Evaluating risk factors for cirrhosis progression and response to statin therapy among a cohort of patients with cirrhosis

University Of Miami School Of Medicine, Coral Gables FL

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Abstract

E Despite advances in the treatment of hepatitis C virus (HCV), the number of liver disease-related deaths has increased annually since 2009 due to: 1) liver disease from non-alcoholic steatohepatitis (NASH) and alcohol-induced liver disease; and 2) mortality from hepatocellular carcinoma (HCC). The time course to progress from compensated to decompensated cirrhosis varies based on many factors, such as etiology of liver disease and medical co-morbidities. To better identify patients at greatest risk of hepatic decompensation requires a cohort of patients with varying etiologies of liver disease leading to compensated cirrhosis. Another population that has been shown to have increased risk of hepatic decompensation, and worse survival are HIV-infected patients. However, these data have been largely restricted to patients with HIV and viral hepatitis. In addition to identifying the trajectory of compensated cirrhosis, there is a need to identify therapeutics to slow progression. There are several lines of evidence to suggest that statins slow cirrhosis progression and/or decrease the risk of decompensation. However, there are limited prospective data to identify a benefit of statins among patients with compensated cirrhosis. This underscores the need to establish the safety and efficacy of statins to prevent hepatic decompensation in a US population, and to assess what may affect the response to statin therapy among patients with compensated cirrhosis. Our overarching goal is to develop a longitudinal prospective cohort study of patients with compensated cirrhosis to assess trajectories of hepatic stiffness and time to hepatic decompensation. We will enroll a subset with clinically significant portal hypertension in a randomized controlled trial of rosuvastatin. We seek to address these aims to: 1) identify factors associated with progression from compensated to decompensated cirrhosis; 2) develop risk models to stratify patients with compensated cirrhosis at risk for hepatic decompensation; and 3) determine whether rosuvastatin slows progression of liver stiffness among patients with compensated cirrhosis.