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肌肉减少症和肌内脂肪变性在经颈静脉肝内门体分流术后显性肝性脑病发展和死亡率中的作用。

Contributory roles of sarcopenia and myosteatosis in development of overt hepatic encephalopathy and mortality after transjugular intrahepatic portosystemic shunt.

机构信息

Department of Interventional Radiology, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230022, Anhui Province, China.

Infection Hospital, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230000, Anhui Province, China.

出版信息

World J Gastroenterol. 2023 May 14;29(18):2875-2887. doi: 10.3748/wjg.v29.i18.2875.

DOI:10.3748/wjg.v29.i18.2875
PMID:37274064
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10237102/
Abstract

BACKGROUND

Skeletal muscle abnormalities, such as muscle mass depletion (sarcopenia) and fatty infiltration of the muscle (myosteatosis), are frequent complications in cirrhotic patients scheduled for transjugular intrahepatic portosystemic shunt (TIPS).

AIM

To investigate the association and predictive value of sarcopenia and myosteatosis for overt hepatic encephalopathy (HE) and mortality after TIPS.

METHODS

The records of cirrhotic patients who underwent the TIPS procedure at our hospital between January 2020 and June 2021 were retrospectively retrieved. The transversal psoas muscle thickness (TPMT) and psoas muscle attenuation (PMA) measured from the unenhanced abdominal computed tomography (CT) at the level of the third lumbar vertebrae were used to analyze the sarcopenia and myosteatosis, respectively. The area under curve (AUC) was used to evaluate the discriminative power of TPMT, PMA, and relevant clinical parameters. Fur-thermore, log-rank test was performed to compare the incidence of overt HE and survival between the different groups, and the association of risk factors with overt HE and mortality was analyzed using Cox proportional hazards regression models.

RESULTS

A total of 108 patients were collected. Among these patients, 45.4% of patients developed overt HE after TIPS treatment. Furthermore, 32.4% and 28.7% of these patients were identified to have myosteatosis and sarcopenia, respectively. Myosteatosis (51.0% 16.9%, < 0.001) and sarcopenia (40.8 18.6%, = 0.011) were found to be more frequent in patients with overt HE, when compared to patients without overt HE. The receiver operating characteristics analysis indicated that the predictive power of TPMT and PMA in overt HE (AUC = 0.713 and 0.778, respectively) was higher when compared to the neutrophil lymphocyte ratio (AUC = 0.636). The cumulative incidence of overt HE was the highest in patients with concomitant sarcopenia and myosteatosis, followed by patients with myosteatosis or sarcopenia, while this was the lowest in patients without sarcopenia and myosteatosis. In addition, sarcopenia and myosteatosis were inde-pendently associated with overt HE and mortality after adjusting for confounding factors in post-TIPS patients.

CONCLUSION

CT-based estimations for sarcopenia and myosteatosis can be used as reliable predictors for the risk of developing overt HE and mortality in cirrhotic patients after TIPS.

摘要

背景

骨骼肌异常,如肌肉质量减少(肌肉减少症)和肌肉脂肪浸润(肌脂病),是接受经颈静脉肝内门体分流术(TIPS)治疗的肝硬化患者常见的并发症。

目的

研究肌肉减少症和肌脂病与 TIPS 后显性肝性脑病(HE)和死亡率的相关性及其预测价值。

方法

回顾性检索 2020 年 1 月至 2021 年 6 月在我院接受 TIPS 治疗的肝硬化患者的病历。使用未增强腹部 CT 测量第三腰椎水平的横截面积比 (TPMT) 和比衰减值 (PMA) 分别分析肌肉减少症和肌脂病。使用曲线下面积 (AUC) 评估 TPMT、PMA 和相关临床参数的区分能力。此外,对数秩检验用于比较不同组之间显性 HE 和生存的发生率,使用 Cox 比例风险回归模型分析危险因素与显性 HE 和死亡率的关系。

结果

共纳入 108 例患者。这些患者中,45.4%在 TIPS 治疗后发生显性 HE。此外,这些患者中有 40.8%和 28.7%分别存在肌脂病和肌肉减少症。与无显性 HE 的患者相比,显性 HE 患者的肌脂病(51.0%比 16.9%, < 0.001)和肌肉减少症(40.8%比 18.6%, = 0.011)更为常见。受试者工作特征分析表明,与中性粒细胞与淋巴细胞比值(AUC = 0.636)相比,TPMT 和 PMA 对显性 HE 的预测能力更高(AUC = 0.713 和 0.778)。伴有肌肉减少症和肌脂病的患者显性 HE 的累积发生率最高,其次是仅存在肌脂病或肌肉减少症的患者,而无肌肉减少症和肌脂病的患者最低。此外,在 TIPS 后患者中,调整混杂因素后,肌肉减少症和肌脂病与显性 HE 和死亡率独立相关。

结论

CT 估计的肌肉减少症和肌脂病可用作 TIPS 后肝硬化患者发生显性 HE 和死亡率的可靠预测指标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b85d/10237102/f7f30b7a11e1/WJG-29-2875-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b85d/10237102/400cd1afb0e0/WJG-29-2875-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b85d/10237102/400cd1afb0e0/WJG-29-2875-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b85d/10237102/384cb87be200/WJG-29-2875-g002.jpg
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