Abstract
Methods Liver stiffness measurements (LSM) have been serially assessed 1, 3, and 5 years after HCV clearance in 655 patients who have been treated with DAAs. Results The mean age was 51.44 ± 10 years. 73% of patients were males. 48% were cirrhotics. In noncirrhotics, the mean LSM was significantly decreased from 8.29 ± 2.3 kPa to 4.03 ± 1.0 kPa (p < 0.0001) at the end of the follow-up. Likewise, LSM decreased in cirrhotics from 29.66 ± 14.25 kPa to 22.50 ± 11.16 kPa (p < 0.0001). The proportions of F1, F2, F3, and F4 patients at the baseline were 17.7%, 17.9%, 16.6%, and 47.8%, which became 56.5%, 4.1%, 4.9%, and 34.5%, respectively, with a substantial reversal of cirrhosis in 87 patients (27.7%) at the end of follow-up. Conclusions There was an overall significant regression of liver stiffness in all patients after sustained HCV eradication. Liver stiffness reflecting mild fibrosis (F0–F2) usually improves shortly after treatment, while measurements reflecting advanced fibrosis (F3–F4) take a longer time to regress to lower fibrosis stages.
Highlights
Hepatitis C virus (HCV) infection is a major worldwide health problem
Around 70% of persons acutely infected with HCV will develop chronic HCV infection. e global estimate of chronic HCV is about 71 million people (1% of the world population). e progression of hepatic fibrosis with excess deposition of an extracellular matrix is the most serious consequence of chronic hepatitis if left untreated. 15–30% of those with chronic liver injury will end in liver cirrhosis within 20 years with risk of cirrhosis-related complications including portal hypertension and hepatocellular carcinoma (HCC). e overall HCV related mortality is about 400,000 deaths every year [1, 2]
HCV is a major leading cause of liver cirrhosis and its related complications. e annual rates of liver decompensation, transplantation, and HCC attributed to HCV are 6.37%, 4.58%, and 3.36%, respectively [25]
Summary
Hepatitis C virus (HCV) infection is a major worldwide health problem. Around 70% of persons acutely infected with HCV will develop chronic HCV infection. e global estimate of chronic HCV is about 71 million people (1% of the world population). e progression of hepatic fibrosis with excess deposition of an extracellular matrix is the most serious consequence of chronic hepatitis if left untreated. 15–30% of those with chronic liver injury will end in liver cirrhosis within 20 years with risk of cirrhosis-related complications including portal hypertension and hepatocellular carcinoma (HCC). e overall HCV related mortality is about 400,000 deaths every year [1, 2].HCV treatment has been revolutionized since the introduction of direct acting antiviral agents (DAAs) in 2014. E global estimate of chronic HCV is about 71 million people (1% of the world population). 15–30% of those with chronic liver injury will end in liver cirrhosis within 20 years with risk of cirrhosis-related complications including portal hypertension and hepatocellular carcinoma (HCC). E overall HCV related mortality is about 400,000 deaths every year [1, 2]. DAAs have been associated with high rates of sustained virological response (SVR) exceeding 95% with an excellent safety and tolerability profile [3]. The primary goal of HCV therapy is to achieve SVR, and the improvement of liver fibrosis remains the most important prognostic indicator. Erefore, it is necessary to determine how far virological clearance is associated with fibrosis regression [4]. Liver biopsy is the gold standard for the evaluation of liver fibrosis, it has been gradually replaced by TE because of its potential
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