Acute pancreatitis and cytokines: "second attack" by septic complication leads to organ failure

Abstract

Acute pancreatitis is accompanied by destruction and digestion of tissues, causing hypercytokinemia and hyperreactivity of leukocytes (macrophages and neutrophils) and vascular endothelial cells. As one of the biological defense mechanisms in this condition, neutrophils infiltrate vital organs such as the lung, liver, and digestive organs. When acute pancreatitis is complicated by infection, hyperreactive macrophages release a large amount of proinflammatory cytokines that activate primed neutrophils, as a "second attack." Utilizing proteolytic enzymes and oxidant, neutrophils injure the infiltrated vital organs, causing cellular damage and dysfunction of vital organs distant from the pancreas. Multiple organ failure in acute pancreatitis with septic complications can develop, at least in part, by proinflammatory cytokine release and neutrophil activation.