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Pancreatic triglyceride lipase mediates lipotoxic systemic inflammation.胰腺甘油三酯脂肪酶介导脂毒性全身炎症。
J Clin Invest. 2020 Apr 1;130(4):1931-1947. doi: 10.1172/JCI132767.
2
Tobacco smoking and the risk of pancreatitis: A systematic review and meta-analysis of prospective studies.吸烟与胰腺炎风险:前瞻性研究的系统评价和荟萃分析。
Pancreatology. 2019 Dec;19(8):1009-1022. doi: 10.1016/j.pan.2019.09.004. Epub 2019 Sep 11.
3
Transgenic Expression of PRSS1 Sensitizes Mice to Pancreatitis.PRSS1 的转基因表达使小鼠易患胰腺炎。
Gastroenterology. 2020 Mar;158(4):1072-1082.e7. doi: 10.1053/j.gastro.2019.08.016. Epub 2019 Aug 13.
4
Risk Stratification and Early Conservative Treatment of Acute Pancreatitis.急性胰腺炎的风险分层与早期保守治疗
Visc Med. 2019 Apr;35(2):82-89. doi: 10.1159/000497290. Epub 2019 Mar 25.
5
The multifaceted contributions of mitochondria to cellular metabolism.线粒体对细胞代谢的多方面贡献。
Nat Cell Biol. 2018 Jul;20(7):745-754. doi: 10.1038/s41556-018-0124-1. Epub 2018 Jun 27.
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The Combination of Alcohol and Cigarette Smoke Induces Endoplasmic Reticulum Stress and Cell Death in Pancreatic Acinar Cells.酒精与香烟烟雾的联合作用诱导胰腺腺泡细胞内质网应激和细胞死亡。
Gastroenterology. 2017 Dec;153(6):1674-1686. doi: 10.1053/j.gastro.2017.08.036. Epub 2017 Aug 25.
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Genome-wide association study identifies inversion in the locus to modify risk for alcoholic and non-alcoholic chronic pancreatitis.全基因组关联研究鉴定出 基因座的倒位可改变酒精性和非酒精性慢性胰腺炎的风险。
Gut. 2018 Oct;67(10):1855-1863. doi: 10.1136/gutjnl-2017-314454. Epub 2017 Jul 28.
8
Validation of Demographics, Etiology, and Risk Factors for Chronic Pancreatitis in the USA: A Report of the North American Pancreas Study (NAPS) Group.美国慢性胰腺炎人口统计学、病因学及风险因素的验证:北美胰腺研究(NAPS)小组报告
Dig Dis Sci. 2017 Aug;62(8):2133-2140. doi: 10.1007/s10620-017-4621-z. Epub 2017 Jun 9.
9
Length of Variable Numbers of Tandem Repeats in the Carboxyl Ester Lipase (CEL) Gene May Confer Susceptibility to Alcoholic Liver Cirrhosis but Not Alcoholic Chronic Pancreatitis.羧基酯酶(CEL)基因中可变串联重复序列的长度可能与酒精性肝硬化易感性相关,但与酒精性慢性胰腺炎无关。
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10
Lysosome associated membrane proteins maintain pancreatic acinar cell homeostasis: LAMP-2 deficient mice develop pancreatitis.溶酶体相关膜蛋白维持胰腺腺泡细胞内稳态:LAMP-2缺陷小鼠会发生胰腺炎。
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我们目前对酒精性胰腺炎的病理生理学了解多少:简要综述。

What Do We Currently Know about the Pathophysiology of Alcoholic Pancreatitis: A Brief Review.

作者信息

Żorniak Michał, Sirtl Simon, Mayerle Julia, Beyer Georg

机构信息

Medical Department II, University Hospital, LMU Munich, Munich, Germany.

Department of Gastroenterology, Medical University of Silesia, Katowice, Poland.

出版信息

Visc Med. 2020 Jun;36(3):182-190. doi: 10.1159/000508173. Epub 2020 Jun 10.

DOI:10.1159/000508173
PMID:32775348
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7383280/
Abstract

BACKGROUND

Alcoholic pancreatitis is a serious medical concern worldwide and remains to be one of the common causes of pancreatic disease.

SUMMARY

While alcohol consumption causes direct damage to pancreatic tissue, only a small percentage of active drinkers will develop pancreatitis. An explanation of this phenomenon is probably that alcohol increases pancreatic vulnerability to damage; however, the simultaneous presence of additional risk factors and pancreatic costressors is required to increase the risk of pancreatitis and its complications caused by alcohol misuse. Recently, a number of important genetic as well as environmental factors influencing the risk of alcoholic pancreatitis have been described.

KEY MESSAGES

In brief, this review reports established factors for the development of alcoholic pancreatitis and summarizes recent progress made in basic and clinical research.

摘要

背景

酒精性胰腺炎是全球范围内严重的医学问题,仍是胰腺疾病的常见病因之一。

总结

虽然饮酒会对胰腺组织造成直接损伤,但只有一小部分经常饮酒者会患上胰腺炎。这种现象的一种解释可能是酒精会增加胰腺对损伤的易感性;然而,需要同时存在其他风险因素和胰腺协同应激源,才能增加因酒精滥用导致胰腺炎及其并发症的风险。最近,已经描述了一些影响酒精性胰腺炎风险的重要遗传和环境因素。

关键信息

简而言之,本综述报告了酒精性胰腺炎发生的既定因素,并总结了基础和临床研究的最新进展。