[Pathogenetic concepts of chronic pancreatitis].
Summary. The understanding of the pathogenesis of chronic pancreatitis is limited. Several theories (i. e. obstruction hypothesis) were suggested in the past but could not be confirmed by experimental data. As a formal description of the course of the disease, the necrosis-fibrosis concept seems to be very attractive. According to this theory, there is no significant difference in the pathogenesis of acute and chronic pancreatitis. A major step was the identification of mutations of the cationic trypsinogen, the secretory trypsin inhibitor (SPINK 1) and the cystic-fibrosis protein (CFTR) in some patients. Investigation of these mutations may significantly contribute to a better understanding of the pathogenesis of chronic pancreatitis.
Teich
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Medizinische Klinik und Poliklinik II, Universität Leipzig, Germany.
Keim
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D000328:Adult; D002908:Chronic Disease; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics; D005355:Fibrosis; D006801:Humans; D009154:Mutation; D009336:Necrosis; D010179:Pancreas / Q000473:pathology; D010190:Pancreatic Neoplasms / Q000209:etiology / Q000235:genetics; D010195:Pancreatitis / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D012307:Risk Factors; D014361:Trypsin Inhibitors / Q000235:genetics; D014362:Trypsinogen / Q000235:genetics
C505032:CFTR protein, human; D014361:Trypsin Inhibitors; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D014362:Trypsinogen