Nora T Oliver1, Christine M Hartman, Jennifer R Kramer, Elizabeth Y Chiao. 1. aDepartment of Medicine, Section of Infectious Diseases and Health Services Research, Baylor College of Medicine bCenter for Innovations in Quality, Effectiveness and Safety, Michael E. DeBakey VA Medical Center, Houston, Texas, USA.
Abstract
INTRODUCTION: Chronic HIV/hepatitis C virus (HCV) coinfection carries increased risk of cirrhosis, hepatocellular carcinoma, and death. Due to anti-inflammatory properties, 3-hydroxy-3methylglutaryl coenzyme A (HMG-CoA) inhibitors (statins) may be useful adjunctive therapy to reduce liver disease progression. METHODS: Clinical information was extracted from the Veterans Affairs HIV and HCV Clinical Case Registries (1999-2010). HIV-related variables included combination antiretroviral therapy era of diagnosis, CD4 cell count, and percentage time with undetectable HIV viral load. Metabolic variables included diabetes, low high-density lipoprotein (HDL), and hypertension. Statin use was measured as percentage time with active prescription (time-updated throughout the follow-up period). Cox proportional hazards analysis was used to determine risk factors for cirrhosis (International Classification of Diseases-9 or aminotransferase-to-platelet ratio index >2) overall and in groups stratified by alanine aminotransferase (ALT) level above and below 40 IU/l. RESULTS: The cohort included 5985 HIV/HCV coinfected veterans. The majority was black race, and the mean age at index date was 45 years. Statin use was significantly protective of cirrhosis for patients with ALT 40 IU/l or less; for every 30% increase in time on statin, there was a 32% decreased risk of developing cirrhosis (hazard ratio 0.68, 95% confidence interval 0.47-0.98). Diabetes and low HDL were significantly associated with cirrhosis in patients with ALT greater than 40 IU/l (hazard ratio 1.15, P < 0.04 and hazard ratio 1.3, P < 0.0001). CONCLUSION: Statin drug use is beneficial in mitigating the risk of liver disease progression for HIV/HCV coinfected patients without advanced liver disease. Low HDL and diabetes in coinfected patients with abnormal ALT have greater risk of cirrhosis development.
INTRODUCTION:Chronic HIV/hepatitis C virus (HCV) coinfection carries increased risk of cirrhosis, hepatocellular carcinoma, and death. Due to anti-inflammatory properties, 3-hydroxy-3methylglutaryl coenzyme A (HMG-CoA) inhibitors (statins) may be useful adjunctive therapy to reduce liver disease progression. METHODS: Clinical information was extracted from the Veterans Affairs HIV and HCV Clinical Case Registries (1999-2010). HIV-related variables included combination antiretroviral therapy era of diagnosis, CD4 cell count, and percentage time with undetectable HIV viral load. Metabolic variables included diabetes, low high-density lipoprotein (HDL), and hypertension. Statin use was measured as percentage time with active prescription (time-updated throughout the follow-up period). Cox proportional hazards analysis was used to determine risk factors for cirrhosis (International Classification of Diseases-9 or aminotransferase-to-platelet ratio index >2) overall and in groups stratified by alanine aminotransferase (ALT) level above and below 40 IU/l. RESULTS: The cohort included 5985 HIV/HCV coinfected veterans. The majority was black race, and the mean age at index date was 45 years. Statin use was significantly protective of cirrhosis for patients with ALT 40 IU/l or less; for every 30% increase in time on statin, there was a 32% decreased risk of developing cirrhosis (hazard ratio 0.68, 95% confidence interval 0.47-0.98). Diabetes and low HDL were significantly associated with cirrhosis in patients with ALT greater than 40 IU/l (hazard ratio 1.15, P < 0.04 and hazard ratio 1.3, P < 0.0001). CONCLUSION: Statin drug use is beneficial in mitigating the risk of liver disease progression for HIV/HCV coinfectedpatients without advanced liver disease. Low HDL and diabetes in coinfectedpatients with abnormal ALT have greater risk of cirrhosis development.
Authors: Juan Berenguer; Elena Rodríguez; Pilar Miralles; Miguel A Von Wichmann; José López-Aldeguer; Josep Mallolas; María J Galindo; Eva Van Den Eynde; María J Téllez; Carmen Quereda; Antoni Jou; José Sanz; Carlos Barros; Ignacio Santos; Federico Pulido; Josep M Guardiola; Enrique Ortega; Rafael Rubio; Juan J Jusdado; María L Montes; Gabriel Gaspar; Herminia Esteban; José M Bellón; Juan González-García Journal: Clin Infect Dis Date: 2012-05-18 Impact factor: 9.079
Authors: Juan A Pineda; Manuel Romero-Gómez; Fernando Díaz-García; José A Girón-González; José L Montero; Julián Torre-Cisneros; Raúl J Andrade; Mercedes González-Serrano; José Aguilar; Manuela Aguilar-Guisado; José M Navarro; Javier Salmerón; Francisco J Caballero-Granado; José A García-García Journal: Hepatology Date: 2005-04 Impact factor: 17.425
Authors: Jennifer R Kramer; Marc A Kowalkowski; Zhigang Duan; Elizabeth Y Chiao Journal: J Acquir Immune Defic Syndr Date: 2015-04-01 Impact factor: 3.731
Authors: A H Mohsen; P J Easterbrook; C Taylor; B Portmann; R Kulasegaram; S Murad; M Wiselka; S Norris Journal: Gut Date: 2003-07 Impact factor: 23.059
Authors: Sehrish Kamal; Muhammad Ali Khan; Ankur Seth; George Cholankeril; Deepansh Gupta; Utkarsh Singh; Faisal Kamal; Colin W Howden; Christopher Stave; Satheesh Nair; Sanjaya K Satapathy; Aijaz Ahmed Journal: Am J Gastroenterol Date: 2017-06-06 Impact factor: 10.864
Authors: Vanessa El Kamari; Corrilynn O Hileman; Pierre M Gholam; Manjusha Kulkarni; Nicholas Funderburg; Grace A McComsey Journal: Clin Gastroenterol Hepatol Date: 2018-06-14 Impact factor: 11.382
Authors: Dana D Byrne; Janet P Tate; Kimberly A Forde; Joseph K Lim; Matthew Bidwell Goetz; David Rimland; Maria C Rodriguez-Barradas; Adeel A Butt; Cynthia L Gibert; Sheldon T Brown; Roger Bedimo; Matthew S Freiberg; Amy C Justice; Jay R Kostman; Jason A Roy; Vincent Lo Re Journal: Clin Infect Dis Date: 2017-10-16 Impact factor: 9.079