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- W4385563308 abstract "Acute pancreatitis is initiated by premature intracellular activation of zymogens and perpetuated by an overwhelming inflammatory response triggered by the disintegrating often necrotic pancreatic tissue. Whether the extent of zymogen activation in the exocrine pancreas determines severity of the disease or whether other mechanisms drive the organ over the edge to fall prey to its own digestive capacity is still a matter of debate. However, an initially primarily sterile inflammatory disorder can proceed to microbial superinfection of the pancreatic necrosis which frequently results in multiorgan failure and is closely associated with a rise in mortality. Mortality in severe acute pancreatitis peaks at two different time points: patients either pass away during the first 7 days after the onset of pain from an overwhelming inflammatory response syndrome resulting in multiorgan failure (approx. 30%) or they die late in the disease course facilitated by a compensatory anti-inflammatory response syndrome which permits translocation of gut bacteria into pancreatic necrosis which results in uncontrollable sepsis and again persistent multiorgan failure. Within this chapter the pathophysiology of individual organ failure during the course of pancreatitis is reviewed." @default.
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- W4385563308 date "2023-08-04" @default.
- W4385563308 modified "2023-09-27" @default.
- W4385563308 title "Molecular, Biochemical, and Metabolic Abnormalities of Acute Pancreatitis" @default.
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- W4385563308 doi "https://doi.org/10.1002/9781119876007.ch16" @default.
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