Pathogenese der akuten Pankreatitis

Acute pancreatitis is characterized by the autodigestion of the pancreas by its own digestive enzymes. The pathophysiological onset of the disease occurs in the acinar cells. The normally inactive precursors of secreted proteases are prematurely activated and as a result digest the cells from within. The activation of trypsinogen to trypsin represents the key event as active trypsin activates further digestive enzymes and can therefore initiate the activation of the complete protease cascade. This premature activation of proteases results in the cell death of acinar cells and in the induction of a strong proinflammatory immune response. Cells of the innate immune system migrate into the damaged organ and potentiate the local damage again via the release of inflammatory cytokines, such as tumor necrosis factor alpha and reactive oxygen species. Concomitant to the local immune reaction, a systemic activation of the immune system also occurs, which can develop into a systemic inflammatory response syndrome (SIRS). In the course of the SIRS severe complications such as organ failure can occur. The consequence of this pronounced SIRS in the later course of the disease is a strong immunological counter-regulation, the so-called compensatory anti-inflammatory reaction syndrome (CARS). In the course of this immunosuppression commensal bacteria from the intestines can colonize the pancreatic necrosis. The outcome of the SIRS/CARS balance is decisive for the course and the prognosis of the patient.