Acute pancreatitis

Acute pancreatitis is associated with a significant morbidity and a mortality as high as 10%. This review summarizes the most relevant articles in the past year that have contributed to understanding and management of this disease.

Pathologic activation of both digestive zymogens and the transcription factor nuclear factor kappaB are early events in acute pancreatitis; these pathologic processes are inhibited in experimental pancreatitis by curcumin and the pH modulator chloroquine. Primary sensory neurons may constitute a final common pathway for pancreatic inflammation. Experimental acute pancreatitis and associated lung injury are attenuated by inhibiting the prostanoid mediators cyclo-oxygenase-2 and 5-lipoxygenase and CC chemokine receptor antagonist Met-RANTES. Endoscopic retrograde cholangiopancreatography-induced acute pancreatitis can be reduced experimentally by intraductal neurokinin-1 receptor antagonist and clinically by use of diclofenac and pancreatic duct stenting. MRI in the setting of acute pancreatitis is a reliable method of staging disease severity. Distinct patterns of cytokine response are observed in acute pancreatitis.

Early events within the acinar cell and the regulation of inflammation by transcription factors continue to be elucidated. Although experimental acute pancreatitis can be successfully ameliorated by use of cytokine and inflammatory inhibitors, this has not been demonstrated in clinical disease. The finding of a compartmentalization of the inflammatory response in acute pancreatitis may be important for planning therapeutic interventions. Pancreatic duct stenting reduces the risk of developing postendoscopic retrograde cholangiopancreatography pancreatitis in high-risk people.