Acute pancreatitis

Numerous pathophysiologic concepts and effective therapeutic trials in experimentally induced acute pancreatitis stand in opposition to inefficient therapeutic effects and missing knowledge of pathomechanisms in human acute pancreatitis, Disruption of cell cytoskeleton and tight junctions is an early event in experimental pancreatitis. Further evidence was presented that oxygen-derived free radicals and impairment of microcirculation determine the severity of pancreatitis. The role of nitric oxide and kinins has to be clarified further. The antiinflammatory cytokines interleukin-2 and interleukin-10 showed a protective effect in experimental pancreatitis. In men, a platelet-activating factor antagonist reduced the incidence of organ failure. It is hoped that these findings will lead to new therapeutic options, Chronic alcohol consumption induces subclinical pancreatic damage before the onset of acute pancreatitis. Pancreatitis-associated protein as a marker of acute pancreatic injury was significantly increased in chronic alcoholism without signs of acute pancreatitis. The mortality rate in acute pancreatitis is significantly lower in patients admitted directly rather than in patients transferred from other units 2 weeks after diagnosis. Infectious complications, surgical intervention, and mortality are reduced in patients with early antibiotic administration.