酒精和胰腺

S Schenker, R Montalvo
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引用次数: 57

摘要

酒精性胰腺炎可能是酒精滥用最严重的不良后果之一。它的诊断,正如多年来一样,主要依赖于临床对腹部窘迫症状和体征的正确解释,并以胰腺酶(淀粉酶和脂肪酶)升高为依据。最近,在特定情况下使用计算机断层扫描(CT)已具有确认和预后价值。CT异常的严重程度与各种临床-实验室分类(APACHE系统、Ranson标准等)和辅助治疗有相当好的相关性。酒精性胰腺炎的发病机制尚未完全明确。最终的图像是被激活的蛋白水解酶的组织自溶。然而,这种激活的触发因素尚不清楚。主要有三种理论:(1)胰管梗阻较大和/或相对于胰腺分泌的通透性增加,(2)蛋白质沉淀物引起的胰管梗阻较小,以及(3)乙醇对胰腺腺泡细胞的直接毒性代谢作用。虽然不是相互排斥的,但我们倾向于最后一种假设,因为它与乙醇对其他器官系统的影响最一致。乙醇和/或其代谢物的直接作用可通过氧化应激或脂肪酸乙酯的生成介导,至少部分介导。自溶(无论其近似机制如何)可能通过释放各种细胞因子介导导致炎症。还应该认识到,“急性”胰腺炎(本章的主题)可能代表了酒精滥用引起的慢性胰腺暴露和损伤的急性过程。为什么胰腺炎只发生在少数酒精滥用者的关键问题还没有解决。治疗取决于酒精性胰腺炎的严重程度,这是由临床-实验室和CT标准确定的。轻度胰腺炎通常在戒酒和支持性治疗下急性消退。重症胰腺炎具有显著的发病率和死亡率,主要与胰腺坏死程度和感染程度有关。它需要细致的内外科结合护理。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Alcohol and the pancreas.

Alcoholic pancreatitis may be one of the most serious adverse consequences of alcohol abuse. Its diagnosis, as it has for many years, depends primarily on clinical acumen in interpreting properly the symptoms and signs of abdominal distress, buttressed by elevated pancreatic enzymes (amylase and lipase). More recently, the use of computerized tomography (CT) in selected situations has been both of confirmatory and prognostic value. Severity of abnormality by CT correlates reasonably well with a variety of clinical-laboratory clusters (APACHE system, Ranson's criteria, etc.) and aids in therapy. The pathogenesis of alcoholic pancreatitis is not fully defined. The ultimate picture is one of tissue autolysis by activated proteolytic enzymes. The triggers for such activation, however, are still not known. They are represented by three main theories: (1) large duct obstruction and/or increased permeability relative to pancreatic secretion, (2) small duct obstruction due to proteinaceous precipitates, and (3) a direct toxic-metabolic effect of ethanol on pancreatic acinar cells. While not mutually exclusive, we favor the last hypothesis as being most consistent with the effects of ethanol on other organ systems. The direct effects of ethanol and/or its metabolites may be mediated, at least in part, via oxidative stress or the generation of fatty acid ethyl esters. Autolysis (regardless of proximate mechanism(s)) leads to inflammation likely mediated via release of various cytokines. It also should be appreciated that "acute" pancreatitis (the topic of this chapter) likely represents an acute process within a chronic pancreatic exposure and injury from alcoholic abuse. The key question of why pancreatitis develops in only a small number of alcohol abusers is not resolved. Therapy depends on the severity of alcoholic pancreatitis, which is defined by clinical-laboratory and often CT criteria. Mild pancreatitis usually resolves acutely with alcohol abstention and supportive therapy. Severe pancreatitis has a significant morbidity and mortality, mainly related to the degree of pancreatic necrosis and infection. It requires meticulous combined medical-surgical care.

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