肝衰竭并发急性胰腺炎的机制及预防

陆星宇; 杨晶; 李盼; 彭建平

doi:10.12449/JCH240434

肝衰竭并发急性胰腺炎的机制及预防

DOI: 10.12449/JCH240434

湖南中医药大学第一附属医院肝病科，长沙 410000

基金项目:

湖南省自然科学基金项目 (2022JJ30458);

长沙市科技计划项目 (kq2202451)

利益冲突声明：本文不存在任何利益冲突。

作者贡献声明：陆星宇、彭建平参与起草和修改文章关键内容；李盼、杨晶对研究的思路有关键贡献。

详细信息

通信作者:
彭建平， jppeng@126.com （ORCID： 0009-0001-2437-9153）

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出版历程
- 收稿日期: 2023-08-17
- 录用日期: 2023-09-13
- 出版日期: 2024-04-25

Mechanism and prevention of liver failure complicated by acute pancreatitis

Department of Hepatology，The First Affiliated Hospital of Hunan University of Chinese Medicine，Changsha 410000，China

Research funding:

Natural Science Foundation of Hunan Province (2022JJ30458);

Science and Technology Plan Project of Changsha (kq2202451)

More Information

Corresponding author: PENG Jianping， jppeng@126.com （ORCID： 0009-0001-2437-9153）

摘要

摘要: 肝衰竭病情进展快，并发症多，病情十分凶险。在肝衰竭发展过程中，并发急性胰腺炎十分常见；而急性胰腺炎的临床症状及体征与肝衰竭并发自发性腹膜炎极其相似，易被忽略。本文通过炎症反应、十二指肠乳头功能障碍、肠道菌群失调、氧化应激、微循环障碍等5个方面对肝衰竭并发急性胰腺炎的机制进行阐述，并根据其作用机制提出相应预防手段。
- 肝功能衰竭 /
- 胰腺炎，急性坏死性 /
- 病理过程 /
- 早期医疗干预
Abstract: Liver failure often has rapid progression， multiple complications， and dangerous conditions. Acute pancreatitis is a common comorbidity during the progression of liver failure， and since acute pancreatitis has extremely similar clinical symptoms and signs to liver failure complicated by spontaneous peritonitis， it is often neglected in clinical practice. This article elaborates on the mechanisms of liver failure complicated by acute pancreatitis from the five aspects of inflammatory response， duodenal papillary dysfunction， gut microbiota dysbiosis， oxidative stress， and microcirculatory disturbance and proposes corresponding preventive measures based on these mechanisms.
- Liver Failure /
- Pancreatitis， Acute Necrotizing /
- Pathologic Processes /
- Early Medical Intervention

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图 1 肝衰竭并发急性胰腺炎的炎症反应机制

Figure 1. Inflammatory reaction of liver failure complicated with acute pancreatitis

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图 2 肝衰竭并发急性胰腺炎的氧化应激反应机制

Figure 2. Mechanism of oxidative stress in liver failure complicated with acute pancreatitis

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表 1 肝衰竭过程中细胞因子对胰腺的作用

Table 1. Effect of cytokines on pancreas during liver failure

细胞因子	作用机制
IL-1β	通过改变Ca²⁺稳态失衡诱导胰蛋白酶活化并降低胰腺腺泡细胞的细胞活力^［6］；诱导炎性细胞产生IL-6、IL-18、TNF-α等，介导炎症反应等过程^［7］
IL-6	通过gp130蛋白激活JAK-STAT信号通路诱导胰腺炎的发生^［8］；IL-6激活胰腺腺泡细胞中STAT-3磷酸化，增加急性胰腺炎的严重程度
IL-18	协同IL-12诱导IFN-γ的生成，从而提升T淋巴细胞以及NK细胞的功能；激活MAPK和PI3K/AKT信号通路，导致大量细胞因子的产生，进一步加剧了炎症损害^［9］
IL-33	触发腺泡释放炎症因子，使得急性胰腺炎病情加重；诱导IL-6及IL-8等炎症因子的产生，介入炎症反应^［10］
TNF-α	刺激NF-κB信号通路的激活，有助于炎症反应的全身性进展^［11］。激活T淋巴细胞，促进炎症因子释放，诱发炎症反应^［12］
MCP-1	诱导单核细胞的趋化与激活，使其积极参与免疫应答^［13］
MIF	激活MAPK、NF-κB信号通路，刺激巨噬细胞产生IL-1、IL-6、IL-12、TNF等炎症因子^［14］
ICAM-1	其通过激活白细胞和血管内皮细胞的黏连与聚集过程，从而增加微血管的通透性，引致血管内皮的损害，形成微循环障碍^［15］
ROS	激活JNK、NF-κB、MAPK、AP-1信号通路，诱导IL-1、IL-6、TNF-α、iNOS等炎症因子产生^［16］
注：MCP-1，单核细胞趋化蛋白-1；ROS，活性氧；ICAM-1，细胞间黏附分子-1。

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