@article{3421eb6771eb4a9480ea5104e2c86bd1,
title = "Biomarkers of asthma relapse and lung function decline in adults with spontaneous asthma remission: A population-based cohort study",
abstract = "Background: The extent to which biomarkers of asthma activity persist in spontaneous asthma remission and whether such markers are associated with future respiratory outcomes remained unclear. We investigated the association between sub-clinical inflammation in adults with spontaneous asthma remission and future asthma relapse and lung function decline. Methods: The Tasmanian Longitudinal Health Study is a population-based cohort (n = 8583). Biomarkers of systemic inflammation were measured on participants at age 45, and latent profile analysis was used to identify cytokine profiles. Bronchial hyperresponsiveness (BHR) and nitric oxide products in exhaled breath condensate (EBC NOx) were measured at age 50. Participants with spontaneous asthma remission at ages 45 (n = 466) and 50 (n = 318) were re-evaluated at age 53, and associations between baseline inflammatory biomarkers and subsequent asthma relapse and lung function decline were assessed. Results: We identified three cytokine profiles in adults with spontaneous asthma remission: average (34%), Th2-high (42%) and Th2-low (24%). Compared to the average profile, a Th2-high profile was associated with accelerated decline in post-BD FEV1/FVC (MD −0.18% predicted per-year; 95% CI −0.33, −0.02), while a Th2-low profile was associated with accelerated decline in both post-BD FEV1 (−0.41%; −0.75, −0.06) and post-BD FVC (−0.31%; −0.62, 0.01). BHR and high TNF-α during spontaneous remission were associated with an increased risk of asthma relapse. In contrast, we found no evidence of association between EBC NOx and either asthma relapse or lung function decline. Conclusion: BHR and serum inflammatory cytokines have prognostic value in adults with spontaneous asthma remission. At-risk individuals with BHR, Th2-high or Th2-low cytokine profiles may benefit from closer monitoring and on-going follow-up.",
keywords = "asthma, biomarkers, endotypes, precision medicine",
author = "Tan, {Daniel J.} and Lodge, {Caroline J.} and Walters, {Eugene Haydn} and Lowe, {Adrian J.} and Bui, {Dinh S.} and Gayan Bowatte and Rangi Kandane-Rathnayake and Aldakheel, {Fahad M.} and Bircan Erbas and Hamilton, {Garun S.} and Thomas, {Paul S.} and Mark Hew and Tang, {Mimi L.K.} and Abramson, {Michael J.} and Perret, {Jennifer L.} and Dharmage, {Shyamali C.}",
note = "Funding Information: We acknowledge the TAHS study participants, previous investigators and current investigators who are not co‐authors of this manuscript. We also acknowledge the study site coordinators and respiratory scientists who collected data in lung function laboratories in Tasmania, Victoria, Queensland and New South Wales, the research interviewers and data entry operators. DJT was supported by a NHMRC Postgraduate Scholarship and Royal Australian College of Physicians (RACP) Woolcock Scholarship. Open access publishing facilitated by The University of Melbourne, as part of the Wiley ‐ The University of Melbourne agreement via the Council of Australian University Librarians. Funding Information: CJL, EHW, AJL, DSB, MJA, JLP and SCD hold an investigator‐initiated grant from GlaxoSmithKline for unrelated research. SCD holds an investigator‐initiated grant from AstraZeneca for unrelated research. MJA holds investigator‐initiated grants from Pfizer, Boehringer‐Ingelheim and Sanofi for unrelated research; has undertaken an unrelated consultancy for and received assistance with conference attendance from Sanofi; and received a speaker's fee from GlaxoSmithKline. AJL has received non‐financial support from Primus Pharmaceuticals for unrelated research. MH has received unrestricted grants, speaker fees, and consulted for; GlaxoSmithKline, AstraZeneca, Novartis, Teva, Sanofi and Seqirus; with all payments to his employer Alfred Health. All other authors declare no competing interests. Funding Information: This study was supported by funds from the National Health and Medical Research Council (NHMRC) of Australia; the University of Melbourne, Clifford Craig Foundation; the Victorian, Queensland and Tasmanian Asthma Foundations; Royal Hobart Hospital Research Foundation; Helen MacPherson Smith Trust; and GlaxoSmithKline. The funding bodies had no direct role in the conduct of the study, statistical analysis or interpretation of the data, and preparation or approval of the manuscript. Publisher Copyright: {\textcopyright} 2022 The Authors. Allergy published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.",
year = "2023",
month = apr,
doi = "10.1111/all.15566",
language = "English",
volume = "78",
pages = "957--967",
journal = "Allergy",
issn = "0105-4538",
publisher = "Wiley-Blackwell",
number = "4",
}