Effects of a Sustained Virologic Response on Outcomes of Patients With Chronic Hepatitis C
For patients with chronic hepatitis C virus infection, the goal of antiviral therapy is to achieve a sustained virologic response (SVR). We review the durability of the SVR and its effects on liver-related mortality, hepatic decompensation, and the development of hepatocellular carcinoma. We performed a systematic review of the effects of the SVR on liver-related hepatic outcomes and found the SVR to be durable (range, 98.4%-100%). An SVR reduced liver-related mortality among patients with chronic hepatitis C (3.3- to 25-fold), the incidence of hepatocellular carcinoma (1.7- to 4.2-fold), and hepatic decompensation (2.7- to 17.4-fold). An SVR can lead to regression of fibrosis and cirrhosis, and has been associated with a reduced rate of hepatic decompensation, a reduced risk for hepatocellular carcinoma, and reduced liver-related mortality.
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- "Progression to cirrhosis is estimated to be about 5-20% after 20 years of infection.It is estimated that 13.1% of patients with HCV in 2005 will die of liver-related causes by 2030, increasing to 36.8% by 2060.While HCV is considered cured if the patient achieves sustained viral response (SVR), achieving SVR using older therapies [pegylated interferon-alpha and ribavirin] has been daunting. Standard therapy requires 24 to 48 weeks of weekly injections and is associated with significant side effect burden. "
- "SVR, most commonly measured as SVR12, is defined as having undetectable viral replication in the blood 12 weeks after completion of therapy. The obtainment of SVR has been significantly associated with a decrease in all-cause mortality, liver-related mortality , the incidence of hepatocellular carcinoma (HCC) as well as fibrosis regression [Ng and Saab, 2011] and cirrhosis resolution in 50–60% of patients with CHC [D'Ambrosio et al. 2012; Shiffman et al. 2014]. The benefits of being cured also improve worker productivity and healthrelated QOL [as measured by patient-reported outcomes (PROs)] in patients who achieve SVR [Younossi et al. 2014a, 2014c, 2014d]. "
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ABSTRACT: Chronic hepatitis C (CHC) affects over 185 million individuals worldwide, approximately 3% of the world's population. CHC can lead to quality of life impairment, cirrhosis, hepatocellular carcinoma (HCC), liver failure and liver-related death. While CHC has been associated with increases in HCC, liver-related mortality and all-cause mortality, being cured of CHC is associated with improvement in these outcomes. Older interferon-based regimens were complex and toxic and required 6-12 months of therapy, with cure rates averaging around 40-45% for HCV genotype 1. Newer interferon-free regimens are now available in the US, Europe, Japan and in other countries. These regimens have short durations, minimal side effects, low pill burden and efficacy approaching 90-100%. We may eventually see single-tablet regimens lasting no more than 4-6 weeks. This review will summarize the data regarding these interferon-free regimens, including Gilead's Harvoni (sofosbuvir/ledipasvir), AbbVie's Viekira Pak (paritaprevir/ritonavir/ombitasvir with dasabuvir), and Janssen's Olysio (simeprevir) with sofosbuvir. Some practical considerations as we move into an interferon-free era will also be discussed, such as patient adherence and drug-drug interactions.
- "The information of the Charlson comorbidity index (CCI) was also collected and considered as one possible confounding risk . We collected exposure information of other drugs that might alter the risk of cirrhosis, such as anti-HCV treatment (interferon or ribavirin) , aspirin , angiotensin-converting enzyme inhibitors (ACEIs) (captopril, enalapril, lisinopril, perindopril, ramipril, quinapril, benazepril, cilazapril, and fosinopril) , and metformin . We also considered sociodemographic characteristics (age, sex, income, and level of urbanization) in the modeling. "
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ABSTRACT: Several animal studies have shown that statins can inhibit the progression of cirrhosis; however, few clinical studies have been conducted. Previous study has indicated that statins can prevent the progression of hepatic fibrosis in patients with hepatitis C virus (HCV) infection and advanced hepatic fibrosis but data for human not progress to cirrhosis yet is lacking. This study investigated the association between the use of statin and the risk of cirrhosis development in patients with HCV infection.
We conducted a population-based cohort study by using the Taiwan National Health Insurance Research Database. A total of 226,856 patients with HCV infection were included as the study cohort. Each patient was followed from 1997 to 2010 to identify incident cases of cirrhosis. A Cox proportional hazard regression was performed to evaluate the association between statin use and cirrhosis risk.
A total of 34,273 cases of cirrhosis were identified in the cohort with HCV infection during the follow-up period of 2,874,031.7 person-years. The incidence rate was 445.5 cases of cirrhosis per 100,000 person-years (95% confidence interval (CI), 423.3 to 465.7) for statin users (defined as those who used more than 28 cumulative defined daily doses (cDDD)), and 1311.2 cirrhosis cases per 100,000 person-years (95% CI, 1,297.1 to 1,325.6) for nonusers. A dose-response relationship between statin use and cirrhosis risk was observed. The adjusted hazard ratios were 0.33 (95% CI, 0.31 to 0.36), 0.24 (95% CI, 0.22 to 0.25), and 0.13 (95% CI, 0.12 to 0.15) for statin use of 28 to 83, 84 to 365, and more than 365 cDDD, respectively, relative to no statin use (< 28 cDDD).
Among the patients with HCV infection, statin use was associated with a reduced risk of cirrhosis development in a dose-dependent manner. Further clinical research is required.
Copyright © 2015. Published by Elsevier B.V.
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