# Clinical Outcomes and Non‐Invasive Testing in Metabolic Dysfunction‐Associated Steatohepatitis With Cirrhosis: A Systematic Review

**Authors:** Hannes Hagström, Chris Hellmund, Jeffrey V. Lazarus, Riku Ota, Mary E. Rinella, Giada Sebastiani, Fotis Tefos, Zobair M. Younossi, Mazen Noureddin

PMC · DOI: 10.1111/liv.70608 · 2026-03-28

## TL;DR

This systematic review summarizes clinical outcomes and non-invasive testing in MASH-related cirrhosis, highlighting gaps in evidence and the need for better prognostic tools.

## Contribution

The study systematically reviews clinical outcomes and non-invasive tests for MASH-related cirrhosis, identifying key risk factors and evidence gaps.

## Key findings

- Transplant-free survival is lower in MASH-related cirrhosis patients with type 2 diabetes.
- Male sex, T2D, and high Child–Turcotte–Pugh score increase HCC risk in MASH-related cirrhosis.
- Few studies evaluated non-invasive tests for predicting liver-related events in MASH-related cirrhosis.

## Abstract

Metabolic dysfunction‐associated steatohepatitis (MASH) with cirrhosis lacks definitive treatments and poses an increasing healthcare burden globally. We undertook a systematic literature review (SLR) to better understand the disease burden in cirrhosis due to MASH.

The SLR was conducted according to Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines and registered with PROSPERO (CRD4202458650). Embase, MEDLINE, and the Cochrane Library were searched for clinical trials, observational studies, and SLRs/meta‐analyses published in 2014–2024 in MASH‐related cirrhosis. This study focuses on clinical outcomes, including the role of non‐invasive tests (NITs) for predicting these outcomes in patients with MASH‐related cirrhosis.

Following full‐text review, 317 studies were considered eligible for inclusion. Studies on transplant‐free survival, decompensation events, and hepatocellular carcinoma (HCC) in cirrhosis due to MASH were few and heterogeneous. In patients with MASH and compensated cirrhosis, transplant‐free survival was lower in patients with type 2 diabetes (T2D) than in those without. Risks of decompensation increased with factors that included the presence of varices and T2D. Male sex, T2D, and high Child–Turcotte–Pugh score were risk factors for developing HCC. Three studies compared the performance of NITs for predicting liver‐related events, including decompensation, but used varying definitions for these outcomes.

This SLR identified data on a range of clinical outcomes in patients with MASH‐related cirrhosis. However, there was limited evidence for certain outcomes including the role of prognostic prediction models for liver‐related events in this patient population.

A better understanding of clinical outcomes and the disease burden of metabolic dysfunction‐associated steatohepatitis (MASH) with cirrhosis will help us to estimate the potential impact of future treatments.Here, we report clinical outcomes specific to MASH with cirrhosis identified via a systematic review of the literature, published from 2014 to 2024.Few included studies reported data on survival without transplant, decompensation, factors linked to the risk of developing hepatocellular carcinoma, and prediction of cirrhosis‐related complications using non‐invasive tests (NITs).We also identified evidence gaps, including the relative performance of different NITs for predicting cirrhosis‐related complications.

A better understanding of clinical outcomes and the disease burden of metabolic dysfunction‐associated steatohepatitis (MASH) with cirrhosis will help us to estimate the potential impact of future treatments.

Here, we report clinical outcomes specific to MASH with cirrhosis identified via a systematic review of the literature, published from 2014 to 2024.

Few included studies reported data on survival without transplant, decompensation, factors linked to the risk of developing hepatocellular carcinoma, and prediction of cirrhosis‐related complications using non‐invasive tests (NITs).

We also identified evidence gaps, including the relative performance of different NITs for predicting cirrhosis‐related complications.

## Linked entities

- **Diseases:** Metabolic dysfunction-associated steatohepatitis (MONDO:0007027), cirrhosis (MONDO:0005155), hepatocellular carcinoma (MONDO:0007256), type 2 diabetes (MONDO:0005148)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, COL3A1 (collagen type III alpha 1 chain) [NCBI Gene 1281] {aka EDS4A, EDSVASC, PMGEDSV}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}
- **Diseases:** hypertensive gastropathy (MESH:D006973), hepatic encephalopathy (MESH:D006501), hepatic decompensation (MESH:D006333), infectious disease (MESH:D003141), Chronic Liver Disease (MESH:D008107), metabolic syndrome (MESH:D024821), LSM (MESH:D017093), fatigue (MESH:D005221), ALBI (MESH:D007647), ELF (MESH:D008103), MASH (MESH:D005234), AIH (MESH:D019693), inflammation (MESH:D007249), cardiac arrhythmias (MESH:D001145), thrombocytopenia (MESH:D013921), cryptogenic cirrhosis (MESH:C562577), Ascites (MESH:D001201), myocardial infarction (MESH:D009203), Metabolic Dysfunction (MESH:D008659), ALD (MESH:D008108), encephalopathy (MESH:D001927), sepsis (MESH:D018805), malignancy (MESH:D009369), weight loss (MESH:D015431), Cirrhosis (MESH:D005355), alcohol-related cirrhosis (MESH:D008104), Cardiovascular disease (MESH:D002318), portal hypertension (MESH:D006975), HCC (MESH:D006528), NITs (MESH:C537770), VCTE (MESH:D053421), diabetes (MESH:D003920), AC (MESH:D055577), coronary artery disease (MESH:D003324), Model (MESH:D004195), gastroesophageal varices (MESH:D014648), stroke (MESH:D020521), bleeding (MESH:D006470), infection (MESH:D007239), NASH (MESH:D005235), splenomegaly (MESH:D013163), Child-Turcotte-Pugh (MESH:C562515), gastrointestinal bleeding (MESH:D006471), -Stage Liver Disease (MESH:D058625), NAFLD (MESH:D065626), T2D (MESH:D003924), cardiac death (MESH:D003643)
- **Chemicals:** Metformin (MESH:D008687), cyclosporine A (MESH:D016572), bilirubin (MESH:D001663), resmetirom (MESH:C588408), alcohol (MESH:D000438), hyaluronic acid (MESH:D006820), CTP (-)
- **Species:** hepatitis C virus [taxon 11103], Hepatitis B virus (no rank) [taxon 10407], Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC13032177/full.md

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Source: https://tomesphere.com/paper/PMC13032177