The impact of cystic fibrosis and PSTI/SPINK1 gene mutations on susceptibility to chronic pancreatitis.
This article reviews current concepts regarding the pathobiology of cystic fibrosis pancreatic disease. It summarizes recent studies on the relationship between CFTR mutations and pancreatitis, and it reviews several unresolved issues in the field.
Cohn
Jonathan A
JA
Veterans Administration Medical Center, 508 Fulton Street, Durham, NC 27705, USA. cohn0001@mc.duke.edu
Mitchell
R Michael
RM
Jowell
Paul S
PS
D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D002908:Chronic Disease; D003550:Cystic Fibrosis / Q000453:epidemiology / Q000235:genetics* / Q000503:physiopathology; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics* / Q000378:metabolism; D020022:Genetic Predisposition to Disease; D006801:Humans; D010195:Pancreatitis / Q000453:epidemiology / Q000235:genetics* / Q000503:physiopathology; D012307:Risk Factors; 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