TITLE:Chronic pancreatitis: challenges and advances in pathogenesis, genetics, diagnosis, and therapy.
AUTHOR:Witt H, Apte MV, Keim V, Wilson JS.
RESOURCE:Gastroenterology. 2007 Apr;132(4):1557-73.
ABSTRACT:
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.
PMID: 17466744
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初译：
TITLE:Chronic pancreatitis: challenges and advances in pathogenesis, genetics, diagnosis, and therapy. 慢性胰腺炎在发病、遗传、诊断、治疗上的进展和挑战
AUTHOR: Witt H, Apte MV, Keim V, Wilson JS.
RESOURCE: Gastroenterology. 《胃肠病学》2007 Apr;132(4):1557-73.
ABSTRACT: 摘要：
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.
慢性胰腺炎以胰腺的进展性损伤为特征，最终导致腺体的内外分泌功能显著损害。在西方国家，导致慢性胰腺炎最常见的因素为酒精滥用。
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.
虽然慢性胰腺炎重要的进展在于阐述反复急性胰腺坏死性炎症（坏死－纤维化观点）后胰囊性纤维化（慢性胰腺炎的永久特性）的发生机制方面，但最近几年我们对于慢性胰腺炎发病机理的理解已有所更新。胰脏的星状细胞现在已经被认为是在纤维形成中的关键性细胞，特别是在与胰腺炎相关的毒性因子（如酒精的代谢产物或氧化剂应激物）或在胰脏坏死性炎症时释放细胞因子的直接激活情况下。
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.
最近一些年来，研究成就也集中在遗传异常方面，其可能是造成慢性胰腺炎的因素。基因调节胰蛋白酶原激活/失活以及囊性纤维化跨膜通道调节因子功能已经受到特别的关注。这些基因上的突变现在已经逐渐被认为是慢性胰腺炎不同形式（包括酒精性胰腺炎，热带胰腺炎以及自发性胰腺炎）的潜在疾病调节角色。
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.
非复杂性慢性胰腺炎的治疗总是主要采用有效保守手段减轻疼痛，治疗消化不良以及糖尿病，从而提高患者的生活质量。
Surgical and endoscopic interventions are reserved for complications such as pseudocysts, abscess, and malignancy.
手术和内窥镜干预可能产生如假性囊肿，脓肿以及恶性肿瘤的并发症。
PMID: 17466744
编译投稿：
共507字
【据《胃肠病学》2007年4月报道】题：慢性胰腺炎在发病、遗传、诊断、治疗上的进展和挑战（作者Witt等）
慢性胰腺炎以胰腺的进展性损伤为特征，最终导致腺体的内外分泌功能显著损害。在西方国家，导致慢性胰腺炎最常见的因素为酒精滥用。虽然慢性胰腺炎重要的进展在于阐述反复急性胰腺坏死性炎症（坏死－纤维化观点）后胰囊性纤维化（慢性胰腺炎的永久特性）的发生机制方面，但最近几年我们对于慢性胰腺炎发病机理的理解已有所更新。胰脏的星状细胞现在已经被认为是在纤维形成中的关键性细胞，特别是在与胰腺炎相关的毒性因子（如酒精的代谢产物或氧化剂应激物）或在胰脏坏死性炎症时释放细胞因子的直接激活情况下。最近一些年来，研究成就也集中在遗传异常方面，其可能是造成慢性胰腺炎的因素。基因调节胰蛋白酶原激活/失活以及囊性纤维化跨膜通道调节因子功能已经受到特别的关注。这些基因上的突变现在已经逐渐被认为是慢性胰腺炎不同形式（包括酒精性胰腺炎，热带胰腺炎以及自发性胰腺炎）的潜在疾病调节角色。非复杂性慢性胰腺炎的治疗总是主要采用有效保守手段减轻疼痛，治疗消化不良以及糖尿病，从而提高患者的生活质量。手术和内窥镜干预可能产生如假性囊肿，脓肿以及恶性肿瘤的并发症。
