ArticleHepatology international2026
Low lysosomal acid lipase activity is associated with histological progression of metabolic dysfunction-associated steatotic liver disease.
Article in Hepatology international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
background and purpose of the studyLiver inflammation and fibrosis are the key determinants of long-term adverse outcomes in metabolic dysfunction-associated steatotic liver disease (MASLD). Therefore, identifying progressive forms of MASLD is crucial. Lysosomal acid lipase (LAL), a central enzyme in intracellular lipid hydrolysis, has been reported to be reduced in MASLD and linked to liver injury.
aimTo evaluate whether baseline LAL activity predicts long-term progression of MASLD.
methodsWe prospectively followed up 144 adults with biopsy-proven MASLD for a minimum of 5 years (median 8.1). All patients underwent a FibroScan® at baseline and follow-up and 94 of them also had paired liver biopsies. LAL activity (expressed as LAL/platelet-LAL/ptls) was measured on dried blood spots. Liver disease progression was defined by meeting of the histological endpoint at follow-up (i.e., development of MASH and/or NAS worsening ≥ 1 point and/or fibrosis progression ≥ 1 stage) or by liver stiffness measurement (LSM) worsening at Fibroscan.
resultsAmong the 94 biopsied patients, 26% met the composite histological endpoint and had significantly lower baseline LAL/ptls ratio, higher HOMA-IR, CAP and LSM. In particular, lower LAL/ptls was strongly related to the worsening of inflammation. In multivariate analysis, lower ln-transformed LAL/ptls ratio independently predicted histological progression (OR 0.51, 95% CI 0.04-0.60, p = 0.018). No association emerged between baseline LAL/ptls ratio and non-invasive progression by FibroScan.
conclusionsLower LAL/ptls ratio identifies MASLD patients at increased risk of histological progression and complements non-invasive tools by reflecting biological pathways linked to inflammation.
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