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Drug-Induced Sleep Endoscopy (DISE) with Target Controlled Infusion (TCI) and Bispectral Analysis in Obstructive Sleep Apnea
Published on: December 6, 2016
Association of Obstructive Sleep Apnea Risk with Hypoxia-Inducible Factor Expression in Chronic Rhinosinusitis by
Hye Kyu Min1,2, Sung-Wan Kim1, Jin-Young Min1
1Department of Otorhinolaryngology-Head and Neck Surgery, Kyung Hee University Hospital, Kyung Hee University College of Medicine, Seoul 02447, Republic of Korea.
Journal of Clinical Medicine
|May 27, 2026
Summary
Obstructive sleep apnea (OSA) increases hypoxia-inducible factor-2α (HIF-2α) in non-eosinophilic chronic rhinosinusitis (NECRS) but not eosinophilic CRS (ECRS). OSA risk impacts HIF expression differently based on CRS endotype.
Area of Science:
- Otorhinolaryngology
- Sleep Medicine
- Molecular Biology
Background:
- Hypoxia and hypoxia-inducible factors (HIFs) are implicated in chronic rhinosinusitis (CRS) pathophysiology.
- Obstructive sleep apnea (OSA) may worsen hypoxia-driven sinonasal inflammation.
Purpose of the Study:
- To investigate the association between OSA risk and sinonasal HIF expression in CRS patients.
- To differentiate these associations based on eosinophilic CRS (ECRS) and non-eosinophilic CRS (NECRS) endotypes.
Main Methods:
- Ethmoid mucosal tissues were analyzed from 64 CRS patients.
- Patients were categorized by OSA risk (polysomnography/sleep score) and CRS endotype (blood eosinophils).
- Protein levels of HIF-1α, HIF-2α, and inflammatory mediators were quantified using multiplex immunoassay.
Main Results:
- HIF-2α was significantly higher in high-risk OSA patients (p < 0.05).
- HIF-1α was higher in NECRS compared to ECRS (p < 0.05).
- High-risk OSA elevated HIF-2α specifically in NECRS (p < 0.05), with endotype-specific inflammatory marker correlations.
Conclusions:
- Sinonasal HIF expression in CRS is modulated by OSA risk and endotype.
- OSA-related hypoxia impacts HIF-2α in NECRS, but this is less pronounced in ECRS.
- Type 2 inflammation likely influences the attenuated HIF-2α response in ECRS.
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