Abstract
Rationale Chronic obstructive pulmonary disease (COPD) comprises distinct phenotypes, all characterised by airflow limitation.
Objectives We hypothesised that somatotype changes – as a surrogate of adiposity – from early adulthood follow different trajectories to reach distinct phenotypes.
Methods Using the validated Stunkard's Pictogram, 356 COPD patients chose the somatotype that best reflects their current body build and those at ages 18, 30, 40 and 50 years. An unbiased group-based trajectory modelling was used to determine somatotype trajectories. We then compared the current COPD-related clinical and phenotypic characteristics of subjects belonging to each trajectory.
Measurements and main results At 18 years of age, 88% of the participants described having a lean or medium somatotype (estimated body mass index (BMI) between 19 and 23 kg·m−2) while the other 12% a heavier somatotype (estimated BMI between 25 and 27 kg·m−2). From age 18 onwards, five distinct trajectories were observed. Four of them demonstrating a continuous increase in adiposity throughout adulthood with the exception of one, where the initial increase was followed by loss of adiposity after age 40. Patients with this trajectory were primarily females with low BMI and DLCO (diffusing capacity of the lung for carbon monoxide). A persistently lean trajectory was seen in 14% of the cohort. This group had significantly lower forced expiratory volume in 1 s (FEV1), DLCO, more emphysema and a worse BODE (BMI, airflow obstruction, dyspnoea and exercise capacity) score thus resembling the multiple organ loss of tissue (MOLT) phenotype.
Conclusions COPD patients have distinct somatotype trajectories throughout adulthood. Those with the MOLT phenotype maintain a lean trajectory throughout life. Smoking subjects with this lean phenotype in early adulthood deserve particular attention as they seem to develop more severe COPD.
Abstract
In smoking-related COPD, somatotype trajectories are associated with the final COPD phenotype. Specifically, the “pink puffer” or multiorgan loss of tissue (MOLT) phenotype occurs where the patient remains lean. https://bit.ly/2YNhwfu
Footnotes
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Author contributions: The above listed authors attest that they made substantial contributions to the conception and design, acquisition of data, or analysis and interpretation of data; drafting the article or revising it critically for important intellectual content; and final approval of the version to be submitted for revision. All authors had full access to all the data in the study and accept responsibility for the submission of this work.
Conflict of interest: M.J. Divo has nothing to disclose.
Conflict of interest: M. Marin Oto has nothing to disclose.
Conflict of interest: C. Casanova Macario reports, in the last 3 years, to have received lectures and/or scientific advice from Laboratorios Bial, Boehringer Ingelheim, Gebropharma, GSK, Esteve, Menarini, Novartis and Rovi.
Conflict of interest: C. Cabrera Lopez has nothing to disclose.
Conflict of interest: J.P. de-Torres has nothing to disclose.
Conflict of interest: J.M. Marin Trigo has nothing to disclose.
Conflict of interest: C.P. Hersh reports grants from National Institutes of Health during the conduct of the study; and grants from Boehringer Ingelheim and Novartis, and personal fees from 23 and Me, outside the submitted work.
Conflict of interest: A. Ezponda Casajús has nothing to disclose.
Conflict of interest: C. Maguire has nothing to disclose.
Conflict of interest: V.M. Pinto-Plata has nothing to disclose.
Conflict of interest: F. Polverino has nothing to disclose.
Conflict of interest: J.C. Ross reports grants from NIH during the conduct of the study.
Conflict of interest: D. DeMeo has nothing to disclose.
Conflict of interest: G. Bastarrika reports personal fees from General Electric, nonfinancial support from Siemens and grants from Guerbet, outside the submitted work.
Conflict of interest: E.K. Silverman reports grants from NIH during the conduct of the study, and grants and travel support from GlaxoSmithKline outside the submitted work.
Conflict of interest: B.R. Celli has nothing to disclose.
Support statement: The COPDGene cohort (NCT00608764) is funded by National Institutes of Health (NIH) grants U01HL089856 and U01HL089897 and is also supported by the COPD Foundation through contributions made to an Industry Advisory Committee comprised of AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Novartis, and Sunovion. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received March 18, 2020.
- Accepted June 15, 2020.
- Copyright ©ERS 2020
This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.