Witt Heiko, Apte Minoti V, Keim Volker, Wilson Jeremy S
Department of Hepatology and Gastroenterology, Charité, Campus Virchow-Klinikum, Universitätsmedizin Berlin, Berlin, Germany.
Gastroenterology. 2007 Apr;132(4):1557-73. doi: 10.1053/j.gastro.2007.03.001.
Chronic pancreatitis (CP) is characterized by progressive pancreatic damage that eventually results in significant impairment of exocrine as well as endocrine functions of the gland. In Western societies, the commonest association of chronic pancreatitis is alcohol abuse. Our understanding of the pathogenesis of CP has improved in recent years, though important advances that have been made with respect to delineating the mechanisms responsible for the development of pancreatic fibrosis (a constant feature of CP) following repeated acute attacks of pancreatic necroinflammation (the necrosis-fibrosis concept). The pancreatic stellate cells (PSCs) are now established as key cells in fibrogenesis, particularly when activated either directly by toxic factors associated with pancreatitis (such as ethanol, its metabolites or oxidant stress) or by cytokines released during pancreatic necroinflammation. In recent years, research effort has also focused on the genetic abnormalities that may predispose to CP. Genes regulating trypsinogen activation/inactivation and cystic fibrosis transmembrane conductance regulator (CFTR) function have received particular attention. Mutations in these genes are now increasingly recognized for their potential 'disease modifier' role in distinct forms of CP including alcoholic, tropical, and idiopathic pancreatitis. Treatment of uncomplicated CP is usually conservative with the major aim being to effectively alleviate pain, maldigestion and diabetes, and consequently, to improve the patient's quality of life. Surgical and endoscopic interventions are reserved for complications such as pseudocysts, abscess, and malignancy.
慢性胰腺炎（CP）的特征是胰腺进行性损伤，最终导致该腺体的外分泌和内分泌功能严重受损。在西方社会，慢性胰腺炎最常见的相关因素是酗酒。近年来，我们对慢性胰腺炎发病机制的理解有所提高，尽管在明确反复急性胰腺坏死性炎症发作（坏死-纤维化概念）后导致胰腺纤维化（慢性胰腺炎的一个持续特征）发展的机制方面取得了重要进展。胰腺星状细胞（PSC）现已被确立为纤维化形成中的关键细胞，特别是当它直接被与胰腺炎相关的毒性因子（如乙醇、其代谢产物或氧化应激）或胰腺坏死性炎症期间释放的细胞因子激活时。近年来，研究工作也集中在可能易患慢性胰腺炎的基因异常上。调节胰蛋白酶原激活/失活的基因和囊性纤维化跨膜传导调节因子（CFTR）功能受到了特别关注。这些基因的突变现在越来越被认为在包括酒精性、热带性和特发性胰腺炎在内的不同形式的慢性胰腺炎中具有潜在的“疾病修饰”作用。单纯性慢性胰腺炎的治疗通常是保守的，主要目的是有效缓解疼痛、消化不良和糖尿病，从而提高患者的生活质量。手术和内镜干预适用于诸如假性囊肿、脓肿和恶性肿瘤等并发症。
