Obstructive sleep apnea (OSA) is a common sleep disorder associated with intermittent hypoxia, systemic inflammation, oxidative stress, and an increased risk of cardiovascular and metabolic diseases. Current diagnostic methods are effective but have limited availability and do not adequately predict disease burden or treatment response. The purpose of this study is to identify and validate blood biomarkers that may improve the screening, diagnosis, risk stratification, and monitoring of adults with OSA. A total of 120 participants will undergo clinical evaluation and overnight polysomnography. Participants with moderate-to-severe OSA will be randomly assigned to either immediate or delayed positive airway pressure (PAP) therapy, while participants without OSA will serve as controls. Blood samples will be collected at predefined time points and analyzed for inflammatory, metabolic, oxidative stress, and other candidate biomarkers. The study aims to determine which biomarkers are associated with OSA severity and how they change in response to PAP therapy. The results may contribute to the development of more accessible and personalized diagnostic and monitoring strategies for patients with OSA.
Obstructive sleep apnea (OSA) is a highly prevalent disorder characterized by recurrent upper airway obstruction during sleep, resulting in intermittent hypoxia, sleep fragmentation, oxidative stress, systemic inflammation, endothelial dysfunction, and metabolic disturbances. Untreated OSA is associated with an increased risk of cardiovascular disease, diabetes mellitus, stroke, impaired quality of life, and all-cause mortality. Despite the availability of polysomnography as the reference diagnostic method, current diagnostic approaches have limited accessibility and do not adequately reflect disease burden or predict treatment response. The primary objective of this study is to identify and validate blood biomarkers associated with the presence, severity, and treatment response of OSA. The investigators hypothesize that selected circulating proteins, inflammatory mediators, oxidative stress markers, and metabolic profiles can improve the screening, diagnosis, risk stratification, and monitoring of patients with OSA. A total of 120 adults will undergo standardized clinical evaluation and overnight polysomnography. Participants diagnosed with moderate-to-severe OSA will be randomly assigned to either immediate or delayed initiation of positive airway pressure (PAP) therapy, whereas participants without OSA will serve as the control group. Blood samples will be collected at predefined study visits to evaluate changes in candidate biomarkers before and during treatment. The study will investigate a broad panel of biomarkers representing inflammatory pathways, endothelial dysfunction, oxidative stress, and metabolomic alterations using validated laboratory techniques, including multiplex immunoassays, enzyme-linked immunosorbent assays (ELISA), and metabolomic analyses. Changes in biomarker profiles will be evaluated in relation to OSA severity and response to PAP therapy. The results of this study are expected to improve the understanding of the biological mechanisms underlying OSA and facilitate the development of novel biomarker-based approaches for screening, diagnosis, disease monitoring, and personalized management of patients with obstructive sleep apnea.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
DIAGNOSTIC
Masking
NONE
Enrollment
120
Positive airway pressure (PAP) therapy will be administered according to current clinical practice guidelines for the treatment of obstructive sleep apnea. PAP settings will be individually titrated based on clinical assessment and sleep study findings to ensure effective treatment. Participants assigned to PAP therapy will use the device during sleep for the duration specified in the study protocol. Adherence to therapy will be monitored using device-recorded usage data.
Department of Otolaryngology, Medical University of Bialystok
Bialystok, Podlaskie Voivodeship, Poland
RECRUITINGDifference in blood biomarker concentrations between participants with obstructive sleep apnea (OSA) and non-OSA controls at baseline
Comparison of baseline serum and plasma concentrations of a predefined panel of circulating protein biomarkers (osteoprotegerin, cardiotrophin-1, chitinase-3-like protein 1/YKL-40, CRP, HbA1c, erythropoietin, thioredoxin, PD-L1) and a predefined multiplex panel of 48 cytokines, chemokines and growth factors, measured by ELISA and multiplex ELISA (Luminex), between adults with moderate-to-severe OSA (AHI \>=15) and non-OSA controls (AHI \<5) defined by polysomnography. Results will be reported in assay-appropriate units, including pg/mL, ng/mL, mg/L, or percentage, as applicable.
Time frame: At enrollment, prior to initiation of PAP therapy (baseline, Month 0).
Change in blood biomarker concentrations in OSA participants after positive airway pressure (PAP) therapy.
Change from baseline in serum and plasma concentrations of the predefined biomarker panel after positive airway pressure (PAP) therapy. In the Early Treatment Group change is assessed after 3 and 6 months of continuous PAP; in the Delay-TG after 3 months of PAP delivered between months 3 and 6. Aim: determine whether and to what degree biomarker values change in response to standard OSA treatment.
Time frame: Baseline, 3 months and 6 months.
Correlation between baseline blood biomarker concentrations and OSA severity (AHI)
Correlation between baseline concentrations of the studied blood biomarkers and OSA severity expressed by the apnea-hypopnea index (AHI), as well as mean and lowest nocturnal oxygen saturation, in OSA participants. Goal: evaluate suitability of biomarkers for grading OSA severity.
Time frame: At enrollment, prior to initiation of PAP therapy (baseline, Month 0).
Normalization of blood biomarker concentrations toward control values after PAP therapy in OSA participants.
Comparison of post-PAP-treatment biomarker concentrations in OSA participants (Early-TG and Delay-TG) with the enrollment values of the non-OSA control group, to assess whether treatment shifts biomarker values toward those of healthy controls. Goal: identify biomarkers specific to OSA-related hypoxia that approach the concentrations observed in participants without OSA.
Time frame: Control: baseline; Early-TG: Month 3 and Month 6; Delay-TG: Month 6.
Effect of PAP treatment duration (3 vs 6 months) on blood biomarker concentrations
Assessment of the impact of PAP treatment duration on biomarker values: (a) comparison of post-treatment values between the Early Treatment Group (6 months of PAP) and the Delay Treatment Group (3 months of PAP); (b) within Early-TG, comparison of values after 3 versus 6 months to evaluate whether changes become more robust with continued treatment. Goal: determine whether longer therapy produces greater biomarker change.
Time frame: 3 months and 6 months
Stability of blood biomarker concentrations in untreated OSA (3-month observation period).
Comparison of biomarker concentrations in the Delay-TG between baseline and after the 3-month observation period without any treatment, to verify that biomarker values do not change spontaneously in the absence of PAP therapy. Serves as the internal untreated reference for the treatment effect.
Time frame: Baseline and 3 months (Delay-TG)
Differences in serum and plasma metabolomic profiles between OSA and controls and in response to PAP therapy.
Targeted and untargeted metabolomic profiling (GC-MS and LC-QTOF-MS; amino acids, carbohydrates, fatty acids, and specific lipids including phosphatidylcholines, ceramides, triglycerides and lysophosphatidylcholines) compared between OSA participants and controls at baseline, and before versus after PAP therapy in OSA participants. Goal: identify known and novel metabolite biomarkers of OSA.
Time frame: Baseline, 3 months and 6 months
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