Exhaled Nitric Oxide in Systemic Sclerosis Lung DiseaseReport as inadecuate




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Canadian Respiratory Journal - Volume 2017 2017, Article ID 6736239, 8 pages - https:-doi.org-10.1155-2017-6736239

Research Article

University Health Network Pulmonary Hypertension Programme, Toronto General Hospital, Department of Medicine, University of Toronto, Toronto, ON, Canada

Department of Medicine, Temple University, Philadelphia, PA, USA

University Health Network Pulmonary Hypertension Programme, Toronto General Hospital, Toronto, ON, Canada

University Health Network Pulmonary Hypertension Programme, Toronto General Hospital, Toronto Scleroderma Program, Toronto Western Hospital, Mount Sinai Hospital, Department of Medicine, Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, ON, Canada

Correspondence should be addressed to Sindhu R. Johnson

Received 28 September 2016; Revised 9 December 2016; Accepted 9 January 2017; Published 14 February 2017

Academic Editor: Djuro Kosanovic

Copyright © 2017 Natalie K. Kozij et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Exhaled nitric oxide eNO is a potential biomarker to distinguish systemic sclerosis SSc associated pulmonary arterial hypertension PAH and interstitial lung disease ILD. We evaluated the discriminative validity, feasibility, methods of eNO measurement, and magnitude of differences across lung diseases, disease-subsets SSc, systemic lupus erythematosus, and healthy-controls. Methods. Consecutive subjects in the UHN Pulmonary Hypertension Programme were recruited. Exhaled nitric oxide was measured at 50 mL-s intervals using chemiluminescent detection. Alveolar and conducting airway NO were partitioned using a two-compartment model of axial diffusion CMAD and the trumpet model of axial diffusion TMAD. Results. Sixty subjects were evaluated. Using the CMAD model, control subjects had lower median IQR alveolar NO than all PAH subjects 2.0 1.5, 2.5 versus 3.14 ppb 2.3, 4.0, . SSc-ILD had significantly lower median conducting airway NO compared to controls 1009.5 versus 1342.1 mlppb-s, . SSc-PAH had increased median IQR alveolar NO compared to controls 3.3 3.0, 5.7 versus 2.0 ppb 1.5, 2.5, . SSc-PAH conducting airway NO inversely correlated with DLCO r −0.88 95% CI −0.99, −0.26. Conclusion. We have demonstrated feasibility, identified that CMAD modeling is preferred in SSc, and reported the magnitude of differences across cases and controls. Our data supports discriminative validity of eNO in SSc lung disease.





Author: Natalie K. Kozij, John T. Granton, Philip E. Silkoff, John Thenganatt, Shobha Chakravorty, and Sindhu R. Johnson

Source: https://www.hindawi.com/



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