Black race and increased hepatic iron stores predict poor response to interferon treatment for chronic hepatitis C virus (HCV) infection. We tested the hypothesis that these 2 observations are linked by investigating whether HCV-infected African-Americans have increased iron stores relative to uninfected persons. Using data from the third National Health and Nutrition Examination Survey (NHANES III), we determined the risk of having increased iron stores, defined as elevation of both serum ferritin and transferrin-iron saturation (TS), in HCV-RNA-positive blacks (n ؍ 100) and nonblacks (n ؍ 126) relative to HCV-RNAnegative blacks (n ؍ 4,002) and nonblacks (n ؍ R elative to whites, black patients with hepatitis C virus (HCV) infection are more resistant to antiviral treatment with interferon, pegylated interferon, or combination of interferon and ribavirin. [1][2][3][4][5][6] Interracial differences in viral loads and the prevalence of HCV genotype 1 infection only partly account for the observed differences in response to antiviral treatments.Previous studies have suggested that patients with chronic HCV commonly have elevated levels of serum markers of iron stores (ferritin, transferrin-iron saturation [TS], or iron). [7][8][9][10][11][12][13] The presence of elevated body iron stores and, in particular, elevated hepatic iron levels, is one of the strongest predictors of resistance to interferon treatment for HCV. [14][15][16][17][18][19][20][21][22] We used data from the third National Health and Nutrition Examination Survey (NHANES III) to determine whether there are differences between HCV-infected blacks and HCV-infected nonblacks with respect to the likelihood of increased iron stores. We hypothesized that among persons with HCV infection, a greater percentage of blacks than nonblacks would have elevated iron stores, because such a finding would be in agreement with the observed lower response of blacks to antiviral treatment. Also, we asked whether any difference in iron stores between HCV-infected blacks and other races might be attributed to a response to the HCV infection itself, rather than an underlying excess of iron stores in blacks without HCV infection.