α-Glutathione S-transferase as a marker of hepatocellular damage in chronic hepatitis C virus infection

α-Glutathione S-transferase (αGST) may be a good serologic marker of hepatocellular damage because of its low molecular weight, uniform hepatic distribution, high cytosolic concentration, and short half-life. To determine the clinical utility of αGST in patients with chronic hepatitis C virus (HCV) infection, serum αGST levels were measured in 96 patients with chronic HCV infection, of whom 47 subsequently underwent interferon-α therapy. Patients were simultaneously evaluated with conventional liver biochemistry, serum HCV RNA levels, and liver histology. Different methods of serum collection did not affect αGST values, indicating that this was a stable serum marker. In 93% of patients with chronic HCV infection, αGST was elevated and showed an excellent correlation with serum aminotransferases. Histologic analysis revealed a correlation of αGST with both lobular inflammation and bile duct lesions. There was no correlation between serum αGST levels and the demographic features, mode of transmission, virologic, other histologic parameters, or subsequent response to interferon-α. During serial monitoring in patients undergoing interferon-α therapy, elevation of serum αGST correlated with biochemical relapse and in some patients virologic relapse in the presence of normal liver biochemistry. αGST was persistently elevated in all nonresponders. Four of six of those patients who responded completely followed by early relapse had elevated αGST intermittently or continuously during therapy despite normalization of serum aminotransferases. Two of five of those with a complete and sustained response had elevated αGST during treatment and follow-up, and both were also seropositive for HCV RNA during follow-up. These data demonstrate that αGST is a stable marker, has similar diagnostic utility as serum aminotransferases, and may have a role in the monitoring of patients undergoing interferon-α therapy. (Key words : α-Glutathione S-transferase ; Hepatitis C virus ; Alanine aminotransferase; Cell damage ; HCV RNA ; Interferon) Am J Clin Pathol 1995 ;104 :193-198.