CROI 2016 Abstract eBook

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Poster Abstracts

demonstrated in HCV mono-infected individuals and may be due to anti-proliferative effects. We sought to evaluate the association of statin use and progression to cirrhosis in patients with HIV/HIV coinfection.

Methods: We used the health information from the HIV Clinical Care Registry, which is a comprehensive clinical VA database on all HIV-infected Veterans nationwide. Patients included were ≥18 years and had ≥1 confirmed positive HIV test or ICD-9 code and confirmed HIV-infected by the HIV registry. HCV infection was confirmed by positive HCV RNA or genotype test. Cirrhosis (primary outcome) was defined by ICD-9 code or AST to platelet ratio > 2. Variables including diabetes (DM), hypertension (HTN), low-HDL, obesity, and statin use were based upon ICD-9 codes, laboratory tests, and presence of drug prescription. Predictors of cirrhosis included demographics, HIV-specific lab values, statin drug use, and components of metabolic syndrome were analyzed using Cox proportional hazard regression analysis with SAS version 9.1 (SAS Institute Inc, Cary, NC). These variables were modeled as time dependent. Results: There were 6033 HIV/HCV co-infected patients in our cohort (excluding cirrhosis diagnosis prior to HIV diagnosis); 2313 developed cirrhosis.Demographic data can be found in the table.Factors associated with cirrhosis were older age at HIV diagnosis, greater cormorbidities, and CD4 count below 200 cells/uL.Greater time with undetectable HIV viral load was protective. Metabolic risk factors significantly associated with cirrhosis development were diabetes and low-HDL.Statin use was found to be significantly protective against cirrhosis (HR 0.73, CI 0.58-0.92). Conclusions: Cirrhosis development was greater in the HIV/HCV co-infected patients who were diagnosed with HIV later in life and had greater immunosuppression. Metabolic risk factors were prevalent in the cohort, and diabetes and low-HDL were each associated with progression to cirrhosis. HIV VL suppression was protective of liver fibrosis.Statin use was independently protective against cirrhosis development, which suggests statins may be beneficial as adjunctive therapy in the group.

551 Statin Type and Dose Reduce the Risk of Cirrhosis and HCC in HCV Infected Patients Tracey Simon 1 ; Hector Bonilla 2 ; RaymondT. Chung 3 ; Adeel A. Butt 4 1 Massachusetts General Hosp, Boston, MA, USA; 2 ImmunoSci Inc, Pleasanton, CA, USA; 3 Harvard Med Sch, Boston, MA, USA; 4 Hamad Hlthcare Quality Inst, Doha, Qatar Background: HMG-CoA reductase inhibitors (statins) have been associated with delayed fibrosis progression and a reduced risk of hepatocellular carcinoma (HCC), in patients with chronic hepatitis C virus (HCV) infection. The potency and optimal dose for this statin-mediated effect have not yet been defined. We investigated the impact of statin type and dose upon fibrosis progression and the development of incident HCC. Methods: Within the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES), a national Veterans Affairs (VA) database, we identified all subjects initiated on anti-HCV therapy. Patients were followed annually from 2001 to 2014, and incident cases of cirrhosis and HCC were identified. Statin administration was defined according

Poster Abstracts

to the World Health Organization definition of cumulative defined daily dose (cDDD) [1], with “use” defined as >28 cDDD. Multivariable Cox proportional hazard regression models were used to examine the relationship between statin use and the development of cirrhosis as well as HCC. Results: A total of 9,135 subjects with confirmed HCV were included. We identified 1649 cases of cirrhosis and 239 cases of incident HCC. Statin use was associated with a 44% reduction in risk of cirrhosis (adjusted HR 0.6, 95% CI 0.53, 0.68, p<0.0001). A significant dose-response relationship between statins and cirrhosis was observed: the adjusted HR of fibrosis progression with statin use of 28-89 cDDDs, 89-180 cDDDs, and >180 cDDDs were 0.74 (95% CI 0.59, 0.93), 0.71 (95% CI 0.59, 0.88), and 0.6 (95% CI 0.53, 0.68), respectively, compared to non-users. Mean change in FIB-4 score with atorvastatin (n=944) and fluvastatin (n=34) was -0.17 and -0.13 respectively, p=0.04 after adjustment for baseline FIB-4 score and established predictors of cirrhosis. Statin use was also associated with a 49% reduction in risk of developing incident HCC, compared to non-users (adjusted HR 0.51, 95% CI 0.36, 0.72). A similar dose-response relationship was observed.

Conclusions: In patients with chronic HCV infection, statin use appears to reduce the risk of fibrosis progression and decrease the risk of incident HCC, in a dose-dependent manner. Atorvastatin and fluvastatin are each associated with significantly reduced fibrosis progression to cirrhosis, compared to other types of statins. Further prospective clinical studies with clinical and histological endpoints are needed.

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