Review article: nonalcoholic fatty liver disease and hepatitis C virus--partners in crime.

@article{citeulike:2690362, abstract = {BACKGROUND: Both nonalcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CHC) are frequent causes of chronic liver disease. In recent years, there have been significant revelations as regards the relationship between NAFLD and CHC. AIM: To conduct a systematic, evidence-based review of the epidemiology, pathophysiology and potential treatments of coexistent NAFLD and CHC. METHODS: The terms such as hepatitis C, fatty liver, NAFLD, nonalcoholic steatohepatitis and steatosis were searched on PubMed up to January 2008. References from selected articles and pertinent abstracts were also included. RESULTS: Hepatic steatosis affects up to 80\% of patients with CHC and is dependent on both viral and host factors. While insulin resistance (IR) is associated with hepatic steatosis and hepatitis C virus, genotype-specific pathogenic mechanisms have been identified and are currently the focus of intense investigation in the literature. Clinical implications of concurrent NAFLD, CHC and IR include increased disease progression, elevated risk of hepatocellular carcinoma, and decreased response to antiviral therapy. CONCLUSIONS: NAFLD and IR are common in patients with CHC virus infection. IR is a driving force in the development of hepatic steatosis. Because of the clinical implications of hepatic steatosis and IR in the setting of CHC, further studies evaluating treatments, which may increase response to antiviral therapy, are needed.}, address = {Division of Gastroenterology and Hepatology, Brooke Army Medical Center, Fort Sam Houston, TX 78234, USA.}, author = {Blonsky, J. J. and Harrison, S. A. }, citeulike-article-id = {2690362}, doi = {http://dx.doi.org/10.1111/j.1365-2036.2008.03672.x}, issn = {1365-2036}, journal = {Alimentary pharmacology \& therapeutics}, month = {May}, number = {10}, pages = {855--865}, posted-at = {2008-04-19 10:45:54}, priority = {2}, title = {Review article: nonalcoholic fatty liver disease and hepatitis C virus--partners in crime.}, url = {http://dx.doi.org/10.1111/j.1365-2036.2008.03672.x}, volume = {27}, year = {2008} }

TY - JOUR ID - citeulike:2690362 L3 - citeulike-article-id:2690362 TI - Review article: nonalcoholic fatty liver disease and hepatitis C virus--partners in crime. JF - Alimentary pharmacology & therapeutics VL - 27 IS - 10 SP - 855 EP - 865 AD - Division of Gastroenterology and Hepatology, Brooke Army Medical Center, Fort Sam Houston, TX 78234, USA. SN - 1365-2036 N2 - BACKGROUND: Both nonalcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CHC) are frequent causes of chronic liver disease. In recent years, there have been significant revelations as regards the relationship between NAFLD and CHC. AIM: To conduct a systematic, evidence-based review of the epidemiology, pathophysiology and potential treatments of coexistent NAFLD and CHC. METHODS: The terms such as hepatitis C, fatty liver, NAFLD, nonalcoholic steatohepatitis and steatosis were searched on PubMed up to January 2008. References from selected articles and pertinent abstracts were also included. RESULTS: Hepatic steatosis affects up to 80% of patients with CHC and is dependent on both viral and host factors. While insulin resistance (IR) is associated with hepatic steatosis and hepatitis C virus, genotype-specific pathogenic mechanisms have been identified and are currently the focus of intense investigation in the literature. Clinical implications of concurrent NAFLD, CHC and IR include increased disease progression, elevated risk of hepatocellular carcinoma, and decreased response to antiviral therapy. CONCLUSIONS: NAFLD and IR are common in patients with CHC virus infection. IR is a driving force in the development of hepatic steatosis. Because of the clinical implications of hepatic steatosis and IR in the setting of CHC, further studies evaluating treatments, which may increase response to antiviral therapy, are needed. AU - Blonsky, JJ AU - Harrison, SA PY - 2008/05// UR - http://dx.doi.org/10.1111/j.1365-2036.2008.03672.x ER -