Nagar Anil B, Gorelick Fred S
Section of Digestive Diseases, Department of Medicine, West Haven Veteran's Administration Hospital, Yale University, West Haven, Connecticut 06516-2700, USA.
Curr Opin Gastroenterol. 2002 Sep;18(5):552-7. doi: 10.1097/00001574-200209000-00005.
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.
急性胰腺炎始于急性胰腺损伤，并可能引发全身炎症反应，进而发展为多器官功能衰竭，导致死亡。多种诱发因素，如毒素（酒精）、胆结石或内镜逆行胰胆管造影术，会引发一系列事件，始于腺泡内酶原的激活以及细胞因子和其他促炎介质的释放。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。通过阻断特定炎症介质来减轻急性胰腺炎严重程度的尝试取得的成功有限。本综述分为实验性急性胰腺炎和临床急性胰腺炎两部分。之所以保持这种区分，是因为尽管疾病的动物模型有助于明确急性胰腺炎的发病机制，但它们并不能完全重现人类急性胰腺炎的临床综合征，也不能保证治疗方法在人类身上同样成功。
