Determinants of lung function across childhood in the Severe Asthma Research Program (SARP) 3 - 04/01/23
, Carter R. Petty, MA a, Ronald L. Sorkness, PhD b, Loren C. Denlinger, MD, PhD b, Brenda R. Phillips, MA c, Ngoc P. Ly, MD, MPH d, Benjamin Gaston, MD e, Kristie Ross, MD, MS f, Anne Fitzpatrick, PhD, RN, CPNP, MSCR g, Leonard B. Bacharier, MD h, Mark D. DeBoer, MD i, W. Gerald Teague, MD i, Sally E. Wenzel, MD j, Sima Ramratnam, MD b, Elliot Israel, MD k, David T. Mauger, PhD c, Wanda Phipatanakul, MD, MS afor the
National Heart, Lung, and Blood Institute’s Severe Asthma Research Program-3 Investigators∗
Abstract |
Background |
Children with asthma are at risk for low lung function extending into adulthood, but understanding of clinical predictors is incomplete.
Objective |
We sought to determine phenotypic factors associated with FEV1 throughout childhood in the Severe Asthma Research Program 3 pediatric cohort.
Methods |
Lung function was measured at baseline and annually. Multivariate linear mixed-effects models were constructed to assess the effect of baseline and time-varying predictors of prebronchodilator FEV1 at each assessment for up to 6 years. All models were adjusted for age, predicted FEV1 by Global Lung Function Initiative reference equations, race, sex, and height. Secondary outcomes included postbronchodilator FEV1 and prebronchodilator FEV1/forced vital capacity.
Results |
A total of 862 spirometry assessments were performed for 188 participants. Factors associated with FEV1 include baseline Feno (B, −49 mL/log2 PPB; 95% CI, −92 to −6), response to a characterizing dose of triamcinolone acetonide (B, −8.4 mL/1% change FEV1 posttriamcinolone; 95% CI, −12.3 to −4.5), and maximal bronchodilator reversibility (B, −27 mL/1% change postbronchodilator FEV1; 95% CI, −37 to −16). Annually assessed time-varying factors of age, obesity, and exacerbation frequency predicted FEV1 over time. Notably, there was a significant age and sex interaction. Among girls, there was no exacerbation effect. For boys, however, moderate (1-2) exacerbation frequency in the previous 12 months was associated with −20 mL (95% CI, −39 to −2) FEV1 at each successive year. High exacerbation frequency (≥3) 12 to 24 months before assessment was associated with −34 mL (95% CI, −61 to −7) FEV1 at each successive year.
Conclusions |
In children with severe and nonsevere asthma, several clinically relevant factors predict FEV1 over time. Boys with recurrent exacerbations are at high risk of lower FEV1 through childhood.
Le texte complet de cet article est disponible en PDF.Key words : Severe asthma, lung function, spirometry, asthma exacerbations
Abbreviations used : ACT, BD, COPD, Feno, FVC, GLI, SARP, TA, tdFEV1
Plan
| This work was supported by the National Heart, Lung, and Blood Institute to the Severe Asthma Research Program-3 (SARP3) principal investigators, clinical centers, and the Data Coordinating Center as follows: grant number U10 HL109164 (E.R.B., D.A.M., and W.C.M.), grant number U10 HL109257 (M.C.), grant number U10 HL109250 (S.C.E.), grant number U10 HL109146 (J.V.F.), grant number U10 HL109250 (B.G.), grant number U10 HL109172 (E.I. and B.D.L.), grant number U10 HL109168 (N.N.J.), grant number U10 HL109250 (W.G.T.), grant number U10 HL109152 (S.E.W.), and grant number U10 HL109086–04 (D.T.M.). In addition, this program is supported through the following National Institutes of HealthNational Center for Advancing Translational Sciences awards: grant number UL1 TR001420 (Wake Forest University), grant number UL1 TR000427 (University of Wisconsin), grant number UL1 TR001102 (Harvard University), and grant number UL1 TR000454 (Emory University). The following companies provided financial support for study activities at the coordinating and clinical centers beyond the third year of patient follow-up: AstraZeneca, Boehringer-Ingelheim, Genentech, GlaxoSmithKline, Sanofi-Genzyme-Regeneron, and Teva. These companies had no role in study design or data analysis, and the only restriction on the funds was that they be used to support the SARP initiative. |
|
| Disclosure of potential conflict of interest: J. M. Gaffin receives grant support from the National Institute of Environmental Health Sciences (NIEHS) and Vertex Pharmaceuticals, and personal fees from Syneos Health outside of the submitted work. L. C. Denlinger reports grants from the National Heart, Lung, and Blood Institute (NHLBI) and American Lung Association/Asthma Clinical Research Centers, during the conduct of the study; and other considerations from AstraZeneca, Boehringer-Ingelheim, Genentech, GlaxoSmithKline (GSK), Sanofi-Genzyme-Regeneron, and Teva, outside the submitted work. N. P. Ly reports grants from Vertex, and grants from Gilead, outside the submitted work. B. Gaston is funded by the NHLBI, but has no other conflicts relevant to this publication. K. Ross reports grants from AstraZeneca, GSK, Boehringer-Ingelheim, and Idorsia, and personal fees from Sanofi, outside the submitted work. A. Fitzpatrick reports grants from the National Institutes of Health (NIH), during the conduct of the study. L. B. Bacharier reports grants from NIH/National Institute of Allergy and Infectious Diseases and NHLBI; personal fees from GSK, Genentech/Novartis, DBV Technologies, Teva, Boehringer-Ingelheim, AstraZeneca, WebMD/Medscape, Sanofi/Regeneron, Vectura, Circassia, Kinaset, and Vertex; and royalties from Elsevier outside the submitted work. S. E. Wenzel reports that grants from multiple companies provided broad support to SARP, during the conduct of the study; grants and personal fees from AstraZeneca, Knopp, and Novartis; personal fees from GSK and Sanofi; grants from Regeneron; and nonfinancial support from Aer Therapeutics, outside the submitted work. S. Ramratnam reports consulting fees from Sanofi. E. Israel reports grants from the NIH, the Patient-Centered Outcomes Research Institute, and Gossamer Bio; grants and nonfinancial support from Circassia; grants and personal fees from AstraZeneca, Avillion, and Novartis; personal fees and nonfinancial support from Genentech, GSK, and Teva; personal fees from AB Science, the Allergy and Asthma Network, Amgen, Arrowhead Pharmaceuticals, Biometry, Equillium, Merck, Pneuma Respiratory, the NHLBI, PPS Health, Regeneron, Sanofi Genzyme, Sienna Biopharmaceutical, Teva, and Cowen; nonfinancial support from Boehringer-Ingelheim; and other considerations from Vorso, outside the submitted work. W. Phipatanakul reports grant and clinical trial support from the NIH, Genentech, Novartis, AstraZeneca, Regeneron, GSK, Merck, and Sanofi; and consulting fees from Genentech, Novartis, AstraZeneca, Regeneron, GSK, Merck, Sanofi, and Teva. The rest of the authors declare that they have no relevant conflicts of interest. Each author reports that the following companies provided financial support for study activities at the coordinating and clinical centers beyond the third year of patient follow-up: AstraZeneca, Boehringer-Ingelheim, Genentech, GSK, Sanofi-Genzyme-Regeneron, and Teva. These companies had no role in study design or data analysis, and the only restriction on the funds was that they be used to support the SARP initiative. |
Vol 151 - N° 1
P. 138 - janvier 2023 Retour au numéro
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