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Clinical use of hyaluronic acid as a predictor of fibrosis change in hepatitis C
Author(s) -
PATEL KEYUR,
LAJOIE ADRIANNE,
HEATON SHA,
PIANKO STEPHEN,
BEHLING CYNTHIA A,
BYLUND DAVID,
POCKROS PAULJ,
BLATT LAWRENCE M,
CONRAD ANDREW,
MCHUTCHISON JOHN G
Publication year - 2003
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2003.02930.x
Subject(s) - fibrosis , medicine , hyaluronic acid , gastroenterology , glycosaminoglycan , chronic hepatitis , hepatic fibrosis , pathology , liver fibrosis , immunology , virus , anatomy
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.