Clinical use of hyaluronic acid as a predictor of fibrosis change in hepatitis C
Article first published online: 26 FEB 2003
Journal of Gastroenterology and Hepatology
Volume 18, Issue 3, pages 253–257, March 2003
How to Cite
PATEL, K., LAJOIE, A., HEATON, S., PIANKO, S., BEHLING, C. A., BYLUND, D., POCKROS, P., BLATT, L. M., CONRAD, A. and MCHUTCHISON, J. G. (2003), Clinical use of hyaluronic acid as a predictor of fibrosis change in hepatitis C. Journal of Gastroenterology and Hepatology, 18: 253–257. doi: 10.1046/j.1440-1746.2003.02930.x
- Issue published online: 26 FEB 2003
- Article first published online: 26 FEB 2003
- Accepted for publication 19 July 2002.
- chronic hepatitis C;
- hyaluronic acid;
- non-invasive markers;
Background and Aim: Hyaluronic acid (HA) is a glycosaminoglycan synthesized by hepatic stellate cells that has been shown to correlate with liver fibrosis in chronic hepatitis C (HCV) patients. However, its use in monitoring fibrosis over time has not been established. The aim of the present study was to assess the serial relationships between HA and liver fibrosis before and after treatment.
Methods: Seventy-six previously untreated chronic HCV patients received interferon-based therapy over 48 weeks. Serum HA levels were measured and liver biopsies were obtained at baseline, and 24 weeks post-treatment. Histological fibrosis was assessed by using the Knodell and METAVIR scoring systems.
Results: Knodell fibrosis was evaluated in 76 patients; METAVIR fibrosis in 72 patients. Following treatment, patients were grouped into those with increased fibrosis (Knodell = 17; METAVIR = 16), no change (Knodell = 50; METAVIR = 45), or decreased fibrosis (Knodell = 9; METAVIR = 11), relative to baseline. Moderate correlations between HA and fibrosis scores were found before treatment (Knodell R = 0.45; METAVIR R = 0.40) and post-treatment (Knodell R = 0.45; METAVIR R = 0.61). However, changes in HA correlated poorly with changes in fibrosis scores over the study period (Knodell R = 0.11; METAVIR R = 0.06). There was poor qualitative agreement between the direction of HA change and the direction of change in fibrosis scores (Knodell kappa = 0.04; METAVIR kappa = 0.08). The sus-tained virological response group (n = 18) had a significantly decreased mean HA compared with non-responders (−27.9 vs 21.7 µg/L; P = 0.009), but pretreatment HA did not predict a response.
Conclusions: Serum HA showed a modest association with hepatic fibrosis, and remains a useful non-invasive marker. However, serum HA alone has limited value in predicting histological changes over a treatment period.