Elshaarawy Omar, Mueller Johannes, Guha Indra Neil, Chalmers Jane, Harris Rebecca, Krag Aleksander, Madsen Bjørn Stæhr, Stefanescu Horia, Farcau Oana, Ardelean Andreea, Procopet Bogdan, Thiele Maja, Mueller Sebastian
Department of Medicine and Center for Alcohol Research, Salem Medical Center, University of Heidelberg, Zeppelinstraße 11-33, 69121 Heidelberg, Germany.
NIHR Nottingham Biomedical Research Centre, Nottingham University Hospitals NHS Trust and the University of Nottingham, Nottingham, UK.
JHEP Rep. 2019 Jun 21;1(2):99-106. doi: 10.1016/j.jhepr.2019.05.003. eCollection 2019 Aug.
BACKGROUND & AIMS: Both liver stiffness (LS) and spleen stiffness (SS) are widely used to non-invasively assess liver fibrosis and portal hypertension, respectively. We aimed to identify the impact of disease etiology, namely the localization of inflammation (portal lobular), on the SS/LS ratio.
In this multicenter study, LS and SS were prospectively assessed in 411 patients with alcohol-related liver disease (ALD) or hepatitis C virus (HCV) using FibroScan® (Echosens, Paris); changes in these parameters were also studied in response to treatment (alcohol withdrawal, HCV therapy). LS and spleen length (SL) were further analyzed in a retrospective cohort of 449 patients with long-term data on decompensation/death.
Both, SS and SL were significantly higher in HCV compared to ALD (42.0 32.6 kPa, 0.0001, 15.6 11.9 cm, 0.0001) despite a lower mean LS in HCV. Consequently, the SS to LS ratio and the SL to LS ratio were significantly higher in HCV (3.8 1.72 and 1.46 0.86, 0.0001) through all fibrosis stages. Notably, SL linearly increased with SS and the relation between SS and SL was identical in HCV and ALD. In contrast, livers were much larger in ALD at comparable LS. After treatment, LS significantly decreased in both diseases without significant changes to the SS/LS ratio. In the prognostic cohort, patients with ALD had higher LS values (30.5 21.3 kPa) and predominantly presented with jaundice (65.2%); liver failure was the major cause of death (0.01). In contrast, in HCV, spleens were larger (17.6 12.1 cm) while variceal bleeding was the major cause of decompensation (73.2%) and death (0.001).
Both SS/LS and SL/LS ratios are significantly higher in patients with portal HCV compared to lobular ALD. Thus, combined LS and SS or SL measurements provide additional information about disease etiology and disease-specific complications.
Herein, we show that patients with hepatitis C virus infection (HCV) have higher spleen stiffness and portal pressure than patients with alcohol-related liver disease (ALD), within the same fibrosis stage and matched to liver stiffness. Thus, the spleen stiffness to liver stiffness ratio is significantly higher in patients with HCV compared to ALD. Additionally, patients with HCV more commonly progress to portal hypertension-related complications ( variceal bleeding), while patients with ALD more commonly progress to liver failure ( jaundice). The spleen stiffness to liver stiffness ratio is a useful tool to confirm disease etiology and predict disease-specific complications.
肝脏硬度(LS)和脾脏硬度(SS)分别被广泛用于无创评估肝纤维化和门静脉高压。我们旨在确定疾病病因,即炎症定位(门脉性/小叶性)对SS/LS比值的影响。
在这项多中心研究中,使用FibroScan®(Echosens,巴黎)对411例酒精性肝病(ALD)或丙型肝炎病毒(HCV)患者的LS和SS进行前瞻性评估;还研究了这些参数在治疗(戒酒、HCV治疗)后的变化。在一个有失代偿/死亡长期数据的449例患者的回顾性队列中,对LS和脾脏长度(SL)进行了进一步分析。
尽管HCV患者的平均LS较低,但与ALD患者相比,HCV患者的SS和SL均显著更高(42.0对32.6 kPa,P<0.0001;15.6对11.9 cm,P<0.0001)。因此,在所有纤维化阶段,HCV患者的SS/LS比值和SL/LS比值均显著更高(3.8对1.72和1.46对0.86,P<0.0001)。值得注意的是,SL随SS呈线性增加,且SS与SL之间的关系在HCV和ALD中相同。相比之下,在相同LS水平下,ALD患者的肝脏更大。治疗后,两种疾病的LS均显著降低,而SS/LS比值无显著变化。在预后队列中,ALD患者的LS值更高(30.5对21.(此处原文可能有误,推测为21.3)kPa),主要表现为黄疸(65.2%);肝衰竭是主要死因(P = 0.01)。相比之下,在HCV患者中,脾脏更大(17.6对12.1 cm),而静脉曲张出血是失代偿(73.2%)和死亡(P = 0.001)的主要原因。
与小叶性ALD患者相比,门脉性HCV患者的SS/LS和SL/LS比值均显著更高。因此,联合测量LS和SS或SL可提供有关疾病病因和疾病特异性并发症的额外信息。
在此,我们表明,在相同纤维化阶段且与肝脏硬度匹配的情况下,丙型肝炎病毒感染(HCV)患者比酒精性肝病(ALD)患者具有更高的脾脏硬度和门静脉压力。因此,与ALD患者相比,HCV患者的脾脏硬度与肝脏硬度比值显著更高。此外,HCV患者更常进展为门静脉高压相关并发症(静脉曲张出血),而ALD患者更常进展为肝衰竭(黄疸)。脾脏硬度与肝脏硬度比值是确认疾病病因和预测疾病特异性并发症的有用工具。