# Incorporating parenchymal heterogeneity into FLIS to improve MRI-based liver function assessment

**Authors:** Hande Özen Atalay, Muhammet Selman Sogut, Murat Akyildiz, Afak Durur Karakaya

PMC · DOI: 10.1186/s13244-025-02187-z · Insights into Imaging · 2026-01-12

## TL;DR

This study improves MRI-based liver function assessment by incorporating parenchymal heterogeneity into a scoring system called FLIS.

## Contribution

The novel FLIS-H score integrates parenchymal heterogeneity, enhancing correlations with liver fibrosis and clinical scores.

## Key findings

- FLIS-H showed stronger correlations with fibrosis stage and clinical scores than standard FLIS.
- Incorporating parenchymal heterogeneity significantly improved associations with Child–Pugh, ALBI, and MELD scores.
- FLIS-H provides a fast and reliable method for liver assessment in clinical radiology.

## Abstract

To assess the correlation between the functional liver imaging score (FLIS) and FibroScan®-derived fibrosis stage, and to determine whether incorporating parenchymal heterogeneity (FLIS-H) improves its association with fibrosis and clinical scores.

This retrospective single-centre study included 113 patients who underwent FibroScan® and hepatocyte-specific contrast-enhanced MRI within a median interval of 4 days. FLIS was calculated, and the parenchymal heterogeneity score was added to FLIS (FLIS-H; range 0–8). Inter-reader agreement was evaluated using a two-way random-effects intraclass correlation coefficient (ICC). Correlations between FLIS/FLIS-H and fibrosis stage/clinical scores (Child–Pugh, MELD, ALBI) were assessed using Spearman’s rank correlation. Steiger’s z-test and Zou’s method were used to compare correlations.

A total of 113 patients (67 men; mean age 56.6 ± 13.5 years) were evaluated. Inter-reader agreement was excellent for FLIS (ICC 0.994; 95% CI: 0.975–1.000), heterogeneity (ICC 0.949; 95% CI: 0.901–0.984), and FLIS-H (ICC 0.974; 95% CI: 0.957–0.989). FLIS showed significant negative correlations with Child–Pugh (ρ = −0.2664, p = 0.0087), ALBI (ρ = −0.3076, p = 0.0022), and fibrosis stage (ρ = −0.3207, p < 0.001). FLIS-H demonstrated stronger correlations with Child–Pugh (ρ = −0.4167, p < 0.001), ALBI (ρ = −0.5243, p < 0.001), MELD (ρ = −0.2360, p = 0.020), and fibrosis stage (ρ = −0.5270, p < 0.001). Steiger’s z-test confirmed that correlations were significantly improved with FLIS-H for ALBI (z = −3.03, p = 0.0025), Child–Pugh (z = −2.01, p = 0.045), and fibrosis stage (z = −2.90, p = 0.0038).

FLIS correlates significantly with fibrosis stage and clinical scores. Incorporating parenchymal heterogeneity into FLIS enhances these associations and may provide a superior method for liver assessment.

This study introduces a modified FLIS version (FLIS-H) that integrates parenchymal heterogeneity and demonstrates superior correlation with elastography-derived fibrosis stages and clinical scoring systems, offering a practical improvement for non-invasive assessment in routine practice.

FLIS has no reported correlation with elastography-based liver fibrosis staging.Parenchymal heterogeneity is not included as a parameter in the standard FLIS.Integrating heterogeneity improves correlation with fibrosis stage and clinical scores.FLIS-H enables fast, reliable, structure-function liver assessment in clinical radiology.

FLIS has no reported correlation with elastography-based liver fibrosis staging.

Parenchymal heterogeneity is not included as a parameter in the standard FLIS.

Integrating heterogeneity improves correlation with fibrosis stage and clinical scores.

FLIS-H enables fast, reliable, structure-function liver assessment in clinical radiology.

## Full-text entities

- **Genes:** GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** IgG4-related sclerosing cholangitis (MESH:D000077733), hepatocellular injury (MESH:D056486), acute hepatitis (MESH:D017114), Chronic liver disease (MESH:D008107), deaths (MESH:D003643), cholangiocarcinoma (MESH:D018281), post (MESH:D000094025), viral hepatitis (MESH:D014777), hepatomegaly (MESH:D006529), Metabolic dysfunction (MESH:D008659), inflammation (MESH:D007249), steatosis (MESH:D005234), encephalopathy (MESH:D001927), cryptogenic cirrhosis (MESH:C562577), portal vein thrombosis (MESH:D012170), hereditary haemochromatosis (MESH:D009386), ALD (MESH:D008108), autoimmune hepatitis (MESH:D019693), ALBI (MESH:D007647), primary biliary cholangitis (MESH:D008105), Child (MESH:C562515), liver failure (MESH:D017093), chronic hepatitis B (MESH:D019694), ascites (MESH:D001201), Hepatic encephalopathy (MESH:D006501), primary sclerosing cholangitis (MESH:D015209), cachexia (MESH:D002100), cholestatic (MESH:D002779), liver fibrosis (MESH:D008103), Fibrosis (MESH:D005355), cancer (MESH:D009369), congestive hepatopathy (MESH:D002311), MELD (MESH:D058625)
- **Chemicals:** bilirubin (MESH:D001663), Gadoxetic acid (MESH:C073590), ALBI (-), creatinine (MESH:D003404)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** C282Y, C in 3

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## Figures

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## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12796089/full.md

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Source: https://tomesphere.com/paper/PMC12796089