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Báo cáo y học: "Hepatitis C Virus (HCV) Infection and Hepatic Steatosis"

Tuyển tập các báo cáo nghiên cứu khoa học ngành y học tạp chí Medical Sciences dành cho các bạn sinh viên ngành y tham khảo đề tài: Hepatitis C Virus (HCV) Infection and Hepatic Steatosis. | Int. J. Med. Sci. 2006 3 53 Review International Journal of Medical Sciences ISSN 1449-1907 www.medsci.org 2006 3 2 53-56 2006 Ivyspring International Publisher. All rights reserved Hepatitis C Virus HCV Infection and Hepatic Steatosis Eugene J. Yoon and Ke-Qin Hu Division of Gastroenterology and Hepatology University of California Irvine Medical Center CA 92868 USA Corresponding address Ke-Qin Hu MD Director of Hepatology Services and Associate Professor of Clinical Medicine Division of Gastroenterology Univ. of California Irvine Medical Center 101 The City Drive Building 53 Suite 113 Orange CA 92868 USA. Phone 714-456-6745. Email kqhu@uci.edu Received 2005.12.30 Accepted 2006.02.16 Published 2006.04.01 There are two discrete forms of steatosis that may be found in patients infected with hepatitis C virus HCV . Metabolic steatosis can coexistwith HCV regardless of genotype in patients with risk factors such as obesity hyperlipidemia and insulin resistance. The second form of hepatic steatosis in HCV patients is a result of the direct cytopathic effect of genotype 3 viral infections. There have been proposed mechanisms for this process but it remains elusive. Both categories of steatosis tend to hasten the progression of liver fibrosis and therefore prompt recognition and management should be initiated in patients with HCV and steatosis. The authors review the current understanding of the relationship between hepatitis C infection and hepatic steatosis and discuss future research directions. Key words hepatitis C obesity metabolic syndrome diabetes steatosis NAFLD NASH 1. Introduction The usual progression of liver disease in patients with hepatitis C HCV is a process of inflammation accompanied by periportal necrosis and fibrosis. The inflammation that results from the virus causes stimulation of stellate cells which ultimately leads to the deposition of collagen which leads to fibrosis progression within the liver. If this process is rapid and unhindered then the