Published: 8 October 2026
Author(s): Leonard D. Broekman, Kirsi M.A. van Eekhout, Sophie Porro, Laura A.M. Konings, Sofia Carvalhana, Ioanna P. Kalafati, Manuel Romero-Gómez, Luca Miele, Jörn M. Schattenberg, Manuel Castro Cabezas, Jean W. Muris, Juan M. Mendive, Ghislaine J.M.W. van Thiel, Luisa Vonghia, Sven M. Francque, Maarten E. Tushuizen, Adriaan G. Holleboom, on behalf of the GRIPonMASH Consortium
Issue: October 2026
Section: Original Article

Metabolic dysfunction-associated steatotic liver disease (MASLD), including metabolic dysfunction-associated steatohepatitis (MASH) and its fibrotic and cirrhotic stages, poses a growing burden on healthcare globally [1]. The increasing prevalence and duration of obesity and type 2 diabetes mellitus (T2D) have led to a rapid increase in MASLD, which now affects an estimated 38% of the adult global population and up to 60–80% of individuals with elevated cardiometabolic risk [2,3]. Among patients with T2D in primary care, 5–10% already have MASLD-induced advanced fibrosis or cirrhosis [4], a key predictor of liver-related, cardiovascular, and all-cause mortality [5].

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