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营养状况和营养支持在乙型肝炎病毒相关慢加急性肝衰竭预后中的作用

Role of nutritional status and nutritional support in outcome of hepatitis B virus-associated acute-on-chronic liver failure.

作者信息

Chang Yue, Liu Qin-Yu, Zhang Qing, Rong Ya-Mei, Lu Cheng-Zhen, Li Hai

机构信息

Division of Gastroenterology and Hepatology, Tianjin Xiqing Hospital, Tianjin 300380, China.

Tianjin Key Laboratory of Hepatopancreatic Fibrosis and Molecular Diagnosis and Treatment, Tianjin 300162, China.

出版信息

World J Gastroenterol. 2020 Aug 7;26(29):4288-4301. doi: 10.3748/wjg.v26.i29.4288.

DOI:10.3748/wjg.v26.i29.4288
PMID:32848334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7422541/
Abstract

BACKGROUND

Hepatitis B virus-associated acute-on-chronic liver failure (HBV-ACLF) is an important type of liver failure in Asia. There is a direct relationship between HBV-ACLF and gastrointestinal barrier function. However, the nutritional status of HBV-ACLF patients has been poorly studied.

AIM

To investigate the nutritional risk and nutritional status of HBV-ACLF patients and evaluated the impact of nutritional support on the gastrointestinal barrier and 28-d mortality.

METHODS

Nutritional risk screening assessment and gastrointestinal barrier biomarkers of patients with HBV-ACLF ( = 234) and patients in the compensatory period of liver cirrhosis (the control group) ( = 234) were compared during the period between 2016 and 2018. Changes were analyzed after nutritional support in HBV-ACLF patients. Valuable biomarkers have been explored to predict 28-d death. The 28-d survival between HBV-ACLF patients with nutritional support ( = 234) or no nutritional support (2014-2016) ( = 207) was compared.

RESULTS

The nutritional risk of the HBV-ACLF patients was significantly higher than that of the control group. The nutritional intake of the patients with HBV-ACLF was lower than that of the control group. The decrease in skeletal muscle and fat content and the deficiency of fat intake were more obvious ( < 0.001). The coccus-bacillus ratio, secretory immunoglobulin A, and serum D-lactate were significantly increased in HBV-ACLF patients. The survival group had a lower nutritional risk, lower D-lactate, and cytokine levels (endotoxin, tumor necrosis factor alpha, interleukin-10, and interleukin-1). Interleukin-10 may be a potential predictor of death in HBV-ACLF patients. The 28-d survival of the nutritional support group was better than that of the non-nutritional support group ( = 0.016).

CONCLUSION

Patients with HBV-ACLF have insufficient nutritional intake and high nutritional risk, and their intestinal barrier function is impaired. Individualized and dynamic nutritional support is associated with a better prognosis of 28-d mortality in HBV-ACLF patients.

摘要

背景

乙型肝炎病毒相关性慢加急性肝衰竭(HBV-ACLF)是亚洲肝衰竭的一种重要类型。HBV-ACLF与胃肠屏障功能之间存在直接关系。然而,HBV-ACLF患者的营养状况研究较少。

目的

探讨HBV-ACLF患者的营养风险和营养状况,并评估营养支持对胃肠屏障和28天死亡率的影响。

方法

比较2016年至2018年期间HBV-ACLF患者(n = 234)和肝硬化代偿期患者(对照组)(n = 234)的营养风险筛查评估和胃肠屏障生物标志物。分析HBV-ACLF患者营养支持后的变化。探索有价值的生物标志物以预测28天死亡率。比较接受营养支持的HBV-ACLF患者(n = 234)与未接受营养支持的患者(2014 - 2016年)(n = 207)的28天生存率。

结果

HBV-ACLF患者的营养风险显著高于对照组。HBV-ACLF患者的营养摄入量低于对照组。骨骼肌和脂肪含量的降低以及脂肪摄入不足更为明显(P < 0.001)。HBV-ACLF患者的球菌杆菌比例、分泌型免疫球蛋白A和血清D-乳酸显著升高。存活组的营养风险、D-乳酸和细胞因子水平(内毒素、肿瘤坏死因子α、白细胞介素-10和白细胞介素-1)较低。白细胞介素-10可能是HBV-ACLF患者死亡的潜在预测指标。营养支持组的28天生存率优于非营养支持组(P = 0.016)。

结论

HBV-ACLF患者营养摄入不足且营养风险高,其肠道屏障功能受损。个体化和动态营养支持与HBV-ACLF患者28天死亡率的较好预后相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/64017ae6733d/WJG-26-4288-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/05ae9fea8b42/WJG-26-4288-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/8f247ec2bd8f/WJG-26-4288-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/ed459126d6b2/WJG-26-4288-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/a912da899779/WJG-26-4288-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/5411407e7911/WJG-26-4288-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/64017ae6733d/WJG-26-4288-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/05ae9fea8b42/WJG-26-4288-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/8f247ec2bd8f/WJG-26-4288-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/ed459126d6b2/WJG-26-4288-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/a912da899779/WJG-26-4288-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/5411407e7911/WJG-26-4288-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e524/7422541/64017ae6733d/WJG-26-4288-g006.jpg

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