Abstract

Steatosis is frequently identified when elevated transaminases are noted incidentally during routine laboratory evaluation. Unenhanced hepatic CT is the optimal imaging study for the detection of hepatic steatosis, although it can also be detected by ultrasonography and MRI [6]. However, liver biopsy continues to play a central role in the evaluation of steatosis, because of its ability to detect inflammation, fibrosis, and other associated hepatocyte changes indicative of advanced liver disease. Hepatic steatosis is found in 40% to 180% of HCV-infected patients [7‐9]. In HCV infection, both viral and metabolic factors can lead to steatosis. In patients infected with HCV genotype 3, steatosis is predominantly virus mediated. In these patients, the prevalence and severity of steatosis are elevated (compared with patients who are infected with other HCV genotypes) and correlate with serum and liver HCV RNA levels, and steatosis largely resolves in patients who are successfully treated [10‐13]. In patients with HCV genotype 1 infection, host factors, such as excessive alcohol intake, age, central obesity, and hyperlipidemia, are predominant causes of hepatic steatosis. In these patients, steatosis is increasingly recognized as a component of the metabolic syndrome, a condition generally associated with insulin resistance. Hepatic steatosis is also common in HIV-infected patients

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