Abstract
Acute pancreatitis is increasing in incidence but overall mortality has remained steady in the past decade at approximately 8%.1 Death from acute pancreatitis is usually the result of multiple organ dysfunction syndrome (MODS). Like other acute inflammatory conditions, MODS in acute pancreatitis is associated with the release of cytokines, chemokines and other inflammatory mediators.2–5 Increased expression of a wide variety of mediators has been reported in patients with severe acute pancreatitis although the association between the dynamics of the cytokine response and the development of MODS or death is less clear.2 It seems that the persistence of an inflammatory response is the important factor in the pathophysiology of MODS. In a recent study of 121 patients with predicted severe acute pancreatitis,6 more than 60% of cases met the criteria for the systemic inflammatory response syndrome (SIRS). Forty-four of these patients developed MODS and this was strongly associated with persistence of SIRS for more than 48 h. Mortality overall was 11% and was confined to the small subgroup of patients with deteriorating MODS. Previous studies, based on the original Atlanta criteria,7 have grouped all patients with MODS as having ‘severe’ pancreatitis (including patients with both transient and persisting MODS) and compared these with the larger group of patients with uncomplicated attacks. These recent clinical data suggest that it is only the small subgroup of patients with deteriorating MODS in whom the inflammatory response should be considered pathological. In the remainder of patients, homeostasis is rapidly restored.6
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McKay, C.J., Buter, A. (2004). Cytokine Gene Polymorphisms in Acute Pancreatitis. In: Pancreatic Disease. Springer, London. https://doi.org/10.1007/978-1-85233-904-3_24
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DOI: https://doi.org/10.1007/978-1-85233-904-3_24
Publisher Name: Springer, London
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