Low levels of nitric oxide and carbon monoxide in alpha 1-antitrypsin deficiency

Departments of Pulmonary and Critical Care Medicine and Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195 Quantitations of exhaled nitric oxide (NO) and carbon monoxide (CO) have been proposed as noninvasive markers of airway inflammation. We hypothesized...

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Veröffentlicht in:Journal of applied physiology (1985) 2002-12, Vol.93 (6), p.2038-2043
Hauptverfasser: Machado, Roberto F, Stoller, James K, Laskowski, Daniel, Zheng, Shuo, Lupica, Joseph A, Dweik, Raed A, Erzurum, Serpil C
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Sprache:eng
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Zusammenfassung:Departments of Pulmonary and Critical Care Medicine and Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195 Quantitations of exhaled nitric oxide (NO) and carbon monoxide (CO) have been proposed as noninvasive markers of airway inflammation. We hypothesized that exhaled CO is increased in individuals with 1 -antitrypsin (AT) deficiency, who have lung inflammation and injury related to oxidative and proteolytic processes. Nineteen individuals with 1 -AT deficiency, 22 healthy controls, and 12   patients with non- 1 -AT-deficient chronic obstructive pulmonary disease (COPD) had NO, CO, CO 2 , and O 2 measured in exhaled breath. Individuals with 1 -AT deficiency had lower levels of NO and CO than control or COPD individuals. 1 -AT-deficient and COPD patients had lower exhaled CO 2 than controls, although only 1 -AT-deficient patients had higher exhaled O 2 than healthy controls. NO was correlated inversely with exhaled O 2 and directly with exhaled CO 2 , supporting a role for NO in regulation of gas exchange. Exhaled gases were not significantly related to corticosteroid use or lung function. Demonstration of lower than normal CO and NO levels may be useful as an additional noninvasive method to evaluate 1 -AT deficiency in individuals with a severe, early onset of obstructive lung disease. airway inflammation; chronic obstructive pulmonary disease
ISSN:8750-7587
1522-1601
DOI:10.1152/japplphysiol.00659.2002