严重急性胰腺炎中的炎症和免疫抑制。
Inflammation and immunosuppression in severe acute pancreatitis.
机构信息
Department of Surgery, University of Helsinki, PL 340, 00029 HUS, Helsinki, Finland.
出版信息
World J Gastroenterol. 2010 Jun 21;16(23):2867-72. doi: 10.3748/wjg.v16.i23.2867.
Acute pancreatitis (AP) is a common disease, which usually exists in its mild form. However, in a fifth of cases, the disease is severe, with local pancreatic complications or systemic organ dysfunction or both. Because the development of organ failure is the major cause of death in AP, early identification of patients likely to develop organ failure is important. AP is initiated by intracellular activation of pancreatic proenzymes and autodigestion of the pancreas. Destruction of the pancreatic parenchyma first induces an inflammatory reaction locally, but may lead to overwhelming systemic production of inflammatory mediators and early organ failure. Concomitantly, anti-inflammatory cytokines and specific cytokine inhibitors are produced. This anti-inflammatory reaction may overcompensate and inhibit the immune response, rendering the host at risk of systemic infection. At present, there is no specific treatment for AP. Increased understanding of the pathogenesis of systemic inflammation and development of organ dysfunction may provide us with drugs to ameliorate physiological disturbances.
急性胰腺炎(AP)是一种常见疾病,通常以轻症形式存在。然而,在五分之一的病例中,疾病较为严重,出现局部胰腺并发症或全身器官功能障碍,或两者兼有。由于器官衰竭的发展是 AP 患者死亡的主要原因,因此早期识别可能发生器官衰竭的患者很重要。AP 是由胰腺酶原的细胞内激活和胰腺自身消化引发的。胰腺实质的破坏首先在局部引发炎症反应,但可能导致炎症介质的全身性过度产生和早期器官衰竭。同时,也会产生抗炎细胞因子和特定的细胞因子抑制剂。这种抗炎反应可能过度代偿并抑制免疫反应,使宿主面临全身感染的风险。目前,AP 尚无特异性治疗方法。对全身炎症和器官功能障碍发病机制的深入了解可能为我们提供改善生理紊乱的药物。