Role of Biomarkers in Diagnosis and Prognostic Evaluation of Acute Pancreatitis

Figure 1

Schematic overview of pathogenesis of acute pancreatitis. Acinar cell damage leads to activation of trypsin following impairment of cell membrane trafficking with subsequent activation of zymogen cascade by trypsin. Attraction and activation of leukocyte occur with release of many proinflammatory and anti-inflammatory cytokines and also chemokines. An overt and sustained activation of proinflammatory mediators leads to Systemic Inflammatory Response Syndrome (SIRS) which may further proceed to multiorgan failure and infection of pancreatic necrosis and sepsis with late complications of acute pancreatitis [32, 33].