Pathophysiology of chronic pancreatitis.
Although the most common causes of chronic pancreatitis have not changed, it has become clear that a host of modifying biochemical, inflammatory, neural, and genetic deviations allows the disease to progress. Alterations in biochemical composition allow calcific stone formation, whereas various toxins, cytokines, and neuropeptides contribute to the progression of fibrosis and pain production. The basic cellular structure contributing to fibrosis of the pancreas has been elucidated and factors responsible for its activation delineated. Of most importance is the recent recognition of a set of genetic mutations that results in several aberrations of normal pancreatic physiology, which, in conjunction with other inciting insults or by themselves, allow the disease to begin and progress.
Department of Surgery, University of Tennessee, Memphis, 910 Madison Avenue, 2nd Floor, Room 208, Memphis, TN 38163, USA. sbehrman@utmem.edu
Stephen W
SW
Behrman
Eric S
ES
Fowler
D000428:Alcohol Drinking / Q000009:adverse effects; D002114:Calcinosis / Q000209:etiology; D002352:Carrier Proteins / Q000235:genetics; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics; D005817:Genetic Counseling; D020022:Genetic Predisposition to Disease; D006801:Humans; D009154:Mutation; D010179:Pancreas / Q000473:pathology; D050500:Pancreatitis, Chronic / Q000453:epidemiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D014359:Trypsin Inhibitor, Kazal Pancreatic
C505032:CFTR protein, human; D002352:Carrier Proteins; C486642:SPINK1 protein, human; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D014359:Trypsin Inhibitor, Kazal Pancreatic