Can exhaled nitric oxide differentiate causes of pulmonary fibrosis?

Guilleminault, L.; Saint-Hilaire, A.; Favelle, O.; Caille, Agnès; Boissinot, E; Henriet, Arango; Diot, Patrice; Marchand-Adam, S.

doi:10.1016/j.rmed.2013.07.007

Cited by 20 publications

(29 citation statements)

References 33 publications

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“…Tiev et al (2013) obtained similar results to ours in a very recent study of a population of patients with pulmonary fibrosis associated with systemic sclerosis, in whom increased Calv NO in exhaled breath was associated with severe reduction in TLC and TLCO. Although FeNO at 50 ml/s is recognized as a central airways parameter, its elevation in IPF patients has also been reported by Guilleminault et al (2013), with values comparable to ours, suggesting that elevated alveolar concentrations of NO could drive the increased levels measured at all flow rates.…”

Section: No and Lung Function Testssupporting

confidence: 90%

Exhaled nitric oxide in interstitial lung diseases

Cameli¹,

Bargagli²,

Refini³

et al. 2014

Respiratory Physiology & Neurobiology

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Nitric oxide (NO) is a biomarker of nitrosative stress, which is involved in the pathogenesis of idiopathic interstitial pneumonias (IIP). This study evaluates exhaled NO levels in IIP patients and relates alveolar concentrations of NO (CalvNO) to pulmonary function test (PFT) and 6-minute walking test (6MWT) parameters. We measured fractional exhaled nitric oxide (FeNO), CalvNO and maximum conducting airway wall flux (J'awNO) in 30 healthy subjects and 30 patients with IIP (22 idiopathic pulmonary fibrosis and 8 idiopathic non-specific interstitial pneumonias). IIP patients had higher FeNO at flow rates of 50-100-150 ml/s and higher CalvNO levels than healthy controls (p<0.0001). CalvNO was significantly correlated with 6-minute walking distance (p<0.0001), recovery time (p<0.0005), TLC (p<0.001), FVC (p=0.01) and TLCO (p<0.01). IIP patients showed abnormal nitric oxide production, probably due to lung fibrosis and oxidative-mediated lung injury. CalvNO was correlated with PFT and 6MWT parameters and is proposed as a potential biomarker of lung fibrosis and exercise tolerance.

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Section: No and Lung Function Testssupporting

confidence: 90%

Exhaled nitric oxide in interstitial lung diseases

Cameli¹,

Bargagli²,

Refini³

et al. 2014

Respiratory Physiology & Neurobiology

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“…The HRCT findings that best differentiate chronic HP from NSIP and IPF include the presence of lobular areas with decreased attenuation and vascularity, centrilobular nodules, and lack of lower zone predominance of abnormalities . Interestingly, it has been recently suggested that high FeNO levels could help to differentiate chronic HP from other types of pulmonary fibrosis . HP should also be considered in patients diagnosed with NSIP, as a NSIP pattern without granulomas can be the only pathologic finding of HP .…”

Section: Diagnosismentioning

confidence: 99%

Occupational hypersensitivity pneumonitis: an EAACI position paper

Quirce

Vandenplas

Campo

et al. 2016

Allergy

154

109

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The aim of this document was to provide a critical review of the current knowledge on hypersensitivity pneumonitis caused by the occupational environment and to propose practical guidance for the diagnosis and management of this condition. Occupational hypersensitivity pneumonitis (OHP) is an immunologic lung disease resulting from lymphocytic and frequently granulomatous inflammation of the peripheral airways, alveoli, and surrounding interstitial tissue which develops as the result of a non-IgE-mediated allergic reaction to a variety of organic materials or low molecular weight agents that are present in the workplace. The offending agents can be classified into six broad categories that include bacteria, fungi, animal proteins, plant proteins, low molecular weight chemicals, and metals. The diagnosis of OHP requires a multidisciplinary approach and relies on a combination of diagnostic tests to ascertain the work relatedness of the disease. Both the clinical and the occupational history are keys to the diagnosis and often will lead to the initial suspicion. Diagnostic criteria adapted to OHP are proposed. The cornerstone of treatment is early removal from exposure to the eliciting antigen, although the disease may show an adverse outcome even after avoidance of exposure to the causal agent.

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“…At baseline, none of our patients had FE NO >40 ppb, which is proposed as a cut‐off point to detect chronic HP, and FE NO did not decrease with treatment. Thus, FE NO measurements do not appear to have clinical utility for diagnosis or follow‐up in cases of chronic HP.…”

Section: Discussionmentioning

confidence: 71%

“…26 After treatment, about 40% of our patients exceeded the minimal, clinically significant difference of 30 m in the 6MWD proposed for patients with idiopathic pulmonary fibrosis. 31 At baseline, none of our patients had FE NO >40 ppb, which is proposed as a cut-off point to detect chronic HP, 32 and FE NO did not decrease with treatment. Thus, FE NO measurements do not appear to have clinical utility for diagnosis or follow-up in cases of chronic HP.…”

Section: Demonstrated Thatmentioning

confidence: 75%