Changes in serum levels of cytokeratin-18 fragments in patients with chronic hepatitis C under antiviral therapy

Abstract

Background and Aims: Cytokeratin-18 is the known substrate forcaspases, which are encountered during hepatic and pancreatic acinarapoptosis. Studies performed in recent years have indicated thatthe cleavage level of serum cytokeratin-18 (M30 antigen) is correlatedwith hepatic fibrosis and disease severity in both chronic hepatitis Cand non-alcoholic steatohepatitis. It was shown that antiviral therapyin chronic viral hepatitis C patients significantly reduced hepatocellularapoptosis and cytokeratin-18 is accepted as a reliable marker of hepatocyteapoptosis. Our aim was to determine the correlation between thecytokeratin-18 level and treatment response in patients with chronicviral hepatitis C. Materials and Methods: Sixty patients with chronicviral hepatitis C were included in the study. A 48-week course of peginterferon-ribavirintherapy was given to appropriate patients. Hepatitis Cvirus RNA was measured at 0, 12, and 24 weeks at the end of therapyand 72 weeks. In addition, cytokeratin-18 levels were measured at 0,24, and 72 weeks. Results: The mean age of 60 patients was 52±10.9years. While 31 (51.6%) of patients were in the sustained viral responsegroup, 29 (8.4%) of patients were in the non-sustained viral responsegroup. It was determined that while the cytokeratin-18 level at week 0in the sustained viral response group was 243±21, the cytokeratin-18level at week 24 was 115±12 U/L and the difference between the levelof cytokeratin-18 at weeks 0 and 24 were 127±209 U/L (p: .014). Whilethe cytokeratin-18 level at week 0 in the non- sustained viral responsegroup was 270±14; at week 24, the cytokeratin-18 level was 136±19U/L and the difference between cytokeratin-18 levels at weeks 0 and24 was 136±156 U/L (p > .5). At week 72, the cytokeratin-18 level inthe sustained viral response group was 109±38 and the difference betweenweeks 0 and 72 was 134±215 (p < .002). Conclusion: In chronicviral hepatitis C patients, there was a correlation between sustainedviral response and cytokeratin-18, which is a marker of apoptosis.During treatment, it was found that there was a relationship betweensustained viral response and the decrease in cytokeratin-18 levels. Thisfinding indicates that cytokeratin-18 level monitoring may be used as apredictive marker of sustained viral response.