L.A.M. Konings 1,2, C. Dietvorst 1,3, W. Theel 4, J. Apers5, S. Ter Borg 6, R.E.M. Verstegen 7, E.M. van der Zwan 7, M. Castro Cabezas 1,2,8
1. Department of Internal medicine, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands
2. Department of Internal medicine, division of endocrinology, Erasmus MC Medical Center, Rotterdam, the Netherlands
3. Department of Internal medicine, division of dietetics, Erasmus MC Medical Center, Rotterdam, the Netherlands
4. Department of Internal medicine, division of gastroenterology and hepatology, Erasmus MC Medical Center, Rotterdam, the Netherlands
5. Department of Bariatric surgery, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands
6. Department of Pathology, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands
7. Department of Clinical chemistry, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands
8. Julius Clinical, Zeist, The Netherlands
Background: Metabolic dysfunction–associated steatotic liver disease (MASLD) is prevalent in diabetes and obesity and improves with weight loss. This study evaluates changes after bariatric surgery in hepatic steatosis and fibrosis, measured with vibration-controlled transient elastography (VCTE) in relation to different non-invasive tests (NITs) for MASLD.
Methods: The Franciscus Obesity NASH Study (FONS) is a single centre cohort study including bariatric surgery patients. Steatosis was defined as CAP ≥ 275 dB/m, fibrosis as LSM ≥ 8 kPa measured at two different time points with VCTE. Different blood-based NITs for steatosis (HSI, LAP, FSI) and fibrosis (FIB-4, MAF-5, NFS and APRI) were calculated.
Results: 170 subjects were reanalysed one year after bariatric surgery. At baseline, diabetes was present in 15.3%, MASLD in 64.1% and fibrosis in 27.6%. Baseline CAP and LSM correlated with baseline HbA1c. Diabetes was associated with higher CAP, fibrosis NITs and FSI. Most NITs, with NFS as exception, did not adequately discriminate between participants with steatosis or fibrosis and those without. After one year, steatosis was present in 8.2% and fibrosis in 5.9%. BMI, CAP and LSM decreased significantly, as did most NITs, only FIB-4 rose and APRI remained unchanged. Results were comparable in the diabetes subgroup. In linear regression analysis, HSI, LAP and FSI changes were associated with CAP change, only NFS change was associated with LSM change.
Conclusion: Bariatric surgery reduced hepatic steatosis (CAP) and liver stiffness (LSM), with improvement in most NITs, also in subjects with diabetes. Blood-based NITs, with exception of NFS, did not reliably identify steatosis or fibrosis. However, changes in steatosis NITs and NFS reflected changes in liver steatosis and fibrosis.