[Inflammatory pancreatic disease due to enzyme autodigestion: an exceptional model of glandular crinophagy].
The exocrine pancreas is a functionally dangerous structure since it is exposed to digestion by its most aggressive enzymes (proteases, etc) despite self-protective measures such as the synthesis of some of these enzymes in the form of inactive zymogens (trypsinogen, etc.). We review inflammatory pancreatic disease by separately analyzing its classical forms of onset: acute and chronic pancreatitis (AP and CP). There is general consensus that the initial pathogenic event in AP is intraacinar activation of trypsinogen into trypsin, followed by that of the remaining proenzymes, giving rise to an unusual model of autophagic inflammation. In contrast, consensus is lacking on the initial pathogenic event in CP (toxic-metabolic lesion, oxidative stress, ductal hypertension, etc.?), although in some cases a <<necrosis-fibrosis>> sequence due to recurrent episodes of AP seems evident. The pathogenic features shared by both forms of the disease and which justify some recent attempts to formulate an overall explanation of the pathogenesis of pancreatitis are discussed. Such an explanation would place both forms of pancreatitis within the conceptual framework of an <<inflammatory pancreatic disease due to enzyme autodigestion>>.
Servicio de Aparato Digestivo, Fundación Jiménez Díaz, Universidad Autónoma, Madrid, España. Palomasanchezfayos@wanadoo.es
P
P
Sánchez-Fayos Calabuig
M Jesús
MJ
Martín Relloso
Agustina
A
González Guirado
Juan Carlos
JC
Porres Cubero
D000208:Acute Disease; D005355:Fibrosis; D006801:Humans; D010179:Pancreas / Q000473:pathology; D010195:Pancreatitis / Q000201:enzymology / Q000209:etiology* / Q000473:pathology; D050500:Pancreatitis, Chronic / Q000201:enzymology / Q000209:etiology / Q000473:pathology