# CT-based radiomics-clinical model for risk assessment of parenteral nutrition-associated hepatic steatosis in chronic intestinal failure and its metabolomic interpretation

**Authors:** Yufei Xia, Ruochen Li, Sirui Liu, Pinwen Zhou, Jiaqi Wang, Xin Qi, Minyi Zhu, Guangming Sun, Xuejin Gao, Li Zhang, Gulisudumu Maitiabula, Xinying Wang

PMC · DOI: 10.3389/fnut.2026.1705520 · 2026-02-03

## TL;DR

This study creates a model combining CT scans and clinical data to predict liver fat risk in patients on long-term nutrition support.

## Contribution

A novel radiomics-clinical model for predicting PNAHS in CIF patients with superior performance and metabolic interpretation.

## Key findings

- The combined radiomics-clinical model achieved an AUC of 0.862 in predicting PNAHS risk.
- Key predictors included radiomics score, cholesterol, urea, PN frequency, and intermuscular fat area.
- High-risk PNAHS groups showed distinct metabolic profiles based on serum metabolomics analysis.

## Abstract

Patients with chronic intestinal failure (CIF) dependent on parenteral nutrition (PN) are at risk of developing parenteral nutrition-associated hepatic steatosis (PNAHS), a condition that can progress to hepatic fibrosis. Effective methods for predicting PNAHS risk are lacking.

This retrospective study included 307 CIF patients. Patients were divided into training (n = 219) and testing (n = 88) sets. Radiomic features (n = 1,037 per patient) were extracted from non-contrast abdominal CT scans obtained within 1 week before PN initiation. Clinical characteristics (e.g., demographics, laboratory values) were collected. Multiple predictive models were developed: radiomics, clinical, combined radiomics-clinical, and various deep learning models (e.g., DenseNet121, ResNet18, Unet, etc.). Model performance was evaluated using the area under the receiver operating characteristic curve (AUC), calibration curves, decision curve analysis and Log-rank test. Serum metabolomics analysis was performed to explore biological implications of the model-derived risk scores.

The combined model demonstrated the highest AUC of 0.862 (95% CI: 0.782–0.942) in the testing set, significantly outperforming most other models (p < 0.05). Key predictors in the combined model included the radiomics score, total cholesterol level, urea level, PN frequency, and L3-intermuscular fat area. The combined score also demonstrated considerable capability in stratifying patients by duration of PN dependency. The distinct PNAHS risk groups identified by the combined model exhibited significant differences in their metabolic profiles.

We developed a novel predictive model that integrates CT radiomics features with clinical characteristics to effectively predict the risk of PNAHS in patients with CIF and reflects underlying metabolic disturbance.

## Full-text entities

- **Genes:** GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, ALPP (alkaline phosphatase, placental) [NCBI Gene 250] {aka ALP, PALP, PLAP, PLAP-1}, GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, GGTLC5P (gamma-glutamyltransferase light chain 5 pseudogene) [NCBI Gene 653590] {aka GGT}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}
- **Diseases:** hepatic pathologies (MESH:D005598), liver damage (MESH:D056486), biliary obstruction (MESH:D001658), liver injury (MESH:D017093), PNAHS (MESH:D005234), CIF (MESH:D000090124), splenomegaly (MESH:D013163), renal cell carcinoma (MESH:D002292), sepsis (MESH:D018805), cysts (MESH:D003560), metabolic (MESH:D008659), HCC (MESH:D006528), hypertension (MESH:D006973), Malnutrition (MESH:D044342), viral or autoimmune hepatitis (MESH:D014777), SBS (MESH:D012778), benign liver diseases (MESH:D008107), sarcopenia (MESH:D055948), portal hypertension (MESH:D006975), Fibrosis (MESH:D005355), thrombosis (MESH:D013927), hepatic fibrosis (MESH:D008103), chronic kidney disease (MESH:D051436), NAFLD (MESH:D065626), thrombocytopenia (MESH:D013921), diabetes (MESH:D003920), cancer (MESH:D009369)
- **Chemicals:** lipid (MESH:D008055), iron (MESH:D007501), water (MESH:D014867), citric acid (MESH:D019343), L-glutamine (MESH:D005973), Glucose (MESH:D005947), creatinine (MESH:D003404), Malic acid (MESH:C030298), cholesterol (MESH:D002784), L-asparagine (MESH:D001216), alcohol (MESH:D000438), glutamate (MESH:D018698), acids (MESH:D000143), alpha-ketoglutarate (MESH:D007656), Ammonia (MESH:D000641), PNAHS (-), TG (MESH:D014280), L-phenylalanine (MESH:D010649), creatine (MESH:D003401), carbon (MESH:D002244), TCA (MESH:D014233), L-arginine (MESH:D001120), bicarbonate (MESH:D001639), carbohydrates (MESH:D002241), bilirubin (MESH:D001663), fumaric acid (MESH:C032005), urea (MESH:D014508), amino acid (MESH:D000596)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12909248/full.md

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Source: https://tomesphere.com/paper/PMC12909248