From the Department of Diagnostic, Interventional, and Pediatric Radiology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland (J.B.K., B.J., L.E., A.C., V.C.O., A.T.H.); Institute of Forensic Medicine, University of Bern, Bern, Switzerland (J.B.K.); Dr. Kurz Röntgeninstitut AG, Thun, Switzerland (J.B.K.); Siemens Medical Solutions USA, Tucson, AZ (U.G., M.K.); Siemens Medical Solutions USA, New York, NY (M.B.K.); Department of Hepatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland (A.B.); Department of Radiology and Nuclear Medicine, Lucerne Cantonal Hospital, University of Lucerne, Lucerne, Switzerland (L.E., J.R., A.T.H.); and Liver Elastography Center, Translational Imaging Center, Swiss Institute for Translational and Entrepreneurial Medicine, Bern, Switzerland (A.C., V.C.O., A.T.H.).
Invest Radiol. 2024 Nov 1;59(11):754-760. doi: 10.1097/RLI.0000000000001084.
This study evaluates the impact of liver steatosis on the discriminative ability for liver fibrosis and inflammation using a novel Dixon water-only fat-corrected Look-Locker T1 mapping sequence, compared with a standard shortened Modified Look-Locker Inversion Recovery (shMOLLI) sequence, with the aim of overcoming the limitation of steatosis-related confounding in liver T1 mapping.
3 T magnetic resonance imaging of the liver including the 2 T1 mapping sequences and proton density fat fraction (PDFF) was prospectively performed in 24 healthy volunteers and 38 patients with histologically proven liver fibrosis evaluated within 90 days of liver biopsy. Paired Mann-Whitney test compared sequences between participants with and without significant liver steatosis (PDFF cutoff 10%), and unpaired Kruskal-Wallis test compared healthy volunteers to patients with early (F0-2) and advanced (F3-4) liver fibrosis, as well as low (A0-1) and marked (A2-3) inflammatory activity. Univariate and multivariate logistic regression models assessed the impact of liver steatosis on both sequences.
Dixon_W T1 was higher than shMOLLI T1 in participants without steatosis (median 896 ms vs 890 ms, P = 0.04), but lower in participants with liver steatosis (median 891 ms vs 973 ms, P < 0.001). Both methods accurately differentiated between volunteers and patients with early and advanced fibrosis (Dixon_W 849 ms, 910 ms, 947 ms, P = 0.011; shMOLLI 836 ms, 918 ms, 978 ms, P < 0.001), and those with mild and marked inflammation (Dixon_W 849 ms, 896 ms, 941 ms, P < 0.01; shMOLLI 836 ms, 885 ms, 978 ms, P < 0.001). Univariate logistic regression showed slightly lower performance of the Dixon_W sequence in differentiating fibrosis (0.69 vs 0.73, P < 0.01), compensated by adding liver PDFF in the multivariate model (0.77 vs 0.75, P < 0.01).
Dixon water-only fat-corrected Look-Locker T1 mapping accurately identifies liver fibrosis and inflammation, with less dependency on liver steatosis than the widely adopted shMOLLI T1 mapping technique, which may improve its predictive value for these conditions.
本研究旨在评估一种新的 Dixon 水相校正 Look-Locker T1 映射序列（Dixon_W T1）在评估肝脏纤维化和炎症方面的鉴别能力，与标准缩短的 Modified Look-Locker Inversion Recovery（shMOLLI）序列相比，该序列可克服肝脏 T1 映射中脂肪相关混杂的限制。
对 24 名健康志愿者和 38 名经组织学证实的肝纤维化患者进行前瞻性 3T 磁共振成像，包括 2 个 T1 映射序列和质子密度脂肪分数（PDFF）。对 PDFF 截断值为 10%的有或无明显肝脂肪变性（steatosis）的参与者进行配对 Mann-Whitney 检验，对健康志愿者与早期（F0-2）和晚期（F3-4）肝纤维化以及低（A0-1）和显著（A2-3）炎症活性的患者进行非配对 Kruskal-Wallis 检验。单变量和多变量逻辑回归模型评估了肝脂肪变性对这两种序列的影响。
在无脂肪变性的参与者中，Dixon_W T1 高于 shMOLLI T1（中位数 896ms 比 890ms，P=0.04），但在有肝脂肪变性的参与者中则较低（中位数 891ms 比 973ms，P<0.001）。两种方法均能准确区分志愿者与早期和晚期纤维化（Dixon_W 849ms、910ms、947ms，P=0.011；shMOLLI 836ms、918ms、978ms，P<0.001）以及轻度和显著炎症（Dixon_W 849ms、896ms、941ms，P<0.01；shMOLLI 836ms、885ms、978ms，P<0.001）的患者。单变量逻辑回归显示 Dixon_W 序列在区分纤维化方面的性能略低（0.69 比 0.73，P<0.01），但通过在多变量模型中添加肝 PDFF 进行校正（0.77 比 0.75，P<0.01）。
Dixon 水相校正 Look-Locker T1 映射可准确识别肝纤维化和炎症，其对肝脂肪变性的依赖性低于广泛应用的 shMOLLI T1 映射技术，这可能提高其对这些疾病的预测价值。
