Arpan Mohanty1, Janet P Tate2, Guadalupe Garcia-Tsao3. 1. Section of Digestive Diseases, VA Connecticut Healthcare System, West Haven, Connecticut; Section of Digestive Diseases, Yale University School of Medicine, New Haven, Connecticut. 2. Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut; Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, Connecticut. 3. Section of Digestive Diseases, VA Connecticut Healthcare System, West Haven, Connecticut; Section of Digestive Diseases, Yale University School of Medicine, New Haven, Connecticut. Electronic address: guadalupe.garcia-tsao@yale.edu.
Abstract
BACKGROUND & AIMS: Statins decrease portal pressure in patients with cirrhosis and increase survival times of patients who have bled from varices. However, statins can be hepatotoxic. It is important to determine whether long-term statin use will be beneficial or detrimental for patients with cirrhosis because physicians are reluctant to prescribe statins to patients with liver disease. We investigated the effects of statins on decompensation and survival times in patients with compensated cirrhosis. METHODS: We performed a retrospective cohort using the Veteran Affairs Clinical Case Registry, which contains nationwide data from veterans infected with the hepatitis C virus (HCV). We identified patients with compensated cirrhosis from January 1996 through December 2009. Statin use was according to filled prescriptions. Cirrhosis and decompensation were determined from International Classification of Diseases, 9th revision codes, using a validated algorithm. RESULTS: Among 40,512 patients with HCV compensated cirrhosis (98% male; median age, 56 y), 2802 statin users were identified. We developed a propensity score model using variables associated with statin prescription, and new statin users were matched with up to 5 nonusers; 685 statin users were matched with 2062 nonusers. Discrimination of the propensity score model was 0.92. Statin users had a lower risk of decompensation (hazard ratio [HR], 0.55; 95% confidence interval [CI], 0.39-0.77) and death (HR, 0.56; 95% CI, 0.46-0.69), compared with nonusers. Findings persisted after adjustment for age, FIB-4 index score, serum level of albumin, model for end-stage liver disease and Child-Turcotte-Pugh scores (HR for decompensation, 0.55; 95% CI, 0.39-0.78), and death (HR, 0.55; 95% CI, 0.45-0.68). CONCLUSIONS: Based on data from the Veteran Affairs Clinical Case Registry, statin use among patients with HCV and compensated cirrhosis is associated with a more than 40% lower risk of cirrhosis decompensation and death. Although statins cannot yet be recommended widely for these patients, their use should not be avoided.
BACKGROUND & AIMS: Statins decrease portal pressure in patients with cirrhosis and increase survival times of patients who have bled from varices. However, statins can be hepatotoxic. It is important to determine whether long-term statin use will be beneficial or detrimental for patients with cirrhosis because physicians are reluctant to prescribe statins to patients with liver disease. We investigated the effects of statins on decompensation and survival times in patients with compensated cirrhosis. METHODS: We performed a retrospective cohort using the Veteran Affairs Clinical Case Registry, which contains nationwide data from veterans infected with the hepatitis C virus (HCV). We identified patients with compensated cirrhosis from January 1996 through December 2009. Statin use was according to filled prescriptions. Cirrhosis and decompensation were determined from International Classification of Diseases, 9th revision codes, using a validated algorithm. RESULTS: Among 40,512 patients with HCVcompensated cirrhosis (98% male; median age, 56 y), 2802 statin users were identified. We developed a propensity score model using variables associated with statin prescription, and new statin users were matched with up to 5 nonusers; 685 statin users were matched with 2062 nonusers. Discrimination of the propensity score model was 0.92. Statin users had a lower risk of decompensation (hazard ratio [HR], 0.55; 95% confidence interval [CI], 0.39-0.77) and death (HR, 0.56; 95% CI, 0.46-0.69), compared with nonusers. Findings persisted after adjustment for age, FIB-4 index score, serum level of albumin, model for end-stage liver disease and Child-Turcotte-Pugh scores (HR for decompensation, 0.55; 95% CI, 0.39-0.78), and death (HR, 0.55; 95% CI, 0.45-0.68). CONCLUSIONS: Based on data from the Veteran Affairs Clinical Case Registry, statin use among patients with HCV and compensated cirrhosis is associated with a more than 40% lower risk of cirrhosis decompensation and death. Although statins cannot yet be recommended widely for these patients, their use should not be avoided.
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