Mesropyan Narine, Schneider Franziska, Lutz Pia C, Katemann Christoph, Weber Oliver M, Peeters Johannes M, Dell Tatjana, Lehmann Jennifer, Pieper Claus C, Kuetting Daniel, Strassburg Christian P, Luetkens Julian A, Chang Johannes, Isaak Alexander
Department of Diagnostic and Interventional Radiology, University Hospital Bonn, Venusberg-Campus 1, Bonn, Germany (N.M., T.D., C.C.P., D.K., J.A.L., A.I.); QILaB, Quantitative Imaging Lab Bonn, University Hospital Bonn, Venusberg-Campus 1, Bonn, Germany (N.M., D.K., J.A.L., A.I.); Department of Internal Medicine I, University Hospital Bonn, Venusberg-Campus 1, Bonn, Germany (F.S., P.C.L., J.L., C.P.S., J.C.); Cirrhosis Center Bonn, University Hospital Bonn, Venusberg-Campus 1, Bonn, Germany (F.S., P.C.L., J.L., C.P.S., J.C.); Philips GmbH, Hamburg, Germany (C.K., O.M.W.); and Philips Healthcare, Best, the Netherlands (J.M.P.).
Invest Radiol. 2025 Oct 1;60(10):679-687. doi: 10.1097/RLI.0000000000001193.
The diagnostic value of hepatic native T1, extracellular volume fraction (ECV), and T2 mapping for noninvasive assessment of liver fibrosis is limited in the complex spectrum of steatotic liver disease due to confounding factors, including hepatic fat and inflammation. Therefore, this study aimed to histologically validate T1ρ mapping and compare it with conventional mapping parameters for assessing hepatic fibrosis across different animal models of steatotic liver disease.
In male Sprague-Dawley rats, different models of steatotic liver disease were induced using a high-fat diet (HFD) and carbon-tetrachloride (CCl 4 ) inhalation: (1) 12-week HFD group resulting in steatosis/steatohepatitis without fibrosis; (2) 6-week HFD + CCl 4 group resulting in steatohepatitis with fibrosis; (3) 12-week HFD + CCl 4 resulting in steatohepatitis-associated cirrhosis. Hepatic T1, ECV, T2, and T1ρ were assessed by quantitative MRI. Portal pressure was invasively measured. Hepatic fibrosis was assessed using Sirius red, alpha-smooth muscle actin (α-SMA) staining, and measurement of hydroxyproline content. Hepatic fat content was estimated in Oil red staining and triglyceride content.
Fifty-seven animals were analyzed (12-week HFD, n = 15; 6-week HFD + CCl 4 , n = 14; 12-week HFD + CCl 4 ; n = 16; controls, n = 12). T1ρ values were higher in the fibrosis groups, for example, 12-week HFD + CCl 4 versus HFD group (71 msec ±5 vs 60 msec ±3, P < 0.001). T1ρ values correlated with fibrosis markers (Sirius red r = 0.41; α-SMA: r = 0.67; hydroxyproline: r = 0.76; each P < 0.001) and portal pressure (r = 0.55, P < 0.001). T1ρ had the highest diagnostic performance for the detection of histologically defined fibrosis and invasively measured portal hypertension (eg, for fibrosis, T1ρ: AUC 0.96, P < 0.001; T1: AUC 0.74, P = 0.017; ECV: AUC 0.79, P = 0.043; T2: AUC 0.51, P < 0.001). T1ρ was an independent marker for the detection of histologically defined fibrosis (odds ratio: 3.81, P = 0.02).
In preclinical models of steatotic liver disease, T1ρ mapping could most reliably detect hepatic fibrosis and portal hypertension across different mapping parameters.
在包括肝脂肪和炎症等混杂因素的脂肪性肝病复杂谱系中，肝脏固有T1、细胞外容积分数（ECV）和T2成像对肝纤维化进行无创评估的诊断价值有限。因此，本研究旨在通过组织学方法验证T1ρ成像，并将其与传统成像参数进行比较，以评估不同脂肪性肝病动物模型中的肝纤维化情况。
在雄性斯普拉格-道利大鼠中，采用高脂饮食（HFD）和吸入四氯化碳（CCl4）诱导不同的脂肪性肝病模型：（1）12周HFD组，导致脂肪变性/脂肪性肝炎但无纤维化；（2）6周HFD + CCl4组，导致脂肪性肝炎伴纤维化；（3）12周HFD + CCl4组，导致脂肪性肝炎相关性肝硬化。通过定量MRI评估肝脏T1、ECV、T2和T1ρ。有创测量门静脉压力。使用天狼星红、α-平滑肌肌动蛋白（α-SMA）染色以及羟脯氨酸含量测量评估肝纤维化。通过油红染色和甘油三酯含量估算肝脏脂肪含量。
共分析了57只动物（12周HFD组，n = 15；6周HFD + CCl4组，n = 14；12周HFD + CCl4组，n = 16；对照组，n = 12）。纤维化组的T1ρ值更高，例如，12周HFD + CCl4组与HFD组相比（71毫秒±5对60毫秒±3，P < 0.001）。T1ρ值与纤维化标志物（天狼星红r = 0.41；α-SMA：r = 0.67；羟脯氨酸：r = 0.76；各P < 0.001）和门静脉压力（r = 0.55，P < 0.001）相关。T1ρ在检测组织学定义的纤维化和有创测量的门静脉高压方面具有最高的诊断性能（例如，对于纤维化，T1ρ：AUC 0.96，P < 0.001；T1：AUC 0.74，P = 0.017；ECV：AUC 0.79，P = 0.043；T2：AUC 0.51，P < 0.001）。T1ρ是检测组织学定义的纤维化的独立标志物（优势比：3.81，P = 0.02）。
在脂肪性肝病的临床前模型中，T1ρ成像在不同成像参数中最能可靠地检测肝纤维化和门静脉高压。
