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Relationship between alpha-1 antitrypsin deficiency and obstructive sleep apnea
Lindsay Megenhardt1, Sarah Ransdell2, Jodi Clark-LoCascio2
1Department of Health Care Sciences, Nova Southeastern University, Fort Lauderdale, FL, USA. Lindsay.Megenhardt@asu.edu.
Sleep & Breathing = Schlaf & Atmung
|May 1, 2021
Summary
Individuals with alpha-1 antitrypsin deficiency (AATD) may face a higher risk of obstructive sleep apnea (OSA). Despite lower diagnosed OSA rates, AATD patients show increased symptom scores, suggesting a potential link requiring further investigation.
Area of Science:
- Pulmonary Medicine
- Genetics
- Sleep Medicine
Background:
- Alpha-1 antitrypsin deficiency (AATD) is a genetic disorder that can lead to lung and liver disease.
- Obstructive sleep apnea (OSA) is a common sleep disorder characterized by repeated airway collapse during sleep.
Purpose of the Study:
- To investigate whether individuals with mild to severe alpha-1 antitrypsin deficiency (AATD) have an elevated risk of developing obstructive sleep apnea (OSA) compared to the general population.
Main Methods:
- Utilized the STOP-BAG questionnaire on 2338 participants from the Alpha-1 Coded Testing Study (ACT) and 4638 from the Kentucky Behavioral Risk Factor Survey (KyBRFS).
- Employed propensity score matching based on age and BMI to create a balanced cohort for comparison.
- Analyzed OSA risk using chi-square analysis on the matched cohort.
Main Results:
- While diagnosed OSA prevalence was lower in the AATD cohort (11.2%) than the general population (14.5%), a significantly higher percentage of AATD individuals met high-risk thresholds on the STOP-BAG questionnaire (22.7% vs. 13.0%).
- These findings remained significant after propensity score matching.
- No significant differences in OSA risk were observed among different AATD genotypes.
Conclusions:
- AATD may be associated with an increased risk for OSA, despite lower reported diagnoses.
- The discrepancy between OSA symptoms and diagnoses in AATD patients warrants further research.
- Exploration of elastin loss as a potential factor in OSA pathogenesis is suggested.
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