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Abstract
The treatment of acute pancreatitis has remained virtually unchanged for the past 50 years, in large part due to a poor understanding of the initial intracellular events. Furthermore, there is a lack of knowledge regarding the mediator(s) responsible for the progression of the disease from local pancreatic inflammation to a systemic inflammatory disease, as well as the mediator(s) responsible for distant organ dysfunction and failure. With recent advances in the pathophysiology of pancreatitis, in particular the role of the inflammatory mediators interleukin-1 β, tumour necrosis factor α and platelet-activating factor, the potential for new effective therapies has been realised. At present, a number of inflammatory mediator antagonists are being tested in humans, with the hope that we may soon develop a specific treatment for a disease, which thus far, has none.