Liver cT 1 decreases following direct-acting antiviral therapy in patients with chronic hepatitis C virus
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HEPATOBILIARY
Liver cT1 decreases following direct‑acting antiviral therapy in patients with chronic hepatitis C virus Arjun N. A. Jayaswal1 · Christina Levick1,2 · Jane Collier2 · Elizabeth M. Tunnicliffe1,3 · Matthew D. Kelly4 · Stefan Neubauer1,3 · Eleanor Barnes2,3,5 · Michael Pavlides1,2,3 Received: 27 August 2020 / Revised: 4 November 2020 / Accepted: 7 November 2020 © The Author(s) 2020
Abstract Purpose Direct-acting antiviral therapies (DAAs) for treatment of chronic hepatitis C virus (HCV) have excellent rates of viral eradication, but their effect on regression of liver fibrosis is unclear. The primary aim was to use magnetic resonance imaging (MRI) and spectroscopy (MRS) to evaluate changes in liver fibrosis, liver fat and liver iron content (LIC) in patients with chronic HCV following treatment with DAAs. Methods In this prospective study, 15 patients with chronic HCV due to start treatment with DAAs and with transient elastography (TE) > 8 kPa were recruited consecutively. Patients underwent MRI and MRS at baseline (before treatment), and at 24 weeks and 48 weeks after the end of treatment (EoT) for the measurement of liver cT1 (fibroinflammation), liver fat and T2* (LIC). Results All patients achieved a sustained virological response. Liver cT1 showed significant decreases from baseline to 24 weeks post EoT (876 vs 806 ms, p = 0.002, n = 15), baseline to 48 weeks post EoT (876 vs 788 ms, p = 0.0002, n = 13) and 24 weeks post EoT to 48 weeks post EoT (806 vs 788 ms, p = 0.016, n = 13). Between baseline and 48 weeks EoT significant reduction in liver fat (5.17% vs 2.65%, p = 0.027) and an increase in reported LIC (0.913 vs 0.950 mg/g, p = 0.021) was observed. Conclusion Liver cT1 decreases in patients with chronic HCV undergoing successful DAA treatment. The relatively fast reduction in cT1 suggests a reduction in inflammation rather than regression of fibrosis. Keywords T1 mapping · Iron corrected T1 · Direct-acting antivirals · Hepatitis C virus
Introduction Eleanor Barnes and Michael Pavlides are Joint senior Authors. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00261-020-02860-5) contains supplementary material, which is available to authorized users. * Michael Pavlides [email protected] 1
Oxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK
2
Translational Gastroenterology Unit, University of Oxford, Oxford, UK
3
Oxford NIHR Biomedical Research Centre, Oxford, UK
4
Perspectum Ltd, Oxford, UK
5
Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, UK
Chronic hepatitis C virus (HCV) affects an estimated 71 million people worldwide [1] and is associated with the development of liver cirrhosis, hepatocellular carcinoma (HCC), liver failure and death. Direct-acting antiviral therapies (DAAs) have high rates of viral eradication (> 95%) and have transformed the treatm
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