Role of insulin resistance and hepatic steatosis in the progression of fibrosis and response to treatment in hepatitis C

被引:27
作者
Sanyal, Arun J. [1 ]
机构
[1] Virginia Commonwealth Univ, Dept Internal Med, Div Gastroenterol Hepatol & Nutr, Med Ctr, Richmond, VA 23298 USA
关键词
chronic hepatitis C; insulin resistance; metabolic syndrome; non-alcoholic steatohepatitis; obesity; steatosis; FATTY LIVER-DISEASE; DENSITY-LIPOPROTEIN RECEPTOR; INDEPENDENT RISK-FACTOR; VIRUS-RNA REPLICATION; ANTIVIRAL TREATMENT; METABOLIC SYNDROME; DIABETES-MELLITUS; CORE PROTEIN; INFECTION; HCV;
D O I
10.1111/j.1478-3231.2010.02397.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Hepatitis C is a common cause of chronic viral infection of the liver. It is associated with insulin resistance and the development of type 2 diabetes mellitus. It is also associated with the development of hepatic steatosis. The presence of hepatic steatosis is associated with an increased risk of having hepatic fibrosis. This is also associated with the severity of insulin resistance. These findings are specifically germane for those with genotype1 infection. Genotype 3 infection independently causes steatosis and successful treatment of the virus is followed by resolution of steatosis. In genotype 1 infection, the presence of hepatic steatosis is also a risk factor for failure to respond to pegylated interferon and ribavirin therapy. Unfortunately efforts to treat insulin resistance prior to antiviral therapy have not been very successful. Newer efforts focused on the role of specific micro RNAs in mediating the metabolic effects of hepatitis C virus infection may provide to ameliorate the metabolic risks of HCV infection.
引用
收藏
页码:23 / 28
页数:6
相关论文
共 53 条
[1]   Hepatitis C virus and other Flaviviridae viruses enter cells via low density lipoprotein receptor [J].
Agnello, V ;
Abel, G ;
Elfahal, M ;
Knight, GB ;
Zhang, QX .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (22) :12766-12771
[2]   Steatosis in chronic hepatitis C: Why does it really matter? [J].
Asselah, T ;
Rubbia-Brandt, L ;
Marcellin, P ;
Negro, F .
GUT, 2006, 55 (01) :123-130
[3]   Liver fibrosis is not associated with steatosis but with necroinflammation in French patients with chronic hepatitis C [J].
Asselah, T ;
Boyer, N ;
Guimont, MC ;
Cazals-Hatem, D ;
Tubach, F ;
Nahon, K ;
Daïkha, H ;
Vidaud, D ;
Martinot, M ;
Vidaud, M ;
Degott, C ;
Valla, D ;
Marcellin, P .
GUT, 2003, 52 (11) :1638-1643
[4]   Impaired IRS-1/PI3-kinase signaling in patients with HCV: A mechanism for increased prevalence of type 2 diabetes [J].
Aytug, S ;
Reich, D ;
Sapiro, LE ;
Bernstein, D ;
Begum, N .
HEPATOLOGY, 2003, 38 (06) :1384-1392
[5]  
Banerjee D, 2001, ANN ROY COLL SURG, V83, P268
[6]   High body mass index is an independent risk factor for nonresponse to antiviral treatment in chronic hepatitis C [J].
Bressler, BL ;
Guindi, M ;
Tomlinson, G ;
Heathcote, J .
HEPATOLOGY, 2003, 38 (03) :639-644
[7]   LOWERING PLASMA-CHOLESTEROL BY RAISING LDL RECEPTORS [J].
BROWN, MS ;
GOLDSTEIN, JL .
NEW ENGLAND JOURNAL OF MEDICINE, 1981, 305 (09) :515-517
[8]   Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis [J].
Bugianesi, Elisabetta ;
Marchesini, Gulio ;
Gentilcore, Elena ;
Cua, Ian Homer Y. ;
Vanni, Ester ;
Rizzetto, Mario ;
George, Jacob .
HEPATOLOGY, 2006, 44 (06) :1648-1655
[9]   Effect of antiviral treatment on evolution of liver steatosis in patients with chronic hepatitis C:: indirect evidence of a role of hepatitis C virus genotype 3 in steatosis [J].
Castéra, L ;
Hézode, C ;
Roudot-Thoraval, F ;
Lonjon, I ;
Zafrani, ES ;
Pawlotsky, JM ;
Dhumeaux, D .
GUT, 2004, 53 (03) :420-424
[10]  
CHEUNG O, CURR PHARM IN PRESS