Published online May 21, 2014. doi: 10.3748/wjg.v20.i19.5801
Revised: March 12, 2014
Accepted: April 8, 2014
Published online: May 21, 2014
Acute pancreatitis is an inflammatory disorder of the pancreas that may cause life-threatening complications. Etiologies of pancreatitis vary, with gallstones accounting for the majority of all cases, followed by alcohol. Other causes of pancreatitis include trauma, ischemia, mechanical obstruction, infections, autoimmune, hereditary, and drugs. The main events occurring in the pancreatic acinar cell that initiate and propagate acute pancreatitis include inhibition of secretion, intracellular activation of proteases, and generation of inflammatory mediators. Small cytokines known as chemokines are released from damaged pancreatic cells and attract inflammatory cells, whose systemic action ultimately determined the severity of the disease. Indeed, severe forms of pancreatitis may result in systemic inflammatory response syndrome and multiorgan dysfunction syndrome, characterized by a progressive physiologic failure of several interdependent organ systems. Stress occurs when homeostasis is threatened, and stressors can include physical or mental forces, or combinations of both. Depending on the timing and duration, stress can result in beneficial or harmful consequences. While it is well established that a previous acute-short-term stress decreases the severity of experimentally-induced pancreatitis, the worsening effects of chronic stress on the exocrine pancreas have received relatively little attention. This review will focus on the influence of both prior acute-short-term and chronic stress in acute pancreatitis.
Core tip: Depending on the timing and duration, stress can result in beneficial or harmful consequences. Regarding the exocrine pancreas, a previous acute-short-term stress decreases the severity of experimentally-induced pancreatitis. This protection is conferred by distinct heat shock proteins (HSP) including HSP27, HSP60 and HSP70. Conversely, chronic stress increases the susceptibility of the exocrine pancreas, aggravating pancreatitis episodes. These worsening effects are mainly mediated by tumor necrosis factor alpha.