ReviewPediatric pulmonology2026
Sleep-Disordered Breathing in Primary Ciliary Dyskinesia.
Review in Pediatric pulmonology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Sleep-Disordered Breathing in Primary Ciliary Dyskinesia.Pediatric pulmonology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrimary Ciliary Dyskinesia (PCD) is a rare genetic disorder marked by impaired mucociliary clearance, chronic upper and lower airway infections, and progressive bronchiectasis. Sleep-disordered breathing (SDB) has emerged as an under-recognized comorbidity in this population.
objectiveThis review synthesizes current evidence on the prevalence, pathophysiology, diagnostic approaches, and management of SDB in PCD across pediatric and adult cohorts.
resultsReported prevalence of obstructive sleep apnea (OSA) in PCD ranges widely from ~33% to 100%, markedly exceeding general population norms; however, one large recent pediatric cohort reported a much lower prevalence (~1.2%), indicating that true disease magnitude remains uncertain. Upper-airway abnormalities (chronic rhinosinusitis, nasal polyposis, adeno-tonsillar hypertrophy) are almost universal in PCD, while lower-airway disease and ventilation-perfusion mismatch contribute to nocturnal hypoxemia even in the absence of apneas. Polysomnography (PSG) remains the diagnostic gold standard; subjective questionnaires (e.g., PSQI, SDSC, ESS) show poor correlation with PSG metrics in PCD. Sleep architecture is typically preserved, but sleep efficiency is mildly reduced and arousal indices are elevated, indicative of fragmented yet largely restorative sleep. Psychological and neurocognitive sequelae, including anxiety, depressive symptoms, and attention deficits, may be seen and are associated with SDB in PCD. First-line management focuses on optimization of the upper-airway (adenotonsillectomy, nasal irrigation, intranasal corticosteroids), while residual SDB may necessitate positive airway pressure (PAP) therapy. Optimizing lung function and infection control may further improve nocturnaloxygenation.
conclusionsSDB in PCD represents a multifactorial and potentially modifiable contributor to disease burden. Incorporating sleep assessment into routine PCD care and fostering multicenter, genotype-informed research are imperative to enhance early recognition, management, and quality-of-life outcomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.