title: [Defense mechanism to prevent ectopic activation of pancreatic digestive enzymes under physiological conditions and its breakdown in acute pancreatitis].
abstract: Independent of the etiology, acute pancreatitis is associated with significant morbidity and the potential for mortality. In most patients, acute pancreatitis follows an uncomplicated or mild course. Recent studies in hereditary pancreatitis have clearly revealed that trypsin is the key enzyme at the onset of pancreatitis. However, there are several defense mechanisms to prevent ectopic activation of trypsin under physiological conditions. If the defense mechanisms failed or activation of trypsin occurred over defense ability, trypsin would activate other digestive enzymes and self-digestion of the pancreas would occur.
authors.affiliation: Third Department of Internal Medicine, University of Occupational and Environmental Health, Japan, School of Medicine.
authors.forename: Midori
authors.initials: M
authors.lastname: Kaku
authors.forename: Makoto
authors.initials: M
authors.lastname: Otsuko
mesh_terms: D000208:Acute Disease; D000818:Animals; D002352:Carrier Proteins; D002401:Cathepsin B / Q000502:physiology; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D010179:Pancreas / Q000201:enzymology*; D010195:Pancreatitis / Q000201:enzymology / Q000209:etiology* / Q000503:physiopathology; D014357:Trypsin / Q000378:metabolism; D014359:Trypsin Inhibitor, Kazal Pancreatic; D014362:Trypsinogen / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D036341:Intercellular Signaling Peptides and Proteins; C486642:SPINK1 protein, human; D014359:Trypsin Inhibitor, Kazal Pancreatic; D014362:Trypsinogen; D014357:Trypsin; D002401:Cathepsin B