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Inflammatory markers in exhaled breath condensate following lung resection for bronchial carcinoma


Jungraithmayr, W; Frings, C; Zissel, G; Prasse, A; Passlick, B; Stoelben, E (2008). Inflammatory markers in exhaled breath condensate following lung resection for bronchial carcinoma. Respirology, 13(7):1022-1027.

Abstract

BACKGROUND AND OBJECTIVE: Pulmonary resection may cause inflammatory changes with subsequent injury to the remaining lung and deterioration in respiratory function. This study investigated the pattern of serum inflammatory markers and exhaled breath condensate (EBC) in patients undergoing major lung resection due to bronchial carcinoma compared with minimally invasive thoracic surgery. METHODS: The pro-inflammatory markers IL-1-beta, IL-6, IL-8, tumor necrosis factor-alpha (TNF-alpha) and soluble intercellular adhesion molecule-1 (sICAM-1) were measured preoperatively (day -1) and on three postoperative days (day 1, 3, 7) in serum and EBC in patients after lobectomy or pneumonectomy due to bronchial carcinoma (test group) and in patients undergoing thoracoscopy with minimal wedge resection (control group). RESULTS: All mediators were detectable in serum and all but IL-8 were detectable in EBC. No patient suffered postoperative respiratory failure. In the test group, serum IL-6 was significantly higher postoperatively compared with day -1 (P < 0.001). For EBC (test group), the postoperative values of IL-1-beta were significantly higher compared with day -1 (P = 0.005). In EBC (test group), day -1 TNF-alpha and sICAM-1 were significantly higher compared with controls (P < 0.029 and P = 0.032, respectively). There was no correlation between the levels of mediators and the extent of resection. CONCLUSIONS: Pro-inflammatory markers are detected in EBC following pulmonary surgery. Mediators are detectable in both serum and EBC in patients with bronchial carcinoma undergoing pulmonary resection, but the levels are higher in EBC.

Abstract

BACKGROUND AND OBJECTIVE: Pulmonary resection may cause inflammatory changes with subsequent injury to the remaining lung and deterioration in respiratory function. This study investigated the pattern of serum inflammatory markers and exhaled breath condensate (EBC) in patients undergoing major lung resection due to bronchial carcinoma compared with minimally invasive thoracic surgery. METHODS: The pro-inflammatory markers IL-1-beta, IL-6, IL-8, tumor necrosis factor-alpha (TNF-alpha) and soluble intercellular adhesion molecule-1 (sICAM-1) were measured preoperatively (day -1) and on three postoperative days (day 1, 3, 7) in serum and EBC in patients after lobectomy or pneumonectomy due to bronchial carcinoma (test group) and in patients undergoing thoracoscopy with minimal wedge resection (control group). RESULTS: All mediators were detectable in serum and all but IL-8 were detectable in EBC. No patient suffered postoperative respiratory failure. In the test group, serum IL-6 was significantly higher postoperatively compared with day -1 (P < 0.001). For EBC (test group), the postoperative values of IL-1-beta were significantly higher compared with day -1 (P = 0.005). In EBC (test group), day -1 TNF-alpha and sICAM-1 were significantly higher compared with controls (P < 0.029 and P = 0.032, respectively). There was no correlation between the levels of mediators and the extent of resection. CONCLUSIONS: Pro-inflammatory markers are detected in EBC following pulmonary surgery. Mediators are detectable in both serum and EBC in patients with bronchial carcinoma undergoing pulmonary resection, but the levels are higher in EBC.

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6 citations in Web of Science®
6 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Division of Surgical Research
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:November 2008
Deposited On:13 Feb 2009 13:19
Last Modified:05 Apr 2016 12:58
Publisher:Wiley-Blackwell
ISSN:1323-7799
Publisher DOI:https://doi.org/10.1111/j.1440-1843.2008.01391.x
PubMed ID:18764914

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