Effect of addition of statins to antiviral therapy in hepatitis C virus-infected persons: Results from ERCHIVES

被引:82
作者
Butt, Adeel A. [1 ,2 ,3 ]
Yan, Peng [1 ]
Bonilla, Hector [4 ]
Abou-Samra, Abdul-Badi [3 ]
Shaikh, Obaid S. [1 ,2 ]
Simon, Tracey G. [5 ]
Chung, Raymond T. [6 ,7 ]
Rogal, Shari S. [1 ,2 ]
机构
[1] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA
[2] Univ Pittsburgh, Sch Med, Pittsburgh, PA 15213 USA
[3] Hamad Med Corp, Hamad Healthcare Qual Inst, Doha, Qatar
[4] ImmunoScience Inc, Pleasanton, CA USA
[5] Brigham & Womens Hosp, Boston, MA 02115 USA
[6] Massachusetts Gen Hosp, Boston, MA 02114 USA
[7] Harvard Univ, Sch Med, Boston, MA USA
关键词
HEPATOCELLULAR-CARCINOMA CELLS; CHRONIC LIVER-DISEASE; TREATMENT ELIGIBILITY; RISK; HCV; FIBROSIS; FLUVASTATIN; PRAVASTATIN; SURVIVAL; REPLICATION;
D O I
10.1002/hep.27835
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been variably noted to affect hepatitis C virus (HCV) treatment response, fibrosis progression, and hepatocellular carcinoma (HCC) incidence, with some having a more potent effect than others. We sought to determine the impact of adding statins to antiviral therapy upon sustained virological response (SVR) rates, fibrosis progression, and HCC development among HCV-infected persons using the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES), an established, longitudinal, national cohort of HCV-infected veterans. Within ERCHIVES, we identified those who received HCV treatment and a follow-up of >24 months after treatment completion. We excluded those with human immunodeficiency virus coinfection, hepatitis B surface antigen positivity, cirrhosis, and HCC at baseline. Our main outcomes were liver fibrosis progression measured by FIB-4 scores, SVR rates, and incident HCC (iHCC). Among 7,248 eligible subjects, 46% received statin therapy. Statin use was significantly associated with attaining SVR (39.2% vs. 33.3%; P<0.01), decreased cirrhosis development (17.3% vs. 25.2%; P<0.001), and decreased iHCC (1.2% vs. 2.6%; P<0.01). Statins remained significantly associated with increased odds of SVR (odds ratio=1.44; 95% confidence interval [CI]=1.29, 1.61), but lower fibrosis progression rate, lower risk of progression to cirrhosis (hazard ratio [HR]=0.56; 95% CI=-0.50, 0.63), and of incident HCC (HR=0.51; 95% CI=0.34, 0.76) after adjusting for other relevant clinical factors. Conclusions: Statin use was associated with improved virological response (VR) rates to antiviral therapy and decreased progression of liver fibrosis and incidence of HCC among a large cohort of HCV-positive Veterans. These data support the use of statins in patients with HCV. (Hepatology 2015) Hepatology 2015;62:365-374
引用
收藏
页码:365 / 374
页数:10
相关论文
共 50 条
[21]   Effect of pravastatin on survival in patients with advanced hepatocellular carcinoma. A randomized controlled trial [J].
Kawata, S ;
Yamasaki, E ;
Nagase, T ;
Inui, Y ;
Ito, N ;
Matsuda, Y ;
Inada, M ;
Tamura, S ;
Noda, S ;
Imai, Y ;
Matsuzawa, Y .
BRITISH JOURNAL OF CANCER, 2001, 84 (07) :886-891
[22]   Statin Use in Patients with Cirrhosis: A Retrospective Cohort Study [J].
Kumar, Sonal ;
Grace, Norman D. ;
Qamar, Amir A. .
DIGESTIVE DISEASES AND SCIENCES, 2014, 59 (08) :1958-1965
[23]   Impact of Added Fluvastatin to Standard-of-Care Treatment on Sustained Virological Response in Naive Chronic Hepatitis C Patients Infected with Genotypes 1 and 3 [J].
Kurincic, Tanja Selic ;
Lesnicar, Gorazd ;
Poljak, Mario ;
Volkar, Jelka Meglic ;
Rajter, Mojca ;
Prah, Janja ;
Baklan, Zvonko ;
Kotar, Tadeja ;
Maticic, Mojca .
INTERVIROLOGY, 2014, 57 (01) :23-30
[24]   Statin use and risk of hepatocellular carcinoma [J].
Lai, Shih-Wei ;
Liao, Kuan-Fu ;
Lai, Hsueh-Chou ;
Muo, Chih-Hsin ;
Sung, Fung-Chang ;
Chen, Pei-Chun .
EUROPEAN JOURNAL OF EPIDEMIOLOGY, 2013, 28 (06) :485-492
[25]   Efficacy and safety of high-dose pravastatin in hypercholesterolemic patients with well-compensated chronic liver disease: Results of a prospective, randomized, double-blind, placebo-controlled, Multicenter trial [J].
Lewis, James H. ;
Mortensen, Mary Eflen ;
Zweig, Steven ;
Fusco, Mary Jean ;
Medoff, Jeffrey R. ;
Belder, Rene .
HEPATOLOGY, 2007, 46 (05) :1453-1463
[26]   Dysmetabolic changes associated with HCV: a distinct syndrome? [J].
Lonardo, Amedeo ;
Loria, Paola ;
Carulli, Nicola .
INTERNAL AND EMERGENCY MEDICINE, 2008, 3 (02) :99-108
[27]   The transcription factor KLF2 mediates hepatic endothelial protection and paracrine endothelial-stellate cell deactivation induced by statins [J].
Marrone, Giusi ;
Russo, Lucia ;
Rosado, Eugenio ;
Hide, Diana ;
Garcia-Cardena, Guillermo ;
Carlos Garcia-Pagan, Juan ;
Bosch, Jaime ;
Gracia-Sancho, Jorge .
JOURNAL OF HEPATOLOGY, 2013, 58 (01) :98-103
[28]   Statin use and risk of hepatocellular carcinoma in a US population [J].
McGlynn, Katherine A. ;
Divine, George W. ;
Sahasrabuddhe, Vikrant V. ;
Engel, Lawrence S. ;
VanSlooten, Ashley ;
Wells, Karen ;
Yood, Marianne Ulcickas ;
Alford, Sharon Hensley .
CANCER EPIDEMIOLOGY, 2014, 38 (05) :523-527
[29]  
Nadrous HF, 2004, CHEST, V126, P438, DOI 10.1378/chest.126.2.438
[30]   Statins in Liver Transplant Recipients: Rates of Use, Mortality and Rejection [J].
Selim, R. ;
Abdulhamid, A. ;
Shyamraj, A. ;
Watson, A. ;
Tang, J. ;
Jafri, S. -M. .
AMERICAN JOURNAL OF TRANSPLANTATION, 2017, 17 :585-585