 |
|
|
| |
Insulin Resistance Causes Fibrosis
|
| |
| |
....We propose that in patients with non-3 HCV genotype infection, oxidative stress and insulin resistance have a pathogenic role in the development of steatosis, which in turn accelerate the progression of liver fibrosis..... clear="all" />
Reported by Jules Levin
EASL, April 2007, Barcelona, Spain
"OXIDATIVE STRESS AND INSULIN RESISTANCE CONTRIBUTE TO STEATOSIS IN HCV GENOTYPE NON-3 INFECTED PATIENTS"
M. Vidali 1, R. Zampino 2, G. Occhino 1, A. Ivaldi 1, B. Guerrera 2, R. Serino 1, E. Albano 1, G. Ruggiero 2, L.E. Adinolfi 2
1 Department Of Medical Sciences, University Of East Piedmont, Novara, Italy; 2 Department Of Internal Medicine And Hepatology, Second University Of Naples, Naples, Italy
Background and aims: Hepatic steatosis is common in chronic hepatitis C (CHC) and represents a risk factor in the progression to hepatic fibrosis. However, the mechanisms involved in causing steatosis associated with CHC are still not completely understood. Oxidative stress (OXS) and insulin resistance (IR) are features of both NALFD and CHC and a possible role of OXS in the HCV-related steatosis has been hypothesized. Thus, we investigated in 107 consecutive CHC
patients the relationship between OXS, IR and histological liver damage (steatosis, HAI, fibrosis).
Methods: Serum IgG against human serum albumin (HSA) adducted by malondialdehyde (MDA) were measured as markers of OXS. IR was evaluated by HOMA. Sixty matched healthy subjects were evaluated as controls, and the values of IgG anti-HSA-MDA >95 and HOMA >75 percentile in the control group were considered indicative of OXS and IR, respectively.
Results:
OXS was present in 61% of CHC patients, whereas IR and steatosis were detected in, respectively 80% and 70% of the subjects investigated.
Prevalence of OXS was similar among the patients infected with the different HCV genotypes. Among the patients infected with non-3 HCV genotype those showing OXS had higher steatosis (p<0.05), fibrosis (p<0.05), IR (p<0.05) and ALT (p<0.04) than those without OXS.
In the same patients, univariate analysis showed that IR was associated with age (p<0.02), steatosis (p<0.0005) and OXS (p<0.05), while steatosis was associated with age (p<0.05), IR (p<0.0005), OXS (p<0.05), and fibrosis (p<0.01). No association was evident between OXS and both IR or steatosis in the patients with HCV genotype-3 infection.
In the non-3 HCV genotype infected subjects, multiple regression analysis showed that steatosis (p<0.05) and age (p<0.005), but not OXS were independent predictors of IR.
Steatosis was the only independent variable associated with OXS, whereas IR (p<0.005), OXS (p<0.05) and fibrosis (p<0.01) were the independently associated with the extent of steatosis.
Conclusions: We propose that in patients with non-3 HCV genotype infection, OXS and IR have a pathogenic role in the development of steatosis, which in turn accelerate the progression of liver fibrosis.
|
| |
|
|
|
|
|
