Serge Chooklin1. 1. Department of Surgery, Medical University, Lviv, Ukraine. chooklin_serge@hotmail.com
Abstract
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-1 beta, IL-6, IL-8, IL-18, TNF-alpha) and anti-inflammatory (IL-1 ra, 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-1 beta, IL-6, IL-8, IL-18, and TNF-alpha. 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-1 eta, IL-6, IL-8, IL-18, TNF-alpha, 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-1 beta, IL-6, IL-8, IL-18, TNF-alpha) and anti-inflammatory (IL-1 ra, 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-1 beta, IL-6, IL-8, IL-18, and TNF-alpha. 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-1 eta, IL-6, IL-8, IL-18, TNF-alpha, 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.
Authors: Christos Skouras; Zoe A Davis; Joanne Sharkey; Rowan W Parks; O James Garden; John T Murchison; Damian J Mole Journal: HPB (Oxford) Date: 2015-11-18 Impact factor: 3.647