Artigo Revisado por pares

Statins Reduce the Risk of Cirrhosis and Its Decompensation in Chronic Hepatitis B Patients: A Nationwide Cohort Study

2016; Lippincott Williams & Wilkins; Volume: 111; Issue: 7 Linguagem: Inglês

10.1038/ajg.2016.179

ISSN

1572-0241

Autores

Yi‐Wen Huang, Chia-Long Lee, Sien-Sing Yang, Szu-Chieh Fu, Yun-Yi Chen, Ting‐Chung Wang, Jui-Ting Hu, Ding‐Shinn Chen,

Tópico(s)

Hepatitis B Virus Studies

Resumo

The protective effect of statins in cirrhosis and its decompensation in chronic hepatitis B (CHB) patients remains unknown.We conducted a population-based cohort study using data from the Taiwanese National Health Insurance Research Database from 1997 to 2009. A total of 298,761 CHB patients were identified. CHB patients using statins (n=6,543; defined as ≥28 cumulative defined daily doses (cDDD)) and a 1:1 ratio propensity score and inception point (the date of first use of statins)-matched non-statins (<28 cDDD) were followed up from the inception point until the development of cirrhosis or its decompensation or until withdrawal from insurance or December 2009.After adjustment for competing mortality, CHB patients using statins had a significantly lower cumulative incidence of cirrhosis (relative risk)=0.433; 95% confidence interval (CI)=0.344-0.515; modified log-rank test, P<0.001) and decompensated cirrhosis (relative risk=0.468; 95% CI=0.344-0.637; P<0.001) compared with patients not using statins. After adjustment for age, gender, comorbidity index, hypertension, diabetes, hyperlipidemia, hepatocellular carcinoma, obesity, non-alcoholic fatty liver disease, aspirin use, diabetes medication, CHB treatment, non-statin lipid-lowering drugs, and triglyceride lipid-lowering drugs using the Cox proportional hazard model, statins were still an independent protector against cirrhosis (adjusted hazard ratio (AHR)=0.512; 95% CI=0.413-0.634; P<0.001) and its decompensation (AHR=0.534; 95% CI=0.433-0.659; P 365 cDDD of statins, respectively.CHB patients who receive statin therapy have a dose-dependent reduction in the risk of cirrhosis and its decompensation.

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