Author information
1 Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Australia; Centre for Liver Disease Research, Translational Research Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia.
2 Centre for Liver Disease Research, Translational Research Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia.
3 Faculty of Medicine, University of Queensland, Brisbane Australia.
4 Inala Primary Care, Brisbane, Australia.
5 Pathology Queensland, Brisbane, Australia.
6 Faculty of Medicine, University of Queensland, Brisbane Australia; Department of Radiology, Princess Alexandra Hospital, Brisbane, Australia.
7 Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Australia.
8 Faculty of Medicine, University of Queensland, Brisbane Australia; Department of Diabetes and Endocrinology, Princess Alexandra Hospital, Brisbane, Australia.
9 QIMR Berghofer Medical Research Institute, Brisbane, Australia.
10 Centre for Liver Disease Research, Translational Research Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia; Mater Research, Translational Research Institute, The University of Queensland, Brisbane, Australia.
11 QFAB Bioinformatics, Institute for Molecular Bioscience, Queensland Bioscience Precinct, The University of Queensland, Brisbane, Australia.
12 Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Australia; Centre for Liver Disease Research, Translational Research Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia. Electronic address: e.powell@uq.edu.au.
Abstract
BACKGROUND & AIMS:
There is limited knowledge regarding the longitudinal utility of biomarkers of fibrosis, such as the non-alcoholic fatty liver disease (NAFLD) fibrosis score (NFS) or the fibrosis-4 score (FIB-4) score. We examined longitudinal changes in the NFS and the FIB-4 score in patients with NAFLD, with and without clinically significant fibrosis (CSF).
METHODS:
We performed a retrospective study of 230 patients with NAFLD, collecting clinical and laboratory records to calculate NFS and FIB-4 scores at 6 monthly intervals for 5 years prior to hepatology assessment of fibrosis. Linear mixed models with random intercept and slope and adjusted for age at baseline were used to assess the progression of NFS and log-transformed FIB-4 scores over time in subjects with and without CSF, determined by liver stiffness measurements ≥8.2kPa.
RESULTS:
Patients had a median of 11 (minimum, 10 and maximum, 11) retrospective observations over a median time period of 5 years (minimum, 4.5 years and maximum, 5 years). Of patients with low baseline NFS and FIB-4 scores, 31.11% and 37.76%, respectively, had CSF at the time of hepatology assessment. There was a correlation between NFS and Log10FIB-4 over time (repeated measure r=0.55; 95% CI, 0.52-0.59). The rate of increase in NFS and Log10FIB-4 was significantly higher in patients with than without CSF (both P<.001). Predicted NFS increased by 0.17 and 0.06 units per year in subjects with and without CSF, respectively. Predicted Log10FIB-4 score increased by 0.032 and 3x10-4 units per year in subjects with and without CSF respectively.
CONCLUSIONS:
Non-invasively measured fibrosis scores increase progressively in patients with NAFLD and CSF. Further studies are needed to determine whether repeated measurements can identify patients at risk for CSF.