Molecular basis for pancreatitis.
OBJECTIVE
This timely review will focus on clinical and basic science studies that have greatly advanced our knowledge of the molecular mechanisms of both acute pancreatitis and chronic pancreatitis over the last year.


RESULTS
Animal models of both severe acute pancreatitis and chronic pancreatitis have recently been developed. Several unexpected protective mechanisms, mediated by the protease activated receptor 2 and heat shock protein 70, have been described. A genetic study suggested that polymorphisms in toll-like receptor-4 might affect the risk of developing infections in acute pancreatitis. Studies of chronic pancreatitis have shown that specific neural receptors, transient receptor potential vanilloid subtype 1, mediate pain responses in a model of chronic pancreatitis. The pancreatic zymogen, chymotrypsin C, can degrade pathologically activated trypsin in the acinar cell. Inactivating mutations in chymotrypsin C have been reported to predispose to the development of chronic pancreatitis, especially in those who are prone to alcohol abuse.


CONCLUSIONS
The implications of the last year's findings are widespread. Improved animal models of acute pancreatitis and chronic pancreatitis will be critical for performing pilot studies of therapy. A greater understanding of genetic factors and pain responses could lead to potential treatments. This review will first discuss issues related to acute pancreatitis, and then conclude with studies most relevant to chronic disease.
Thrower
Edwin
E
Department of Internal Medicine, Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT, USA.
Husain
Sohail
S
Gorelick
Fred
F
D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D008967:Molecular Biology; D019283:Pancreatitis, Acute Necrotizing / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D019512:Pancreatitis, Alcoholic / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D050500:Pancreatitis, Chronic / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D011379:Prognosis; D018570:Risk Assessment; D012680:Sensitivity and Specificity