Acute pancreatitis (AP) is a pancreatic inflammatory condition characterized by abdominal pain and increased pancreatic enzyme levels in the blood and urine, with its diagnosis relying on these two premises. Regardless of its trigger, once active the process enters the common pathway of the local and systemic inflammatory response, and severity depends on response intensity (1).The relevance of AP depends not only on potential complicated outcomes but also its high frequency -in our country an incidence of 15,000 new cases yearly was estimated, but it should be highlighted that 3.5-19% of cases experience no pain, and 13-42% are only diagnosed in necropsy studies (2). Clinical course is usually benign, and clinical signs and symptoms, as well as amylasemia/amylasuria levels, decrease within a few days; however, around 20% of cases develop complications both at the local and systemic levels, with pancreatic necrosis being most common and relevant (a good correlation exists between necrosis extent and patient outcome). AP-related mortality still affects around 10% of patients; half of deaths occur during the first two weeks, usually related to distributive shock and multiple organ failure syndrome; the rest occur later in the course of the disease and result from complications related to the development of pancreatic necrosis and its complications.The pathophysiology of AP is complex and involves several inflammatory pathways. The initial trigger is the activation within the pancreatic parenchyma of various proteolytic enzymes, usually promoted by the presence of bile and duodenal contents inside pancreatic ducts. Severe forms also exhibit a disbalance in the protease-antiprotease system, which activates the complement system with release of factor C5a, which in turn stimulates macrophage and neutrophil recruitment; this further promotes intraperitoneal inflammation and cytokine activation via transcription factors such as nuclear factor kappa B (NFκB). The release of activated cytokines involves both proinflammatory (tumor necrosis factor, interleukins IL-1, IL-6 and IL-8, and platelet-activating factor) and antiinflammatory (interleukins IL-2, IL-10 and IL-11) cytokines. Other mediators involved include arachidonic acid metabolites (prostaglandins, plateletactivating factor, and leukotrienes), nitric oxide, various proteolytic and lipolytic enzymes, and reactive oxygen metabolites, which overcome the clearing capacity of endogenous antioxidant systems. The most powerful oxygen metabolite released by leukocytes is ClOH, whereas polymorphonuclear elastase is the most destructive enzyme released (3,4). Finally, acinar damage induces the expression of endothelial adhesion molecules such as VCAM-1 (vascular cell adhesion molecule), which further amplifies the inflammatory response (5) and results in a vicious circle that determines a widespread involvement of the vascular endothelium, which in turn results in vasodilation, increased capillary permeability and interstitial edema. In fact, in most serious cases the inf...