scholarly journals Diagnostic Value of Magnetic Resonance Elastography Radiomics Analysis for the Assessment of Hepatic Fibrosis in Patients With Nonalcoholic Fatty Liver Disease

Author(s):  
Ki Choon Sim ◽  
Min Ju Kim ◽  
Yongwon Cho ◽  
Hyun Jin Kim ◽  
Beom Jin Park ◽  
...  

Abstract Background: To investigate the diagnostic performance of radiomics analysis using magnetic resonance elastography (MRE) toward assessing hepatic fibrosis in patients with nonalcoholic fatty liver disease (NAFLD). Methods: A total of 100 patients with suspected NAFLD were retrospectively enrolled. All patients underwent a liver parenchymal biopsy. MRE was performed using a 3.0-T scanner. Following three-dimensional (3D) segmentation of MRE images, 834 radiomic features were analyzed using a commercial program. Radiologic features, such as median and mean values of two-dimensional (2D) or 3D regions of interest (ROIs) and variable clinical features, were analyzed. A random forest regressor was employed to extract important radiomic, radiological, and clinical features. A random forest classifier model was trained to use these features to classify the fibrosis stage. The area under the receiver operating characteristic curve (AUC) was evaluated using a classifier for fibrosis stage diagnosis. Results: The pathological hepatic fibrosis stage was classified as low-grade fibrosis (stages F0–F1, n = 82) or clinically significant fibrosis (stages F2–F4, n = 18). Eight important features were extracted from radiomics analysis, with the two most important being wavelet-HHL gray level dependence matrix (GLDM)-dependence non-uniformity-normalized and wavelet-HHL GLDM-dependence entropy. The median value of the 2D ROI was identified as the most important radiologic feature. Platelet count was identified as an important clinical feature. The AUC of the classifier using radiomics was comparable to that of radiologic measures (0.97 ± 0.07 vs. 0.96 ± 0.06). Conclusions: MRE radiomics analysis provides diagnostic performance comparable to conventional MRE analysis for the assessment of clinically significant hepatic fibrosis in patients with NAFLD.

2015 ◽  
Vol 24 (3) ◽  
pp. 293-300 ◽  
Author(s):  
Salih Boga ◽  
Huseyin Alkim ◽  
Canan Alkim ◽  
Ali Riza Koksal ◽  
Mehmet Bayram ◽  
...  

Background & Aims: Mild iron overload is frequently reported in patients with nonalcoholic fatty liver disease (NAFLD). Hepcidin is the master iron-regulatory peptide and hemojuvelin (HJV) is the key regulator of iron-dependent secretion of hepcidin. The aims of this study were to evaluate serum HJV and hepcidin levels in patients with biopsy-proven NAFLD with and without hepatic iron overload, and to identify potential associations of HJV and hepcidin with the clinical characteristics of the patients enrolled. Methods: Serum levels of HJV and hepcidin were measured in 66 NAFLD patients with (n=12) and without (n=54) iron overload, and controls (n=35) by enzyme-linked immunosorbent assay. Hemojuvelin and hepcidin levels were assessed in relation to clinical characteristics and liver histologic evaluation of the participants. Results: Significantly lower serum HJV (281.1 [239.2-353.6] vs. 584.8 [440.3-661] ng/ml, p<0.001) and similar serum hepcidin levels (60.5±31.1 vs. 55.8±11.9 ng/ml, p=0.285) were found in NAFLD patients when compared to controls. İron-overloaded NAFLD patients had significantly lower HJV (249.9 [187.6-296.3] vs. 292.9 [243-435] ng/ml, p=0.032) and significantly higher hepcidin (78.4±35.5 vs. 56.5±28.9ng/ml, p=0.027) levels than NAFLD patients without iron overload. Fibrosis stage was significantly higher in iron overloaded NAFLD group (p<0.001). Ferritin levels correlated significantly both with HOMA-IR (r=0.368, p=0.002) and fibrosis stage (r=0.571, p<0.001). Conclusions: Our findings suggest that HJV levels are low in NAFLD and even lower in iron overloaded NAFLD, while hepcidin levels are higher in NAFLD with iron overload. The gradually decreased HJV and increased hepcidin concentrations in our patients most likely reflect the physiological response to iron accumulation in the liver.


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