Outcomes
fibrosis
INFLAMMATION, LIVER FIBROSIS, FIBROSIS, SECONDARY, HEPATIC STEATOSIS, REGRESSION
The primary outcome was regression of liver fibrosis. This was defined as a between-treatment-group comparison of the proportion of patients who had a decrease of at least one fibrosis stage on the end of trial biopsy according to the Kleiner histological scoring system.Secondary histological endpoints were changes from baseline in lobular inflammation, hepatic steatosis, and hepatocyte ballooning. Non-invasive secondary endpoints were change in transient liver elastography, change in Fibrosis-4 (FIB-4) index, and change in N-terminal propeptide of type III collagen (PRO-C3), internal epitope in the 7S domain of type IV collagen (PRO-C4), and C-terminal of type VIII collagen (PRO-C8). The primary and secondary outcomes were all assessed at 18 months after enrolment. Gamma glutamyltransferase, alanine aminotransferase, and self-reported alcohol intake were assessed every second month after enrolment. Secondary outcomes of surrogate markers of fibrosis; hepatic stellate cell activation; blood and urine metabolomics; pro-inflammatory gene expression; quality of life; nutritional status; and gut microbiome composition and gene expression will be reported elsewhere (