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Pathogenic aspects of pulmonary complications in acute pancreatitis patients 被引量:47

Pathogenic aspects of pulmonary complications in acute pancreatitis patients
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摘要 BACKGROUND:Experimental and clinical observations show that proinflammatory cytokines and oxidative stress are involved in the development of local and particularly systemic complications in acute pancreatitis (AP) patients. There are often pulmonary complications in such patients. The mechanisms through which lung injury is induced in AP are not fully clear. METHODS:In order to assess the role of activated neutrophils, pro- and anti-inflammatory cytokines and adhesion molecules at the onset and development of respiratory complications and respiratory failure, we measured the serum levels of pro-inflammatory (IL-1β, IL-6, IL-8, IL-18, TNF-α) and anti-inflammatory (IL-1ra, IL-10) cytokines in 51 AP patients who had been diagnosed with pancreatitis-associated lung injury with and without the development of organ dysfunction. RESULTS:When admitted to the hospital, severe AP patients had increased concentrations of IL-1β, IL-6, IL-8, IL-18, and TNF-α. The concentration of IL-18 alone was considerably increased in the patients who later developed respiratory failure. The onset of acute respiratory distress syndrome in the AP patients was accompanied by an increase in the level of anti-inflammatory cytokines, especially IL-10. It was noted that in severe lung injury, myeloperoxidase activity in the blood increased significantly, but still reflected the processes taking place in the lung parenchyma. Increase in the concentrations of adhesion molecules preceded the development of pulmonary infiltration with respiratory failure symptoms, which provoked endothelial dysfunction and determined the capillary surface permeability for neutrophils and monocytes.CONCLUSIONS:In the pathogenesis of respiratory complications in AP cytokines, chemokines and adhesion molecules, in particular IL-1β, IL-6, IL-8, IL-18, TNF-α, ICAM-1, and E-selectin play major roles. At IL-18 concentrations >650 pg/ml, AP patients are likely to develop pulmonary dysfunction (sensitivity 58%, specificity 100%, LR-positive >58) which allows us to use it as a screening test. BACKGROUND:Experimental and clinical observations show that proinflammatory cytokines and oxidative stress are involved in the development of local and particularly systemic complications in acute pancreatitis (AP) patients. There are often pulmonary complications in such patients. The mechanisms through which lung injury is induced in AP are not fully clear. METHODS:In order to assess the role of activated neutrophils, pro- and anti-inflammatory cytokines and adhesion molecules at the onset and development of respiratory complications and respiratory failure, we measured the serum levels of pro-inflammatory (IL-1β, IL-6, IL-8, IL-18, TNF-α) and anti-inflammatory (IL-1ra, IL-10) cytokines in 51 AP patients who had been diagnosed with pancreatitis-associated lung injury with and without the development of organ dysfunction. RESULTS:When admitted to the hospital, severe AP patients had increased concentrations of IL-1β, IL-6, IL-8, IL-18, and TNF-α. The concentration of IL-18 alone was considerably increased in the patients who later developed respiratory failure. The onset of acute respiratory distress syndrome in the AP patients was accompanied by an increase in the level of anti-inflammatory cytokines, especially IL-10. It was noted that in severe lung injury, myeloperoxidase activity in the blood increased significantly, but still reflected the processes taking place in the lung parenchyma. Increase in the concentrations of adhesion molecules preceded the development of pulmonary infiltration with respiratory failure symptoms, which provoked endothelial dysfunction and determined the capillary surface permeability for neutrophils and monocytes.CONCLUSIONS:In the pathogenesis of respiratory complications in AP cytokines, chemokines and adhesion molecules, in particular IL-1β, IL-6, IL-8, IL-18, TNF-α, ICAM-1, and E-selectin play major roles. At IL-18 concentrations >650 pg/ml, AP patients are likely to develop pulmonary dysfunction (sensitivity 58%, specificity 100%, LR-positive >58) which allows us to use it as a screening test.
机构地区 Department of Surgery
出处 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2009年第2期186-192,共7页 国际肝胆胰疾病杂志(英文版)
关键词 acute pancreatitis pulmonary complications CYTOKINES adhesion molecules acute pancreatitis pulmonary complications cytokines adhesion molecules
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  • 1Xia Zhao,Marwan Dib,Ellen Andersson,Changbin Shi,Bengt Widegren,Xiangdong Wang,Roland Andersson.Alterations of Adhesion Molecule Expression and Inflammatory Mediators in Acute Lung Injury Induced by Septic and Non-septic Challenges[J]. Lung . 2005 (2)
  • 2Bettina Rau,Katja Baumgart,Colin M. Krüger,Martin Schilling,Hans G. Beger.CC-chemokine activation in acute pancreatitis: enhanced release of monocyte chemoattractant protein-1 in patients with local and systemic complications[J]. Intensive Care Medicine . 2003 (4)
  • 3Zoltán Jambrik,Mariann Gy?ngy?si,Péter Hegyi,László Czakó,Tamás Takács,András Farkas,Yvette Mándy,Csaba Góg,Dietmar Glogar,Miklós Csanády.Plasma levels of IL-6 correlate with hemodynamic abnormalities in acute pancreatitis in rabbits[J]. Intensive Care Medicine . 2002 (12)
  • 4Haraldsen P,Wang XD,Sun ZW,Lasson A,Borjesson A,Wallén R et al.Pancreatitis-associated pulmonary injury: Effects of lexipafant, a platelet-activating factor antagonist. J Organ Dysfunction . 2006
  • 5M urakami M,Arm JP,Austen KF.Cytokine regulation of mast cell protease phenotype and arachidonic acid metabolism. Annals of the New York Academy of Sciences . 1994
  • 6Bhatia M;Saluja AK;Singh VP;Frossard JL,Lee HS,Bhagat L,Gerard C,Steer ML.Complement factor C5a exerts an anti-inflammatory effect in acute pancreatitis and associated lung injury,2001.
  • 7Bhatia M,Wong F L,Cao Y,et al.Pathophysiology of acute pancreatitis. Pancreatology . 2005
  • 8Rau B,Baumgart K,Paszkowski A S,et al.Clinical relevance of caspase-1 activated cytokines in acute pancreatitis: High correlation of serum interkeukin18 with pancreatic necrosis and systemic complications. Critical Care Medicine . 2001
  • 9Bernard G R,Artigas A,Brigham K L,et al.The American-European consensus conference on ARDSAmerican Journal of Respiratory and Critical Care Medicine,1994.
  • 10Gukovskaya A S,Gukovsky I,Zaninovic V,et al.Pancreatic acinar cells produce, release, and respond to tumor necrosis factor-alpha.Role in regulating cell death and pancreatitis. The Journal of Clinical Investigation . 1997

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