006), less education (P = 0.008), history of diabetes (15% versus 4%, P < 0.001), insulin resistance (46% versus 33%, p = 0.02), history of hypertension (40% versus 19%, P < 0.001), and higher prevalence of HCV subgenotype 1b (44% versus 28%, P = 0.002). As a group, AAs had higher body mass

index (median 29.3 versus 27.4 kg/m2, P < 0.001), higher HOMA2 scores (median 1.9 versus 1.5, P < 0.001), higher alkaline phosphatase levels (median 83 versus 78 U/L, P = 0.043), higher ferritin levels (median 246 versus 149 ng/mL, P < 0.001), lower alanine aminotransferase levels (median 60 versus 74.5 U/L, P < 0.001), lower total bilirubin levels (median 0.06 versus 0.07 PXD101 datasheet mg/dL, P = 0.004), lower albumin levels (median 4.2 versus 4.2 g/dL, P = 0.004), and lower LDLc levels (median 106.4 versus 118.7 mg/dL, P = 0.009) than CAs. The prevalence of dyslipidemia was 70% overall and did not significantly differ by race. Compared

with pretreatment, there were significant changes in serum lipids during therapy and after completion of therapy (Fig. 1). During the initial 24 weeks of therapy, TG levels increased significantly (median +30 mg/dL), in contrast to significant declines in LDLc (−14.8 mg/dL), HDLc (median −8 mg/dL), and TC (median −17 mg/dL) (P < 0.0001 for all). After therapy, statistically significant changes in lipid measures were limited only to the 24-week virological responders. Among 177 participants who underwent a 48-week course of therapy (24-week virological responders), posttreatment TG levels remained significantly higher than pretreatment levels (median +8 mg/dL, P = 0.03), as did posttreatment Daporinad research buy LDLc (median +7.2 mg/dL, P < 0.0001) and TC levels (median +9 mg/dL, P < 0.0001), whereas HDLc levels

did not significantly change (median +0.8 mg/dL, P = 0.47). Among 62 participants who underwent a 24-week course of therapy before stopping therapy (24-week virological nonresponders), there were no significant changes in posttreatment serum lipids compared with pretreatment levels (TG, median +9 mg/dL, P = 0.41; LDLc, median −3.2 mg/dL, P = 0.36; TC, median −3 mg/dL, P = 0.50; HDLc, +0.3 mg/dL, 上海皓元 P = 0.99). The proportion of PEG-IFN taken was significantly and directly associated with declines in LDLc (r = −0.22, P = 0.005) and TC levels (r = −0.17, P = 0.008) during the initial 24 weeks of therapy. The proportion of ribavirin taken was not significantly associated with any changes in serum lipid levels (P > 0.05 for all). Race was significantly associated with changes in serum lipids during the first 24 weeks of therapy. Compared with CAs, AAs had significantly greater increases in TG and declines in LDLc levels (P = 0.003 and P < 0.0001, respectively) (Fig. 2). The patterns of decreases in TC levels by race were similar to LDLc changes, although the differences were not statistically significant (P = 0.054). Baseline characteristics associated with SVR are summarized in Table 2.