UNLABELLED: Approximately one half of patients who undergo antiviral therapy for chronic hepatitis C virus (HCV) genotype 1 infection do not respond to treatment. African Americans (AAs) are less responsive to treatment than Caucasian Americans (CAs), but the reasons for this disparity are largely unknown. Recent studies suggest that serum lipids may be associated with treatment response. The aims of this study were to evaluate baseline and changes in serum lipids during therapy, determine whether serum lipids are associated with virological response, and assess whether these measures explain the racial difference in efficacy. The study participants were from Virahep-C, a prospective study of treatment-naïve patients with genotype 1 HCV infection who received peginterferon (PEG-IN) alfa-2a plus ribavirin therapy for up to 48 weeks. Fasting serum lipids were analyzed at baseline and during and after therapy in 160 AAs and 170 CAs. A relative risk (RR) model was employed to evaluate characteristics associated with sustained virological response (SVR). Antiviral therapy was associated with changes in serum lipids during and after antiviral therapy, with the changes differing by race and the amount of PEG-IFN taken. Baseline lipid measures independently associated with higher rates of SVR were lower triglyceride and higher low-density lipoprotein cholesterol, with an interaction between high-density lipoprotein cholesterol (HDLc) and gender. Lipid measures did not contribute significantly to an explanation of the racial difference in SVR. CONCLUSION: Serum lipids are associated with SVR, although these paramaters did not explain the racial difference in treatment response. The results of this study are compatible with proposed biological mechanisms of HCV entry, replication, and secretion, and may underscore new potential therapeutic targets for HCV eradication.
UNLABELLED: Approximately one half of patients who undergo antiviral therapy for chronic hepatitis C virus (HCV) genotype 1 infection do not respond to treatment. African Americans (AAs) are less responsive to treatment than Caucasian Americans (CAs), but the reasons for this disparity are largely unknown. Recent studies suggest that serum lipids may be associated with treatment response. The aims of this study were to evaluate baseline and changes in serum lipids during therapy, determine whether serum lipids are associated with virological response, and assess whether these measures explain the racial difference in efficacy. The study participants were from Virahep-C, a prospective study of treatment-naïve patients with genotype 1 HCV infection who received peginterferon (PEG-IN) alfa-2a plus ribavirin therapy for up to 48 weeks. Fasting serum lipids were analyzed at baseline and during and after therapy in 160 AAs and 170 CAs. A relative risk (RR) model was employed to evaluate characteristics associated with sustained virological response (SVR). Antiviral therapy was associated with changes in serum lipids during and after antiviral therapy, with the changes differing by race and the amount of PEG-IFN taken. Baseline lipid measures independently associated with higher rates of SVR were lower triglyceride and higher low-density lipoprotein cholesterol, with an interaction between high-density lipoprotein cholesterol (HDLc) and gender. Lipid measures did not contribute significantly to an explanation of the racial difference in SVR. CONCLUSION: Serum lipids are associated with SVR, although these paramaters did not explain the racial difference in treatment response. The results of this study are compatible with proposed biological mechanisms of HCV entry, replication, and secretion, and may underscore new potential therapeutic targets for HCV eradication.
Authors: Eva Martínez-Bauer; Javier Crespo; Manuel Romero-Gómez; Ricardo Moreno-Otero; Ricard Solá; Nancy Tesei; Fernando Pons; Xavier Forns; José M Sánchez-Tapias Journal: Hepatology Date: 2006-01 Impact factor: 17.425
Authors: Thomas von Hahn; Brett D Lindenbach; Agnès Boullier; Oswald Quehenberger; Matthew Paulson; Charles M Rice; Jane A McKeating Journal: Hepatology Date: 2006-05 Impact factor: 17.425
Authors: Gregory L Armstrong; Annemarie Wasley; Edgar P Simard; Geraldine M McQuillan; Wendi L Kuhnert; Miriam J Alter Journal: Ann Intern Med Date: 2006-05-16 Impact factor: 25.391
Authors: Søren U Nielsen; Margaret F Bassendine; Alastair D Burt; Caroline Martin; Wanna Pumeechockchai; Geoffrey L Toms Journal: J Virol Date: 2006-03 Impact factor: 5.103
Authors: Neal D Freedman; Teresa M Curto; Karen L Lindsay; Elizabeth C Wright; Rashmi Sinha; James E Everhart Journal: Gastroenterology Date: 2011-03-02 Impact factor: 22.682
Authors: P J Clark; A J Thompson; M Zhu; D M Vock; Q Zhu; D Ge; K Patel; S A Harrison; T J Urban; S Naggie; J Fellay; H L Tillmann; K Shianna; S Noviello; L D Pedicone; R Esteban; P Kwo; M S Sulkowski; N Afdhal; J K Albrecht; D B Goldstein; J G McHutchison; A J Muir Journal: J Viral Hepat Date: 2012-02-22 Impact factor: 3.728
Authors: Nikolaos K Gatselis; Kalliopi Zachou; Asterios Saitis; Maria Samara; George N Dalekos Journal: World J Gastroenterol Date: 2014-03-21 Impact factor: 5.742
Authors: Adeel A Butt; Triin Umbleja; Janet W Andersen; Kenneth E Sherman; Raymond T Chung Journal: Clin Infect Dis Date: 2012-05-04 Impact factor: 9.079