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急性胰腺炎的发病机制

Author
Santhi Swaroop Vege, MD
Section Editor
David C Whitcomb, MD, PhD
Deputy Editor
Shilpa Grover, MD, MPH, AGAF

引言

急性胰腺炎是一种以腹痛和血胰酶水平升高为临床特征的胰腺炎症性疾病。已知有多种情况都可引发急性胰腺炎，虽然致病可能性各不相同。但该病的发病机制尚不完全明确。

本专题将重点介绍人们目前对急性胰腺炎发病机制的理解。与急性胰腺炎有关的病因将单独讨论。 (参见“急性胰腺炎的病因”)

动物模型

研究者为探索急性胰腺炎的发病机制而建立了许多动物模型[1]，但皆未严格对应人类的发病情况。例如，75%的人类急性胰腺炎都是由胆石和酗酒所致，但未能在任何动物模型中重现。此外，动物模型中常用的胰腺炎诱导药物(如蛙皮素和无胆碱乙硫氨酸饲料)均不是公认的人类急性胰腺炎病因。

但急性胰腺炎早期的结构和生化改变在各种动物模型中都高度一致，而且人类急性胰腺炎中也发现了相似的改变。此外，不论激发事件为何，人类急性胰腺炎的临床和病理学特点都非常相似。

因此，尽管动物模型存在局限性，但从中得出的数据表明：胰腺炎发生后会产生相似的级联事件，其与激发事件或初始机制无关。动物实验表明，除非实施预防性治疗或在激发事件后数小时内开始治疗，否则不可成功地阻断这种级联事件。这些研究没有阐明为何部分患者仅为间质性或水肿性胰腺炎，而其他患者发展为坏死性胰腺炎。

               

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Literature review current through: 2017-06 . | This topic last updated: 2016-08-10.
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