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Bimodal peaks of liver stiffness in a case of drug-induced liver injury

机译:药物性肝损伤中肝脏僵硬的双峰峰

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A 69-year-old male complained of general fatigue and presented with elevation of liver enzymes without any cause of liver injury. We diagnosed him with hepatocellular drug-induced liver injury (DILI). Liver stiffness, which was evaluated according to the shear wave velocity (SWV) using virtual touch tissue quantification, was serially observed during hospitalization. A fast SWV was noted on the date of admission, indicating a hard degree of liver stiffness. The SWV gradually decreased until the 20th hospital day. However, the patient's liver enzymes again became elevated on the 20th hospital day, and the SWV simultaneously increased in association with a rise in the total bilirubin level. The laboratory data for the second peak of the SWV indicated mixed-type DILI; therefore, the patient's pathological state transitioned from the hepatocellular type to the mixed type. A liver biopsy performed before discharge revealed a state of recovery from acute inflammation without fibrotic changes. We conclude that the second peak of the SWVmay be affected by the presence of intrahepatic cholestasis. We herein report the occurrence of bimodal peaks of liver stiffness in a patient with DILI. In such cases, each peak of liver stiffness may be the result of a different pathological mechanism, namely acute inflammation versus acute intrahepatic cholestasis. Although the detailed mechanisms underlying the development of liver stiffness due to intrahepatic cholestasis remain unclear, this case presented a limitation of virtual touch tissue quantification for evaluation of liver stiffness as fibrosis marker in the liver with intrahepatic cholestasis.
机译:一名69岁的男性主诉总体疲劳,并表现出肝酶升高而没有任何肝损伤的原因。我们诊断出他患有肝细胞药物性肝损伤(DILI)。在住院期间连续观察肝硬度,该硬度根据切波速度(SWV)使用虚拟触摸组织定量进行评估。入院时发现有快速的SWV,表明肝脏僵硬程度较重。 SWV逐渐下降,直到第20住院日。但是,患者的肝酶在医院第20天再次升高,并且SWV与总胆红素水平的升高同时升高。 SWV的第二个峰的实验室数据表明为混合型DILI。因此,患者的病理状态从肝细胞型转变为混合型。出院前进行的肝活检显示从急性炎症中恢复的状态没有纤维化变化。我们得出结论,SWV的第二个高峰可能受到肝内胆汁淤积的影响。我们在此报告了DILI患者肝硬度双峰的发生。在这种情况下,肝脏僵硬的每个高峰可能是不同病理机制的结果,即急性炎症与急性肝内胆汁淤积。尽管尚不清楚由肝内胆汁淤积导致的肝脏僵硬发展的详细机制,但该病例显示了虚拟触摸组织定量方法的局限性,无法评估肝内胆汁淤积性肝中作为肝纤维化标志物的肝硬度。

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