Objectives: To investigate the value of R2* mapping-based radiomics nomograms in staging liver fibrosis in patients with chronic hepatitis B.
Methods: Between January 2020 and December 2020, 151 patients with chronic hepatitis B were randomly divided into training (n = 103) and validation (n = 48) cohorts. From January to February 2021, 58 patients were included in a test cohort. Radiomics features were selected using the interclass correlation coefficient and least absolute shrinkage and selection operator method. Three radiomics nomograms, combining the radiomics score (Radscore) derived from R2* mapping and clinical variables, were used for staging significant and advanced fibrosis, and cirrhosis. Performance of the model was evaluated using the AUC. The utility and clinical benefits were evaluated using the continuous net reclassification index (NRI), integrated discrimination improvement (IDI), and decision curve analysis (DCA).
Results: The Radscore calculated by 12 radiomics features and independent factors (laminin and platelet) of advanced fibrosis were used to construct the radiomics nomograms. In the test cohort, the AUCs of the radiomics nomograms for staging significant fibrosis, advanced fibrosis, and cirrhosis were 0.738 (95% confidence interval [CI]: 0.604-0.872), 0.879 (95% CI: 0.779-0.98), and 0.952 (95% CI: 0.878-1), respectively. NRI, IDI, and DCA confirmed that radiomics nomograms demonstrated varying degrees of clinical benefit and improvement for advanced fibrosis and cirrhosis, but not for significant fibrosis.
Conclusions: Radiomics nomograms combined with R2* mapping-based Radscore, laminin, and platelet have value in staging advanced fibrosis and cirrhosis but limited value for staging significant fibrosis.
Key Points: • Laminin and platelets were independent predictors of advanced fibrosis. • Radiomics analysis based on R2* mapping was beneficial for evaluating advanced fibrosis and cirrhosis. • It was difficult to distinguish significant fibrosis using a radiomics nomogram, which is possibly due to the complex pathological microenvironment of chronic liver diseases.
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