Hanck Christoph, Schneider Alexander, Whitcomb David C
Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, PUH, University of Pittsburgh, 571 Scaife Hall, 3550 Terrace Street, Pittsburgh, PA 15261, USA.
Best Pract Res Clin Gastroenterol. 2003 Aug;17(4):613-23. doi: 10.1016/s1521-6918(03)00048-9.
Chronic, excessive alcohol consumption is clearly associated with acute and chronic pancreatitis. However, both clinical and laboratory studies have demonstrated that alcohol consumption alone does not directly cause pancreatitis. Growing evidence suggests that environmental and possibly genetic cofactors must also be present before the mechanisms protecting the pancreas from pancreatitis are circumvented and pancreatitis develops. The discovery that mutations in the cationic trypsinogen gene (R122H, N29I) predisposed to acute and chronic pancreatitis focused attention on possible genetic predispositions. Mutations in the cationic trypsinogen gene, however, are rarely associated with alcoholic chronic pancreatitis. Mutations in the SPINK1 gene (e.g. N34S) provide a threefold increased risk, and cystic fibrosis transmembrane conductance regulator (CFTR) mutations continue to be investigated. However, the major cofactor associated with alcoholic chronic pancreatitis is yet to be identified.
长期过量饮酒显然与急慢性胰腺炎相关。然而，临床和实验室研究均表明，仅饮酒并不会直接导致胰腺炎。越来越多的证据表明，在保护胰腺免受胰腺炎侵害的机制被规避且胰腺炎发生之前，环境因素以及可能的遗传辅助因素也必定存在。阳离子胰蛋白酶原基因（R122H、N29I）的突变易引发急慢性胰腺炎这一发现，使人们将注意力集中在可能的遗传易感性上。然而，阳离子胰蛋白酶原基因的突变很少与酒精性慢性胰腺炎相关。丝氨酸蛋白酶抑制剂Kazal型1（SPINK1）基因的突变（如N34S）会使患病风险增加两倍，囊性纤维化跨膜传导调节因子（CFTR）突变仍在研究中。然而，与酒精性慢性胰腺炎相关的主要辅助因素尚未确定。
