# Care Pathways for Metabolic Dysfunction‐Associated Steatotic Liver Disease (MASLD): A State‐of‐The‐Art Review

**Authors:** Kirsi M. A. van Eekhout, Leonard D. Broekman, Vivian D. de Jong, Maurice Michel, Rick Grobbee, Douglas Maya‐Miles, Manuel Romero‐Gómez, Jean Muris, Juan M. Mendive, Yasaman Vali, Oscar H. Franco, Jörn M. Schattenberg, Céline Fournier‐Poizat, Manuel Castro Cabezas, Maarten E. Tushuizen, Adriaan G. Holleboom

PMC · DOI: 10.1111/liv.70603 · Liver International · 2026-03-19

## TL;DR

This review evaluates care pathways for MASLD using non-invasive tests to identify severe cases and reduce unnecessary specialist referrals.

## Contribution

The study systematically reviews and compares MASLD care pathways, highlighting the need for standardized protocols and large-scale validation.

## Key findings

- NIT-based pathways improve detection of advanced MASLD and reduce unnecessary hepatology referrals.
- Heterogeneity in pathway design leads to variable screening numbers and challenges in standardization.
- Standardized, large-scale studies are needed to support widespread adoption of MASLD care pathways.

## Abstract

Metabolic dysfunction‐Associated Steatotic Liver Disease (MASLD) is a growing clinical challenge, necessitating effective diagnostic strategies to identify advanced liver fibrosis while minimising unnecessary referrals of mild cases. Current clinical guidelines recommend care pathways utilising non‐invasive tests (NITs) to stratify patients, but the optimal diagnostic algorithm across care settings remains unclear. This state‐of‐the‐art review systematically examines studies describing clinical care pathways for detecting advanced fibrotic MASLD and stratifying patients at risk. A comprehensive literature search of MEDLINE, Embase, Cochrane Library, and Scopus, finalised in January 2026, identified nine relevant studies that met predefined criteria including structured care plans and applicability beyond diagnosis alone. Pathway populations included patients at risk for MASLD (type 2 diabetes (n = 4) or broad range cardiometabolic risk factors (n = 1)) or confirmed MASLD (n = 4). The most frequently employed NITs were FIB‐4 and vibration‐controlled transient elastography (VCTE). Numbers needed to screen (NNS) for hepatology referral and advanced fibrosis detection varied considerably across pathways and populations, reflecting heterogeneity in design and fibrosis assessment methods. All studies reported improved patient risk stratification; attendance rates declined at each pathway step. Findings suggest that NIT‐based clinical care pathways can effectively align patient management and optimise transmural care for MASLD. Nonetheless, heterogeneity in pathway design and fibrosis determination highlights the need for standardised protocols and validation in larger, at‐risk cohorts to strengthen evidence supporting widespread adoption. This review contributes to advancing MASLD management within evolving clinical frameworks.

NIT‐based care pathways improve identification of advanced MASLD and reduce unnecessary hepatology referrals.Considerable heterogeneity exists in pathway design, primarily in terms of target populations, NITs, and definitions of advanced disease, resulting in a widely varied number needed to screen.Present literature underscores the need for a universally accepted outcome framework for MASLD care pathways.Large‐scale, standardised, real‐world studies are urgently needed to guide scalable implementation.

NIT‐based care pathways improve identification of advanced MASLD and reduce unnecessary hepatology referrals.

Considerable heterogeneity exists in pathway design, primarily in terms of target populations, NITs, and definitions of advanced disease, resulting in a widely varied number needed to screen.

Present literature underscores the need for a universally accepted outcome framework for MASLD care pathways.

Large‐scale, standardised, real‐world studies are urgently needed to guide scalable implementation.

## Linked entities

- **Diseases:** Metabolic dysfunction-Associated Steatotic Liver Disease (MONDO:0013209), type 2 diabetes (MONDO:0005148)

## Full-text entities

- **Genes:** SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, FASTK (Fas activated serine/threonine kinase) [NCBI Gene 10922] {aka FAST}
- **Diseases:** gastroesophageal varices (MESH:D014648), NAFLD (MESH:D065626), T2DM (MESH:D003924), cirrhotic (MESH:D000094724), GBD (MESH:D001037), associated (MESH:D018886), HCC (MESH:D006528), VCTE (MESH:D053421), NITs (MESH:C537770), viral hepatitis (MESH:D014777), Metabolic dysfunction (MESH:D008659), ALD (MESH:D008108), CF (MESH:D003550), Fibrosis (MESH:D005355), Liver Diseases (MESH:D008107), metabolic syndrome (MESH:D024821), LSM (MESH:D017093), Liver Fibrosis (MESH:D008103), MASH (MESH:D005234), liver inflammation (MESH:D007249)
- **Chemicals:** Hepta (-), alcohol (MESH:D000438), Resmetirom (MESH:C588408)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

44 references — full list in the complete paper: https://tomesphere.com/paper/PMC13000678/full.md

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Source: https://tomesphere.com/paper/PMC13000678