Abstract
Background Apnoea-hypopnoea index (AHI) forms the basis for severity of obstructive sleep apnoea (OSA), a condition expected to reprogram metabolic pathways in humans. We aimed at identifying the AHI breakpoint from which the majority of significant changes in the systemic metabolome of patients with sleep complaints occur.
Methods In a prospective observational study on symptomatic individuals, who underwent polysomnography for the diagnosis of OSA, profiles of 187 metabolites including amino acids, biogenic amines, acylcarnitines, lysophasphatidylcholines, phosphatidylcholines and sphingomyelins were analysed with liquid chromatography-mass-spectrometry in peripheral blood drawn at 3 different time points overnight. Comparisons of rank-transformed data with general linear model for repeated measures after dichotomizing the study group at different AHI levels were applied to define the best cut-off based on Cohen's f.
Results Sixty-five subjects were recruited with their median AHI of 15.6 events per hour. The mean Cohen's f over the metabolites was highest (0.161) at an AHI level of 5·h−1 representing the metabolomic threshold (MT). Of the particular between-group differences, 8 phosphatidylcholines, 9 acylcarnitines and one amino acid (threonine) had significantly lower concentrations in the individuals with an AHI level equal to or above the MT. The metabolomic changes at AHI levels defining moderate and severe OSA were smaller than at AHI of 5·h−1.
Conclusions The MT for patients with sleep complaints described in this report for the first time coincides with the AHI threshold required to confirm the diagnosis of OSA.
Footnotes
This manuscript has recently been accepted for publication in the ERJ Open Research. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJOR online. Please open or download the PDF to view this article.
Conflicts of interest: O. Kiens has received lecture fees from AstraZeneca, Berlin-Chemie Menarini, GlaxoSmithKline, Norameda, Novartis and Sanofi and sponsorships from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline and Norameda. None of the conflicts of interest has been related to the current study.
Conflicts of interest: V. Ivanova has received lecture fees from AstraZeneca, Berlin-Chemie Menarini and Norameda. K. Veeväli, T. Laurits, R Tamm, E. Taalberg, A. Ottas and K. Kilk report no conflicts of interest.
Conflicts of interest: A. Altraja has received lecture fees from Lecture fees from Abbott, AstraZeneca, Bayer, Berlin-Chemie Menarini, Boehringer Ingelheim, Norameda, GlaxoSmithKline, Janssen, KRKA, MSD, Novartis, Orion, Pfizer, Roche, Sanofi, Takeda, Teva and Zentiva, sponsorships from Abbott, AstraZeneca, Bayer, Boehringer Ingelheim, Norameda, CSL Behring, GlaxoSmithKline, Janssen, KRKA, MSD, Novartis, Roche, Takeda, Teva and AOP Orphan and research support from Bayer, Boehringer Ingelheim, CSL Behring, GlaxoSmithKline, Medis, Norameda, Pfizer and Takeda and has been participated in advisory boards of Actelion, AstraZeneca, Bayer, Boehringer Ingelheim, CSL Behring, GlaxoSmithKline, Janssen, Johnson & Johnson, MSD, Novartis, Roche, Sanofi, Shire Pharmaceuticals and Teva. None of the conflicts of interest has been related to the current study however.
This is a PDF-only article. Please click on the PDF link above to read it.
- Received July 1, 2022.
- Accepted September 20, 2022.
- Copyright ©The authors 2022
This version is distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0. For commercial reproduction rights and permissions contact permissions{at}ersnet.org