Abstract
Background and AimTo investigate the impact of a sustained virological response (SVR) to hepatitis C virus (HCV) treatment on liver stiffness (LS).MethodsLS, measured by transient elastography (FibroScan), demographic and laboratory data of patients treated with interferon (IFN)-containing or IFN-free regimens who had an SVR24 (undetectable HCV viral load 24 weeks after the end of treatment) were analyzed using two-tailed paired t-tests, Mann-Whitney Wilcoxon Signed-rank tests and linear regression. Two time intervals were investigated: pre-treatment to SVR24 and SVR24 to the end of follow-up. LS scores ≥ 12.5 kPa indicated LS-defined cirrhosis. A p-value below 0.05 was considered statistically significant.ResultsThe median age of the patients (n = 100) was 60 years [IQR (interquartile range) 54–64); 72% were male; 60% were Caucasian; and 42% had cirrhosis pre-treatment according to the FibroScan measurement. The median LS score dropped from 10.40 kPa (IQR: 7.25–18.60) pre-treatment to 7.60 kPa (IQR: 5.60–12.38) at SVR24, p <0.01. Among the 42 patients with LS-defined cirrhosis pre-treatment, 25 (60%) of patients still had LS scores ≥ 12.5 kPa at SVR24, indicating the persistence of cirrhosis. The median change in LS was similar in patients receiving IFN-containing and IFN-free regimens: -1.95 kPa (IQR: -5.75 –-0.38) versus -2.40 kPa (IQR: -7.70 –-0.23), p = 0.74. Among 56 patients with a post-SVR24 LS measurement, the LS score changed by an additional -0.90 kPa (IQR: -2.98–0.5) during a median follow-up time of 1.17 (IQR: 0.88–1.63) years, which was not a statistically significant decrease (p = 0.99).ConclusionsLS decreased from pre-treatment to SVR24, but did not decrease significantly during additional follow-up. Earlier treatment may be needed to reduce the burden of liver disease.
Highlights
Hepatitis C Virus (HCV) is a leading cause of liver cirrhosis, end stage liver disease, and hepatocellular carcinoma (HCC) [1,2,3]
The median age of the patients (n = 100) was 60 years [Interquartile range (IQR) 54–64); 72% were male; 60% were Caucasian; and 42% had cirrhosis pre-treatment according to the FibroScan measurement
The median liver stiffness (LS) score dropped from 10.40 kPa (IQR: 7.25– 18.60) pre-treatment to 7.60 kPa (IQR: 5.60–12.38) at SVR24, p
Summary
Hepatitis C Virus (HCV) is a leading cause of liver cirrhosis, end stage liver disease, and hepatocellular carcinoma (HCC) [1,2,3]. By 2007, the age-adjusted mortality for HCV was higher than for human immunodeficiency virus (HIV) in the United States [4]. The goals of HCV treatment are to achieve a sustained virological response (SVR), to halt the progression of liver damage, and to establish conditions that may allow hepatic fibrosis to regress. Hepatic fibrosis stage is a predictor or liver disease progression during chronic infection. To investigate the impact of a sustained virological response (SVR) to hepatitis C virus (HCV) treatment on liver stiffness (LS)
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