Primary end-points were hepatic steatosis (quantified by magnetic resonance imaging) and liver injury (determined by ALT, CK-18). Secondary end-points included insulin resistance measured by the insulin sensitivity index (ISI) and HOMA, and systemic lipid peroxidation determined by plasma F2-isoprostane levels. A total check details of 74 subjects were randomized (33 phlebotomy, 41 control). The phlebotomy group underwent a median (range) of 7 (1-19) venesection sessions and had a significantly greater reduction in ferritin levels over six months compared to controls (-148 ± 114 vs. -38 ± 89 ng/ml, p<0.001). At six months, there was no difference between phlebotomy and control groups in
hepatic steatosis (17.7% vs. 15.5%, p=0.4), serum ALT (36 vs. 46 IU/l, p=0.4) or CK-18 levels
(175 vs. 196 U/l, p=0.9). Similarly, there was no difference in end of study ISI Proteasome purification (2.5 vs. 2.7, p=0.9), HOMA (3.2 vs. 3.2, p=0.6) or F2-isoprostane levels (1332 vs. 1190 pmmol/l, p=0.6) between phlebotomy and control groups. No differences in any end-point were noted in patients with hyperferritinemia at baseline. Among patients undergoing phlebotomy, there was no correlation between number of phlebotomy sessions and change in hepatic steatosis, liver injury or insulin resistance from baseline to end-of-study. Conclusion: Reduction in ferritin by phlebotomy does not improve liver enzymes, hepatic fat or insulin resistance in subjects with NAFLD. This article is protected by copyright. All rights reserved. “
“We sought to clarify the associations between serum cytokines and chemokines, hepatitis B surface antigen (HBsAg), hepatitis B core-related antigen (HBcrAg), and hepatitis B virus (HBV) DNA and response to entecavir therapy in chronic hepatitis B. We analyzed six cytokines (interleukin [IL]-2, IL-6, IL-10, IL-12p70, IL-21 and IL-22) and five chemokines (CCL2, CCL3, CXCL9, CXCL10 and CXCL11) before and at 6, 12 and selleck chemicals 24 months during entecavir therapy in 48 chronic hepatitis B patients. Quantitative measurement of HBsAg, HBcrAg and HBV DNA was performed.
A virological response (VR) was defined as serum HBV DNA of less than 2.1 log copies/mL by treatment month 24. Thirty-nine patients (81%) achieved a VR. Serum IL-6 (P = 0.031), CXCL-9 (P = 0.002), and CXCL-10 (P = 0.001) were high in chronic HBV and correlated positively with transaminases and bilirubin. Before treatment, elevated IL-22 (P = 0.031) and lower HBsAg (P = 0.001) and HBcrAg (P < 0.001), but not HBV DNA, were associated with a favorable treatment outcome. In multivariate analysis, high IL-22 (hazard ratio = 13.67, P = 0.046) and low HBcrAg (hazard ratio = 10.88, P = 0.048) were independently associated with a VR. The levels of IL-22 (P < 0.001), HBsAg (P < 0.001), and HBcrAg (P < 0.001) all decreased from baseline to 24 months of treatment in virological responders. Serum IL-22 and HBcrAg are predictive markers of a VR to entecavir therapy in patients with chronic hepatitis B.