The early phase of both acute and chronic pancreatitis can be characterized by disrupt level and function of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel, decreased bicarbonate secretion, intraductal acidosis, decrease of fluid secretion and elevation of mucoprotein levels. It is almost needless to say that these intrapancreatic changes are very similar to the pathophysiological changes observed in cystic fibrosis. The aim of this mini review is to describe the development of the above mentioned pathological observations in details, moreover highlight some future therapeutic opportunities in pancreatitis.
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