Papachristou Georgios I, Clermont Gilles, Sharma Arun, Yadav Dhiraj, Whitcomb David C
Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Gastroenterol Clin North Am. 2007 Jun;36(2):277-96, viii. doi: 10.1016/j.gtc.2007.03.003.
Acute pancreatitis begins with pancreatic injury, elicits an acute inflammatory response, and encompasses a variety of potential complications in a subset of patients. Early determination of severity and risk of complications is crucial for instituting immediate interventions to improve outcome. The severity of acute pancreatitis is a function of the amount of pancreas that is injured and the intensity of the inflammatory response. Early death is mainly linked to an overwhelming inflammatory response leading to cardiovascular collapse or acute respiratory distress syndrome, whereas late death is associated with infected pancreatic necrosis and sepsis. This article reviews recent advancements in understanding the pathogenesis, immunology, and genetics of severe acute pancreatitis, and the literature on laboratory-based markers, which predict a severe clinical course and pancreatic necrosis.
急性胰腺炎始于胰腺损伤,引发急性炎症反应,并在一部分患者中包含多种潜在并发症。早期确定严重程度和并发症风险对于立即采取干预措施以改善预后至关重要。急性胰腺炎的严重程度取决于胰腺受损的程度和炎症反应的强度。早期死亡主要与导致心血管衰竭或急性呼吸窘迫综合征的压倒性炎症反应有关,而晚期死亡则与感染性胰腺坏死和脓毒症有关。本文综述了在理解重症急性胰腺炎的发病机制、免疫学和遗传学方面的最新进展,以及关于预测严重临床病程和胰腺坏死的基于实验室指标的文献。