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Acute pancreatitis

机译:急性胰腺炎

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摘要

Acute pancreatitis begins as acute pancreatic injury and may generate a systemic inflammatory response that evolves into multiorgan failure, leading to death. Multiple inciting factors such as toxins (alcohol), gallstones, or endoscopic retrograde cholangiopancreatography result in a cascade of events beginning with the intra-acinar activation of zymogens and the release of cytokines and other proinflammatory mediators. Their release is a major determinant of the systemic inflammatory response and distant organ failure. Attempts to attenuate the severity of acute pancreatitis by blocking specific inflammatory mediators have had limited success. This review is divided into experimental acute pancreatitis and clinical acute pancreatitis. The distinction is maintained because although animal models of disease have helped define the pathogenesis of acute pancreatitis, they do not completely reproduce the clinical syndrome of human acute pancreatitis or guarantee equal success of therapies in humans. < copyright > 2002 Lippincott Williams & Wilkins, Inc.
机译:急性胰腺炎始于急性胰腺损伤,并可能产生全身性炎症反应,演变成多器官衰竭,导致死亡。多种刺激因素,例如毒素(酒精),胆结石或内窥镜逆行胰胆管造影术,会导致一系列事件,从酶原的糖内激活,细胞因子和其他促炎介质的释放开始。它们的释放是全身炎症反应和远处器官衰竭的主要决定因素。通过阻断特定的炎症介质来减轻急性胰腺炎的严重程度的尝试取得了有限的成功。这篇综述分为实验性急性胰腺炎和临床急性胰腺炎。之所以保持这种区别,是因为尽管疾病的动物模型已经帮助定义了急性胰腺炎的发病机制,但是它们并不能完全重现人类急性胰腺炎的临床综合征或保证人类疗法的同等成功。 <版权> 2002 Lippincott Williams&Wilkins,Inc.

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