2015
DOI: 10.15279/kpba.2015.20.3.115
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Mechanism of Severe Acute Pancreatitis: Focusing on Development and Progression

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Cited by 10 publications
(5 citation statements)
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“…Regardless of etiology, AP begins as an inflammatory process that is set off by the early release and activation of pancreatic enzymes in the acinar cells of the pancreas (2,3). Key factors for the progression of the process and for the development of pancreatic and extrapancreatic complications include the apoptosis of the acinar cells, release of cytokines, activation of the coagulation system, tissue ischemia, and tissue necrosis (4).…”
Section: Introductionmentioning
confidence: 99%
“…Regardless of etiology, AP begins as an inflammatory process that is set off by the early release and activation of pancreatic enzymes in the acinar cells of the pancreas (2,3). Key factors for the progression of the process and for the development of pancreatic and extrapancreatic complications include the apoptosis of the acinar cells, release of cytokines, activation of the coagulation system, tissue ischemia, and tissue necrosis (4).…”
Section: Introductionmentioning
confidence: 99%
“…Prevalence of acute pancreatitis (AP) equals approximately 10–100 cases per 100,000 people per year. Mortality rates may reach 30%, despite progress in understanding the pathogenesis and implementation of intensive care in patients with moderately severe AP (MSAP) and severe AP (SAP) [ 1 , 2 , 3 ]. AP is related to premature activation of pancreatic proenzymes causing damage to pancreas and adjacent tissues, leading to strong inflammatory response.…”
Section: Introductionmentioning
confidence: 99%
“…In part of the patients, systemic complications develop, including vascular leak syndrome and acute kidney injury (AKI). AKI occurs in nearly 15% of patients with AP and is associated with high mortality, reaching over 80% [ 2 , 3 ]. In older patients (above 60 years of age), the mortality rates in AP increase significantly [ 4 ].…”
Section: Introductionmentioning
confidence: 99%
“…In the evolution of AP, initial changes occur at the level of pancreatic cells where pancreatic enzymes are prematurely activated, which in turn causes vasoconstriction, capillary stasis, reduced oxygen saturation, increased capsular permeability and consequent pancreatic edema [1]. During the further process, leucocytes migrate to the damaged tissue and release proinflammatory cytokines, arachidonic acid metabolites, proteolytic and lipolytic enzymes.…”
Section: Introductionmentioning
confidence: 99%