肝硬度，CAP可预测代偿失调

StephenW

Liver stiffness, controlled attenuation may predict decompensation
April 22, 2017

AMSTERDAM — Assessment of liver stiffness and controlled attenuation parameter may be useful as a novel predictor of decompensation, according to data presented at the International Liver Congress.

“Until recently, a sensitive diagnosis and quantification of liver steatosis was only possible through liver biopsy until the development of controlled attenuation parameter, or CAP,” Cristina Margini, MD, of the Department of Hepatology at UVCM, Inselspital, at the University of Bern, in Switzerland, said in her presentation. “CAP involves a non-invasive standardized numerical quantification of liver fat content based on the degree of ultrasound attenuation.”

Margini and colleagues hypothesized that CAP equal to or greater than 220 dB/m could predict clinical decompensation in compensated advanced chronic liver disease.

The study included 193 patients with liver stiffness equal to or greater than 10 kPa and available CAP measurements who were analyzed between September 2013 and September 2015. Margini highlighted the BMI of the cohort, which was 27.4 ± 4.6, and the Child-Pugh score of 5.4 ± 0.8.

Results indicated that 9.3% of the cohort decompensated, with nine of those events occurring from infection, seven from ascites and one each from variceal bleeding and hepatic encephalopathy. Three of those 18 patients died.

The remainder of the cohort (n = 175; 90.7%) remained compensated, with four fatalities in this group.

At baseline, liver stiffness was 33.6 ± 19.2 in the decompensated group and 19.8 ± 13.0 in those who remained compensated (P < .001).

When the researchers assessed if decompensation was associated with liver stiffness, results showed that 81 patients had stiffness equal to or greater than 13.6 kPa, 48 had stiffness between 13.6 and 21 kPa and 64 had stiffness equal to or greater than 21 kPa (K-W test P = .006). Margini reported a strong association between liver stiffness and decompensation (P < .001).

Similarly, decompensation occurred in just one patient (1.6%) among 61 patients with CAP less than 220 dB/m, and this patient had a BMI of 38 kg/m2. Among 132 patients with CAP equal to or greater than 220 dB/m, 17 (12.9%) developed decompensation.

Among 15 patients with liver stiffness equal to or greater than 21 kPa and CAP less than 220, none developed decompensation. Conversely, however, 12 of 49 patients with both liver stiffness equal to or greater than 21 kPa and CAP equal to or greater than 220 decompensated (P = .03).

Multivariable analysis results showed that among patients with liver stiffness, CAP higher than 220 dB/m significantly increased decompensation risk compared with CAP less than 220 (P = .012).


“Similar results were seen in a multivariate analysis with a CAP cutoff of 235,” Margini said.

At baseline, the researchers evaluate patients for etiology of liver disease, age, gender, BMI, laboratory tests, liver stiffness and CAP. They assessed patients for decompensation, which included ascites, variceal bleeding, jaundice, hepatic encephalopathy, hepatorenal syndrome and severe bacterial infections, along with mortality. Margini noted that 58 patients in the cohort had a viral etiology of liver disease.

“In our cohort of patients with compensated advanced liver disease, liver stiffness was strongly associated with decompensation,” Margini concluded. “CAP value over 220 in our population was significantly associated with clinical decompensation independent of liver stiffness value.” – by Rob Volansky

Reference: Margini C, et al. LBO-05. Presented at: International Liver Congress; April 19-24, 2017; Amsterdam.

Disclosure: Margini reports no relevant financial disclosures.

StephenW

肝硬度，受控衰减可预测代偿失调
2017年4月22日
肝硬度，受控衰减可预测代偿失调
AMSTERDAM - 根据国际肝脏大会提交的数据，肝硬度和受控衰减参数的评估可能有助于作为代偿失调的新型预测因子。

“直到最近，肝脏脂肪变性的敏感诊断和定量只能通过肝脏活检直到发展受控的衰减参数，或CAP，”伯明翰大学UVCM Inselpital肝脏病学系的Cristina Margini医学博士瑞士在演讲中表示。 “CAP涉及基于超声衰减程度的肝脏脂肪含量的非侵入式标准化数值定量。

Margini和同事假设CAP等于或大于220 dB / m可以预测补偿性晚期慢性肝病的临床失代偿。

该研究包括193名肝硬度等于或大于10 kPa的患者，以及2013年9月至2015年9月期间分析的可用CAP测量。Margini强调了队列的BMI，为27.4±4.6，Child-Pugh评分为5.4±0.8。

结果表明，9.3％的队列失代偿，其中9例发生于感染，7例为腹水，1例为静脉曲张出血和肝性脑病。其中三例死亡。

其余的队列（n = 175; 90.7％）仍然得到补偿，其中4人死亡。

基线时，失代偿组的肝硬度为33.6±19.2，其余均为19.8±13.0（P <0.001）。

研究人员评估失代偿与肝硬化有关时，结果显示81例患者的刚度等于或大于13.6 kPa，48例刚度在13.6〜21 kPa之间，64例刚度等于或大于21 kPa（KW检验P = .006）。 Margini报道肝硬化与代偿失调有很强的相关性（P <0.001）。

类似地，61例CAP小于220 dB / m的患者中仅有1例（1.6％）发生失代偿，该患者BMI为38 kg / m2。在132例CAP等于或大于220 dB / m的患者中，17例（12.9％）发生代偿失调。

15例肝硬度等于或大于21 kPa，CAP小于220的患者中，无发展为代偿失调。然而，相反，49例肝硬度等于或大于21 kPa，CAP等于或大于220代谢失代偿患者中的12例（P = 0.03）。

多变量分析结果显示，肝硬化患者CAP高于220 dB / m时，代谢失调风险明显高于CAP，差异有统计学意义（P = 0.012）。
Margini说：“在CAP变化为235的多变量分析中也发现了类似的结果。

在基线时，研究人员评估患者肝病的病因，年龄，性别，BMI，实验室检查，肝硬化和CAP。他们评估了代偿失调的患者，包括腹水，静脉曲张出血，黄疸，肝性脑病，肝肾综合征和严重细菌感染以及死亡率。 Margini指出，该队列中有58名患者患有肝病的病毒性病因。

Margini总结说：“在我们队列患有补偿性晚期肝病的患者中，肝硬化与代偿失调有很强的相关性。 “我们人群中超过220的CAP值与肝硬化值无关的临床失代偿显着相关。” - Rob Volansky

参考文献：Margini C，et al。 LBO-05。主讲：国际肝会; 2017年4月19日至24日阿姆斯特丹

披露：Margini报告没有相关的财务披露。