[Acute pancreatitis: recent advances in understanding its pathophysiology]

This article reviews the recent changes in the understanding of acute pancreatitis pathophysiology emphasizing results deriving from the more detailed comprehension of the local and systemic aspects of the inflammatory process. The authors briefly discuss those theories that have been influencing the basic philosophies of treatment efforts. The role of premature digestive enzyme activation as the principal determinant of the pathoetiology and mortality of this disease has been questioned lately, and the inflammatory explosion has been placed into the center of attention. Simultaneously with the enzyme activation, the pancreatitogenic noxious event rapidly induces the formation of oxygen derived free radicals, activation of the transcription factor NF kappa-B, with consequent citokine production, cellular adhesion molecule upregulation and leukocyte hyperstimulation. Numerous other mediator cascades are activated in parallel, the uncontrolled surge of proinflammatory stimuli, and activity of the effector cells lead to multiple organ failure in severe cases. A genetically determined catastrophe management program is set forth in the acinar cell with pancreatitis associated protein expression and activation of the apoptosis machinery. Therapeutic approaches based on these recent findings are briefly touched upon.