Acute pancreatitis. Export

@article{citeulike:1030315, abstract = {PURPOSE OF REVIEW: This review presents advances in our understanding of the pathobiologic responses of acute pancreatitis from studies using animal models of experimental pancreatitis as well as results of key clinical trials and observations. RECENT FINDINGS: The reports during the past year show significant advances in our understanding of the pathobiology of acute pancreatitis. In particular, there are findings presented that are relevant to our further understanding of pancreatic intracellular digestive enzyme activation; the pancreatic inflammatory response; and cell death responses such as necrosis as apoptosis. Other reports add to understanding of the control of microcirculatory disturbances in acute pancreatitis, and of the role of the pancreatic neural system in regulating the microcirculation as well as the pain associated with the disorder. Finally, there are clinical trials showing benefits of enteral feeding on outcome of acute pancreatitis as well as the finding that diclofenac prevents endoscopic retrograde cholangiopancreatography-induced pancreatitis. SUMMARY: Our understanding of the mechanistic processes that mediate the pathobiologic responses of pancreatitis is rapidly evolving. In addition, we now have initial evidence for potential treatment strategies for this disorder. Testing treatment strategies will lead to improved therapies and outcomes for patients with acute pancreatitis.}, address = {VA Greater Los Angeles Healthcare System, West Los Angeles Healthcare Center, Building 258 Room 340, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. Stephen.Pandol@med.va.gov}, author = {Pandol, S. J.}, citeulike-article-id = {1030315}, citeulike-linkout-0 = {http://dx.doi.org/10.1097/01.mog.0000239861.89209.5f}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/16891878}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=16891878}, doi = {10.1097/01.mog.0000239861.89209.5f}, issn = {0267-1379}, journal = {Curr Opin Gastroenterol}, keywords = {acute, pancreatitis}, month = {September}, number = {5}, pages = {481--486}, posted-at = {2009-01-31 00:48:28}, priority = {3}, title = {Acute pancreatitis.}, url = {http://dx.doi.org/10.1097/01.mog.0000239861.89209.5f}, volume = {22}, year = {2006} }

TY - JOUR ID - citeulike:1030315 L3 - citeulike-article-id:1030315 N2 - PURPOSE OF REVIEW: This review presents advances in our understanding of the pathobiologic responses of acute pancreatitis from studies using animal models of experimental pancreatitis as well as results of key clinical trials and observations. RECENT FINDINGS: The reports during the past year show significant advances in our understanding of the pathobiology of acute pancreatitis. In particular, there are findings presented that are relevant to our further understanding of pancreatic intracellular digestive enzyme activation; the pancreatic inflammatory response; and cell death responses such as necrosis as apoptosis. Other reports add to understanding of the control of microcirculatory disturbances in acute pancreatitis, and of the role of the pancreatic neural system in regulating the microcirculation as well as the pain associated with the disorder. Finally, there are clinical trials showing benefits of enteral feeding on outcome of acute pancreatitis as well as the finding that diclofenac prevents endoscopic retrograde cholangiopancreatography-induced pancreatitis. SUMMARY: Our understanding of the mechanistic processes that mediate the pathobiologic responses of pancreatitis is rapidly evolving. In addition, we now have initial evidence for potential treatment strategies for this disorder. Testing treatment strategies will lead to improved therapies and outcomes for patients with acute pancreatitis. IS - 5 JF - Curr Opin Gastroenterol SN - 0267-1379 AD - VA Greater Los Angeles Healthcare System, West Los Angeles Healthcare Center, Building 258 Room 340, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. Stephen.Pandol@med.va.gov EP - 486 TI - Acute pancreatitis. VL - 22 SP - 481 KW - acute KW - pancreatitis AU - Pandol, SJ PY - 2006/09// UR - http://dx.doi.org/10.1097/01.mog.0000239861.89209.5f ER -