<Review>Pathophysiology and treatment of acute pancreatitis

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Acute pancreatitis is a protean disease capable of wide clinical variation, ranging from mild discomfort to lethal prostration. This variability in presentation and clinical course has plagued the study and management of acute pancreatitis since its original clinical description. Currently, the most widely accepted view as to the mechanism of acute pancreatitis is that the earliest events in acute pancreatitis most likely involve acinar cells and that the earliest evidence of injury occurs in acinar cells themselves. The secretion of digestive enzyme is blocked and colocalization of digestive zymogens and lysosomal hydrolases such as cathepsin B might result in intracellular digestive enzyme activation during the early stages of diet and secretagogue-induced pancreatitis. Moreover, disarray of pancreatic acinar microtubules may be involved in this process. In the case of biliary pancreatitis, the promoting effect on pancreatic secretion by bile acids may trigger the disorder. In addition, intraductal hypertension within the pancreas has been suggested to play an important role in its exacerbation. Regarding remote organ failure in acute severe pancreatitis, the presence of hepatotoxic factors in ascitic fluid as well as the involvement of macrophages in pulmonary dysfunction has been found. Transforming growth factor-beta (TGF-beta) was observed in the asitic fluid by Western blotting analysis using anti-TGF-beta antibody, and the hepatocytocidal effect of ascitic fluid was blocked by anti-TGF-beta antibody. CRP, alpha2-macroglobulin, trypsin activated protein are useful for evaluation of the severity of acute pancreatitis, the serum level of trypsin protein esterase activity was also a striking marker for both prognosis and severity of acute pancreatitis. Pancreatic, hepatic and systemic hemodynamics in the early phase of acute pancreatitis was also studied in dogs. These findings showed that the decreased cardiac output was caused by a decrease in preload, and decrease in gastroduodenal arterial flow was mainly caused by an increase in vascular resistence due to an increase in hematocrit. Moreover a decrease in superior pancreatico-duodenal venous flow revealed that there was a severely depressive outflow from the pancreas because of hemorrhage and destruction of pancreatic parenchyma immediatedly after the onset of pancreatitis. Peritoneal lavage as well as plasma exchange has been certified to be of clinical significance as the special treatment of acute pancreatitis. Necrosectomy and postoperative continuous local lavage have been proved to be effective surgical approaches for necrotizing pancreatitis, but the use of a major pancreatic resection for the surgical management of necrotizing pancreatitis should be excluded from treatment protocols because of its higher morbidity and mortality.
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<Review>Pathophysiology and treatment of acute pancreatitis

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