Hepatology:肝脏硬度可预测癌症、肝功能衰竭及死亡率

2012-07-25 T.Shen 生物谷

近日,来自西班牙的研究者表示,通过瞬时弹性成像(TE)的方法确定的肝脏硬度是肝功能衰竭、肝细胞癌(HCC)以及HIV、HCV相关的疾病死亡的重要预测标准。相关研究成果刊登在了7月份的国际杂志Hepatology上。 据WHO数据,慢性HCV(慢性丙肝)在世界范围内影响着超过1.7亿人的健康,而且每年超过350,000病人因为HCV相关的疾病而死亡。WHO报告说,2010年有3400万感染了HIV

近日,来自西班牙的研究者表示,通过瞬时弹性成像(TE)的方法确定的肝脏硬度是肝功能衰竭、肝细胞癌(HCC)以及HIV、HCV相关的疾病死亡的重要预测标准。相关研究成果刊登在了7月份的国际杂志Hepatology上。

据WHO数据,慢性HCV(慢性丙肝)在世界范围内影响着超过1.7亿人的健康,而且每年超过350,000病人因为HCV相关的疾病而死亡。WHO报告说,2010年有3400万感染了HIV。

文章中,研究者从2006年2月,开展了一项同时感染HIV和HCV的硬化病人的多中心的前瞻性研究,通过TE方法,研究者分析了239个共感染病人代偿性肝硬化的预测价值。

参与者随后进行了9-34个月的长期研究,13%的病人最后发展为肝功能衰竭(代偿失调),代谢失常的发生率一般为100人中有6.7例。医学证据显示,西部国家中,慢性HCV引发的晚期肝病是HIV感染者死亡的主要原因。对于晚期肝病的患者来说,移植是唯一的治疗选择。早期肝硬化的发现以及最优化的疗法至关重要。研究者的研究发现揭示了肝脏硬度可以预测肝功能衰竭以及肝脏相关疾病死亡的风险(患者仅限通知书感染HIV和HCV的个体)。

研究者最后指出,后期深入研究将评估是否肝脏硬度可以作为失代偿肝硬化的一个独立的预后标准,这将结合肝脏移植病人的CTD和MELD分数来判定。

编译自:Liver Stiffness Predicts Liver Failure, Cancer and Mortality

doi:10.1002/hep.25616
PMC:
PMID:

Liver stiffness predicts clinical outcome in human immunodeficiency virus/hepatitis C virus-coinfected patients with compensated liver cirrhosis†

Nicolás Merchante1,‡,*, Antonio Rivero-Juárez2, Francisco Téllez3, Dolores Merino4, Maria José Ríos-Villegas5, Manuel Márquez-Solero6, Mohamed Omar7, Juan Macías1, Ángela Camacho2, Montserrat Pérez-Pérez3, Jesús Gómez-Mateos1, Antonio Rivero2, Juan Antonio Pineda1,§,*, on behalf of the Grupo Andaluz para el Estudio de las Hepatitis Víricas (HEPAVIR) de la Sociedad Andaluza de Enfermedades Infecciosas (SAEI)1 .

Our aim was to assess the predictive value of liver stiffness (LS), measured by transient elastography (TE), for clinical outcome in human immunodeficiency virus / hepatitis C virus (HIV/HCV)-coinfected patients with compensated liver cirrhosis. This was a prospective cohort study of 239 consecutive HIV/HCV-coinfected patients with a new diagnosis of cirrhosis, done by TE, and no previous decompensation of liver disease. The time from diagnosis to the first liver decompensation and death from liver disease, as well as the predictors of these outcomes, were evaluated. After a median (Q1-Q3) follow-up of 20 (9-34) months, 31 (13%, 95% confidence interval [CI]: 9%-17%) patients developed a decompensation. The incidence of decompensation was 6.7 cases per 100 person-years (95% CI, 4.7-9-6). Fourteen (8%) out of 181 patients with a baseline LS < 40 kPa developed a decompensation versus 17 (29%) out of 58 with LS ≥ 40 kPa (P = 0.001). Factors independently associated with decompensation were Child-Turcotte-Pugh (CTP) class B versus A (hazard ratio [HR] 7.7; 95% CI 3.3-18.5; P < 0.0001), log-plasma HCV RNA load (HR 2.1; 95% CI 1.2-3.6; P = 0.01), hepatitis B virus coinfection (HR, 10.3; 95% CI, 2.1-50.4; P = 0.004) and baseline LS (HR 1.03; 95% CI 1.01-1.05; P = 0.02). Fifteen (6%, 95% CI: 3.5%-9.9%) patients died, 10 of them due to liver disease, and one underwent liver transplantation. CTP class B (HR 16.5; 95% CI 3.4-68.2; P < 0.0001) and previous exposure to HCV therapy (HR 7.4; 95% CI 1.7-32.4, P = 0.007) were independently associated with liver-related death; baseline LS (HR 1.03; 95% CI 0.98-1.07; P = 0.08) was of borderline significance. Conclusion: LS predicts the development of hepatic decompensations and liver-related mortality in HIV/HCV-coinfection with compensated cirrhosis and provides additional prognostic information to that provided by the CTP score. (HEPATOLOGY 2012;56:228–238)

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    2012-07-27 gwc384