Metabolomic signatures of asthma-COPD overlap (ACO) are different from asthma and COPD

Introduction Asthma-chronic obstructive pulmonary disease (COPD) overlap, termed as ACO, is a complex heterogeneous disease without any clear diagnostic or therapeutic guidelines. The pathophysiology of the disease, its characteristic features, and existence as a unique disease entity remains unclea...

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Published inMetabolomics Vol. 15; no. 6; pp. 87 - 11
Main Authors Ghosh, Nilanjana, Choudhury, Priyanka, Subramani, Elavarasan, Saha, Dipanjan, Sengupta, Sayoni, Joshi, Mamata, Banerjee, Rintu, Roychowdhury, Sushmita, Bhattacharyya, Parthasarathi, Chaudhury, Koel
Format Journal Article
LanguageEnglish
Published New York Springer US 01.06.2019
Springer Nature B.V
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Summary:Introduction Asthma-chronic obstructive pulmonary disease (COPD) overlap, termed as ACO, is a complex heterogeneous disease without any clear diagnostic or therapeutic guidelines. The pathophysiology of the disease, its characteristic features, and existence as a unique disease entity remains unclear. Individuals with ACO have a faster lung function decline, more frequent exacerbations, and worse quality of life than those with COPD or asthma alone. Objectives The present study aims to determine whether ACO has a distinct metabolic profile in comparison to asthma and COPD. Methods Two different groups of patients were recruited as discovery (D) and validation (V) cohorts. Serum samples obtained from moderate and severe asthma patients diagnosed as per GINA guidelines [n = 34(D); n = 32(V)], moderate and severe COPD cases identified by GOLD guidelines [n = 30(D); 32(V)], ACO patients diagnosed by joint GOLD and GINA guidelines [n = 35(D); 40(V)] and healthy controls [n = 33(D)] were characterized using nuclear magnetic resonance (NMR) spectrometry. Results Multivariate and univariate analysis indicated that 12 metabolites [lipid, isoleucine, N-acetylglycoproteins (NAG), valine, glutamate, citric acid, glucose, l -leucine, lysine, asparagine, phenylalanine and histidine] were dysregulated in ACO patients when compared with both asthma and COPD. These metabolites were further validated in a fresh cohort of patients, which again exhibited a similar expression pattern. Conclusions Our findings suggest that ACO has an enhanced energy and metabolic burden associated with it as compared to asthma and COPD. It is anticipated that our results will stimulate researchers to further explore ACO and unravel the pathophysiological complexities associated with the disease.
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ISSN:1573-3882
1573-3890
DOI:10.1007/s11306-019-1552-z