[Factors involved in the pathogenesis of acute pancreatitis]

Pathophysiological and molecular research have marked the understanding of the primary events taking place in triggering acute pancreatitis, although the early diagnosis of pancreas diseases in general, continues to be a source of frustration in modem medicine. This presents the news about pathogenesis (co-localization theory, auto-activation theory of the tripsynogen), location of early events (acinar pancreatic cells which are the "key" involved: muscarinic receptors, acinar membrane, role of ionized calcium, the phenomenon of apoptosis), extracellular events in initiation of acute pancreatitis with the granting of a central place to enzyme activation and systemic inflammatory response. Aspects of early microvascular changes, disturbances of ischemia-reperfusion and systemic microvascular abnormalities are so important that justifies therapeutic concept of microcirculatory protection. Participation of monocyte/macrophage system, excessive activation of leukocytes that involving activation and release of lysosomal enzymes and oxygen free radicals associated with ischemia-reperfusion mechanism are defining for pathogenesis of acute pancreatitis.