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J Clin Exp Hepatol. 2016 Mar;6(1):15-20. doi: 10.1016/j.jceh.2015.11.004. Epub 2015 Dec 06.

Changes in Liver Volume in Patients with Chronic Hepatitis C Undergoing Antiviral Therapy.

Journal of clinical and experimental hepatology

Julie A Fitzpatrick, Jin Un Kim, Jeremy F L Cobbold, Mark J W McPhail, Mary M E Crossey, Aluel A Bak-Bol, Ashraf Zaky, Simon D Taylor-Robinson

Affiliations

  1. Hepatology Section, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Imperial College London, London W2 1NY, United Kingdom; Robert Steiner MRI Unit, Hammersmith Hospital Campus, Imperial College London, Du Cane Road, London W12 ONN, United Kingdom.
  2. Hepatology Section, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Imperial College London, London W2 1NY, United Kingdom.

PMID: 27194891 PMCID: PMC4862019 DOI: 10.1016/j.jceh.2015.11.004

Abstract

AIM: Liver volumetric analysis has not been used to detect hepatic remodelling during antiviral therapy before. We measured liver volume (LV) changes on volumetric magnetic resonance imaging during hepatitis C antiviral therapy.

METHODS: 22 biopsy-staged patients (median [range] age 45(19-65) years; 9F, 13M) with chronic hepatitis C virus infection were studied. LV was measured at the beginning, end of treatment and 6 months post-treatment using 3D T1-weighted acquisition, normalised to patient weight. Liver outlines were drawn manually on 4 mm thick image slices and LV calculated. Inter-observer agreement was analysed. Patients were also assessed longitudinally using biochemical parameters and liver stiffness using Fibroscan™.

RESULTS: Sustained viral response (SVR) was achieved in 13 patients with a mean baseline LV/kg of 0.022 (SD 0.004) L/kg. At the end of treatment, the mean LV/kg was 0.025 (SD 0.004, P = 0.024 cf baseline LV/kg) and 0.026 (SD 0.004, P = 0.008 cf baseline LV/kg) 6 months post-treatment (P = 0.030 cf baseline, P = 0.004). Body weight-corrected end of treatment LV change was significantly higher in patients with SVR compared to patients not attaining SVR (P = 0.050). End of treatment LV change was correlated to initial ALT (R (2) = 0.479, P = 0.037), but not APRI, AST, viral load or liver stiffness measurements. There was a correlation of 0.89 between observers for measured slice thickness.

CONCLUSIONS: LV increased during anti-viral treatment, while the body weight-corrected LV increase persisted post-antiviral therapy and was larger in patients with SVR.

Keywords: ALT, Alanine aminotransferase; APRI, Aspartate transaminase to platelet ratio index; AST, Aspartate transaminase; CHC, Chronic hepatitis C; CLD, Chronic liver disease; CT, Computed tomography; EASL, European Association for the Study of the Liver; HCC, Hepatocellular carcinoma; HCV, Hepatitis C virus; LV, Liver volume; MRI, Magnetic resonance imaging; NAFLD, Non-alcoholic fatty liver disease; NI, Necroinflammatory; SVR, Sustained viral response; hepatitis C virus; liver volume; magnetic resonance imaging; sustained viral response

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