INFLAMMATORY MEDIATORS IN ACUTE-PANCREATITIS

The cellular events leading to acute pancreatitis are not well defined and the mechanism by which known aetiological factors initiate the di sease process remains to be established. Inflammatory mediators have r ecently been implicated as potential early markers of disease severity and may help elucidate the pathophysiology of the disease. Oxidative stress is emerging as a common effector of the acinar cell injury in e xperimental acute pancreatitis and clinical findings indicate that neu trophil activation is a significant early event. In common with neutro phil-mediated tissue damage in states of tissue hypoperfusion, acute p ancreatitis shows many features of an ischaemia-reperfusion injury. In creased levels of phospholipase A(2) have been demonstrated; this enzy me induces synthesis of prostaglandins and platelet-activating factor, a potent inflammatory mediator. New therapeutic approaches to the com plications of acute pancreatitis may be through manipulation of such m ediators of inflammation.