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ERJ Open Res. 2019 Mar 4;5(1). pii: 00089-2018. doi: 10.1183/23120541.00089-2018. eCollection 2019 Feb.

Dysregulated alveolar function and complications in smokers following oesophagectomy.

Author information

1
Birmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK.
2
These two authors are joint first authors.
3
Birmingham Heartlands Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.
4
Warwick Medical School, University of Warwick, Coventry, UK.
5
These two authors are joint final authors.

Abstract

Acute respiratory distress syndrome (ARDS) has a significant impact on post-operative morbidity and mortality following oesophagectomy. Smoking is a risk factor for the development of ARDS, although the mechanism is unclear. We examined the effect of smoking on alveolar and systemic inflammation, in addition to alveolar-capillary permeability, leading to ARDS in patients undergoing oesophagectomy. We compared clinical, biomarker and PiCCO system data between current smokers (n=14) and ex-smokers (n=36) enrolled into a translational substudy of the BALTI-P (Beta Agonist Lung Injury Trial Prevention) trial. Current smokers compared with ex-smokers had significantly higher numbers of circulating neutrophils, elevated bronchoalveolar lavage (BAL) interleukin (IL)-1 receptor antagonist (IL-1ra), soluble tumour necrosis factor receptor-1 and pre-operative plasma soluble intercellular adhesion molecule-1, and lower BAL vascular endothelial growth factor and post-operative plasma IL-17 (p<0.05). On post-operative day 1, current smokers had higher extravascular lung water index (9.80 versus 7.90; p=0.026) and pulmonary vascular permeability index (2.09 versus 1.70; p=0.013). Current smokers were more likely to develop ARDS (57% versus 25%; p=0.031) and had a significantly reduced post-operative median survival (421 versus 771 days; p=0.023). Smoking prior to oesophagectomy is associated with dysregulated inflammation, with higher concentrations of inflammatory mediators and lower concentrations of protective mediators. This translates into a higher post-operative inflammatory alveolar oedema, greater risk of ARDS and poorer long-term survival.

Conflict of interest statement

Conflict of interest: S.T. Lugg has nothing to disclose. Conflict of interest: P.A. Howells has nothing to disclose. Conflict of interest: D. Parekh has nothing to disclose. Conflict of interest: A. Scott has nothing to disclose. Conflict of interest: R.Y. Mahida has nothing to disclose. Conflict of interest: D. Park has nothing to disclose. Conflict of interest: O. Tucker has nothing to disclose. Conflict of interest: F. Gao has nothing to disclose. Conflict of interest: G.D. Perkins has nothing to disclose. Conflict of interest: D.R. Thickett has nothing to disclose. Conflict of interest: R.C.A. Dancer has nothing to disclose. Conflict of interest: K.A. Aldridge has nothing to disclose.

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