Systemic inflammatory effects of acute pancreatitis; effects of lipid mediators

摘要

Acute pancreatitis is a serious autodigestive and inflammatory process frequently associated with a broad spectrum of systemic complications. It has been long believed those activated hydrolases released from the damaged pancreas gain access to the systemic circulation and are responsible for the induction of the damage in distant organs. However, initial acinar cell damage results in the release of activated hydrolases, but also of inflammatory mediators, altogether leading to the systemic inflammatory response. Between the hydrolases released by pancreas, lipase acts inducing the necrosis of peripancreatic and peritoneal fat tissue. This enzyme hydrolyses triacylglycerols and results in the generation of free fatty acids that could be modified by the oxidative environment generated during pancreatitis. These oxidised fatty acids could interfere on the activity of nuclear receptors, thus promoting an exacerbated inflammatory response in the severe forms of acute pancreatitis.