend to fall in parallel with serum aminotransferase activities. Generally, in patients whose serum aminotransferases reach normal levels, HCV-RNA becomes undetectable. When hepatitis relapses after interferon (IFN) is stopped, HCV-RNA promptly reappears in serum. Patients with a sustained response to interferon have persistently normal serum aminotransferases and undetectable HCV-RNA after stopping interferon. Hepatitis C viral antigen is detectable by immunostaining of liver in the majority of patients with chronic hepatitis C. The intensity of staining for HCV antigen (HCV Ag) before therapy may be a useful predictor of response to treatment. HCV Ag staining decreases with IFN therapy and may become undetectable in patients who respond with normalization of serum aminotransferases and loss of HCV-RNA from serum. Thus, HCV-RNA in serum and HCVAg in liver appear to be useful markers of HCV infection to follow during therapy with IFN-a. Low levels of these markers may indicate an increased likelihood of responding to IFN therapy. Their absence at the end of therapy does not necessarily predict that relapse of hepatitis will not occur. However, their prolonged absence, months or even years after stopping IFN, appears to be a feature of a sustained response to IFN.