Liver disease in patients coinfected with HIV and hepatitis C virus (HCV) has received increasing attention in recent years. Steatosis is accepted as an important contributor to liver disease in patients with HCV, but despite coinfected patients having several reasons to have steatosis, the prevalence and significance of such changes has received scant attention. We examined steatosis in an unselected cohort of coinfected patients and compared its prevalence and predictors with findings in monoinfected patients, where these relationships have been established. We studied 92 coinfected and 372 monoinfected patients undergoing staging liver biopsy. Baseline characteristics of the two groups differed significantly, pointing at different contributors to steatosis in each. Histological inflammation and fibrosis were very similar in the two groups, but steatosis was less in coinfected patients. Steatosis had a univariate association with fibrosis in both groups, but retained a multivariate association only in monoinfected patients. Other multivariate predictors of steatosis in monoinfected patients were the accepted variables of elevated body mass index, male sex, and genotype 3a infection, as well as age. In coinfected patients, however, age was the only multivariate predictor. Undetectable HIV viral load was associated with steatosis in coinfected patients in univariate analysis, but highly active antiretroviral therapy or its individual components could not be initially linked to steatosis. In conclusion, steatosis is less common in HIV/ HCV coinfected patients than similar HCV monoinfected patients, and predictors of steatosis differ between the two groups. (HEPATOLOGY 2005;42:310-316.) H epatic steatosis-collections of triglyceride within hepatocytes-has been found to be a common and important histological finding in patients chronically infected with hepatitis C virus (HCV). [1][2][3][4] It remains unknown exactly what steatosis means to the liver, and whether it is directly associated with liver injury or is a marker, for example, of increased oxidative stress. [5][6] Obesity and type 2 diabetes mellitus seem to contribute to steatosis in a variety of liver diseases, including nonalcoholic fatty liver disease, HCV, and alcoholic liver disease. 1,2,[7][8] HCV genotype 3a is also a specific cause of steatosis. [2][3][4] A number of lines of evidence suggest that steatosis may play a role in the liver disease seen in patients coinfected with HIV and HCV. Hepatic steatosis is quite common in HIV-positive individuals 9-10 and has been associated with medications used to treat HIV, [11][12] as well as with HIV lipodystrophy syndrome [13][14] and HIV-associated lactic acidosis. 15 Steatosis is also common in HCV monoinfected patients, affecting approximately 40%. Hepatic fibrosis is believed to progress more quickly overall in coinfected than monoinfected patients, [16][17][18] and because steatosis has an important association with fibrosis in monoinfected patients, it may also contribute to the accelerated fibrosis observed in coinfected patients. The prevalence and significance of steatosis in coinfected individuals are beginning to be examined; recent reports have found an association between steatosis and fibrosis in this patient group 19,20 and have also suggested that HIV medications may play a role in steatosis in coinfected patients. 20 Abbreviations: HCV, hepatitis C virus; BMI, body mass index; HAART, highly active antiretroviral therapy.