Worsening of steatosis is an independent factor of fibrosis progression in untreated patients with chronic hepatitis C and paired liver biopsies
- 1Department of Virology (EA 3489), Centre Hospitalier Universitaire Henri Mondor, Université Paris-XII, Créteil, France
- 2Department of Hepatology and Gastroenterology, and Department of Virology, Centre Hospitalier Universitaire Henri Mondor, Université Paris-XII, Créteil, France
- 3Department of Public Health, Centre Hospitalier Universitaire Henri Mondor, Université Paris-XII, Créteil, France
- 4Department of Pathology, Centre Hospitalier Universitaire Henri Mondor, Université Paris-XII, Créteil, France
- Correspondence to:
Dr L Castéra, Service de Virologie (EA 3489), Centre Hospitalier Universitaire Henri Mondor, 51 avenue du Maréchal de Lattre de Tassigny, 94010 Créteil, France;
- Accepted 20 August 2002
Background and aims: Steatosis, a frequent histological finding in patients with chronic hepatitis C (CHC), has been suggested to influence liver fibrosis progression. The aim of the present study was to evaluate in patients with CHC and paired liver biopsies the relationship between the evolution of steatosis and that of fibrosis between the two biopsies.
Methods: Ninety six patients were selected according to the following criteria: absence of treatment; absence of cirrhosis at initial biopsy; and serum hepatitis B surface antigen and human immunodeficiency virus antibody negativity. Degrees of necroinflammatory activity, fibrosis, and steatosis grades were assessed in the two biopsies. In addition to histological lesions, parameters studied included the source of infection, duration of infection, body mass index, alcohol intake, alanine aminotransferase levels, hepatitis C virus genotype, and viral load.
Results: The mean interval between the two biopsies was 48 (32) months. Steatosis was found in 54% of patients at first biopsy, and was severe in 9%. Worsening of steatosis was observed in 34% of patients, stability in 50%, and improvement in 16%. Worsening of steatosis was significantly associated with hepatic fibrosis progression in patients with (p=0.03) or without (p<0.03) steatosis at diagnosis. Overall, fibrosis progression was observed in 31% of patients and stability in 69%. In a univariate analysis, fibrosis progression was associated with male sex (p=0.05), worsening of histological activity (p=0.04), and worsening of steatosis (p=0.0003). In a multivariate analysis, the only factor independently associated with fibrosis progression was worsening of steatosis (worsening v improvement/stability: odds ratio 4.7 (95% confidence interval 1.3–10.8); p=0.0001).
Conclusions: Our results suggest that in untreated patients with CHC and serial liver biopsies, fibrosis progression is strongly associated with worsening of steatosis.