Author/Authors :
Alba Muzzi، نويسنده , , Gioacchino Leandro، نويسنده , , Laura Rubbia-Brandt، نويسنده , , Richard James، نويسنده , , Olivia Keiser، نويسنده , , Raffaele Malinverni، نويسنده , , Jean-François Dufour، نويسنده , , Beat Helbling، نويسنده , , Antoine Hadengue، نويسنده , , Jean-Jacques Gonvers، نويسنده , , Beat Müllhaupt، نويسنده , , Andreas Cerny، نويسنده , , Mario U. Mondelli، نويسنده , , Francesco Negro، نويسنده , , For the Swiss Hepatitis C Cohort Study (SCCS)، نويسنده ,
Abstract :
Background/Aims
Liver steatosis is a frequent finding in chronic hepatitis C. An association has been suggested between steatosis and fibrosis progression rate, but the pathogenetic mechanisms linking fatty infiltration and collagen deposition are unknown.
Methods
We measured the levels of insulin resistance (as HOMA score) and leptin in 221 non-diabetic chronic hepatitis C patients, to assess their impact on liver steatosis and fibrosis, relative to other factors, using a multivariable logistic regression.
Results
When all 221 patients were considered, steatosis was associated with excessive alcohol intake, genotype 3, and serum HCV RNA level, whereas fibrosis was associated with HOMA score and age. In 152 patients infected with genotype non-3, steatosis was associated with alcohol abuse and HCV RNA level, and fibrosis with HOMA score and age. In the 69 patients with genotype 3, steatosis and fibrosis were associated with each other. The association between fibrosis and HOMA score held also when 22 obese patients were excluded from the analysis. Levels of insulin resistance were not correlated with the presence of steatosis.
Conclusions
Thus, insulin resistance (but not leptin) may play a role in fibrogenesis in chronic hepatitis C patients infected with genotype non-3.
Keywords :
Insulin resistance , hepatitis C virus , obesity , Diabetes , Liver fibrogenesis , leptin