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
Affiliations
- 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.
- 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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