Nocturnal saturation and glucose tolerance in children with cystic fibrosis
Dharmeshkumar Suratwala1, June S H Chan, Andrea Kelly
1Children's Hospital of Philadelphia, Pulmonary Division, 9NW50, 34th Street & Civic Center Boulevard, Philadelphia, PA 19104, USA.
Insights
In children with cystic fibrosis (CF), lower nocturnal oxygen saturation during sleep is linked to impaired glucose regulation. This suggests a connection between breathing during sleep and glucose metabolism in CF patients.
Area of Science:
- Pediatric Pulmonology
- Endocrinology
- Sleep Medicine
Background:
- Glucose intolerance is prevalent in cystic fibrosis (CF), correlating with poorer health outcomes and increased mortality.
- Sleep-disordered breathing is known to affect glucose metabolism, prompting investigation into its role in CF.
Purpose of the Study:
- To investigate the association between sleep-disordered breathing, inflammation, and glucose intolerance in children with CF.
- To determine if recurrent hypoxemia and sleep disruption impact glucose regulation in CF patients.
Main Methods:
- 25 children with CF underwent polysomnography, actigraphy, inflammatory marker measurement, and oral glucose tolerance testing.
- Blood glucose area under the curve (AUC) was measured; polysomnography data were compared to healthy controls.
Main Results:
- 29% of CF children had impaired glucose tolerance, and 4% had diabetes.
- Lower mean nocturnal oxygen saturation significantly correlated with higher glucose AUC (r=-0.49, p=0.015).
- Nocturnal oxygen saturation was the primary predictor of glucose AUC (R(2)=0.24, p=0.001), independent of other factors.
Conclusions:
- Reduced oxyhemoglobin saturation during sleep is associated with poorer glucose regulation in pediatric CF patients.
- Further research is required to establish causality and understand if sleep-related hypoxia impacts glucose metabolism or vice versa.
Background:
Glucose intolerance is common in cystic fibrosis (CF), and is associated with worsening pulmonary function and nutritional status, and increased mortality. As sleep-disordered breathing is associated with disorders of glucose metabolism, it was hypothesised that recurrent episodes of hypoxaemia during sleep, and sleep disruption, would be associated with inflammation and glucose intolerance in CF.
Methods:
25 children (aged 14±4 (mean±SD) years) with CF underwent polysomnography, actigraphy, measurement of serum inflammatory markers and oral glucose tolerance testing. Blood glucose area under the curve (AUC), as a cumulative measure of glucose response, was determined. Polysomnography data were compared with retrospective data from 25 healthy controls.
Results:
Forced expiratory volume in 1 s was 92±14% predicted. 24 subjects underwent glucose tolerance testing, of whom 29% had impaired glucose tolerance and 4% had diabetes. The mean nocturnal oxygen saturation correlated negatively with glucose AUC at 120 min (r=-0.49, p=0.015). Partial correlations and regression models including age, body mass index, nocturnal saturation and pulmonary function indicated that nocturnal saturation accounted for the majority of the predictive power for glucose AUC (R(2)=0.24, p=0.001). There were no meaningful relationships between sleep quality, inflammation and glucose tolerance.
Conclusions:
Lower oxyhaemoglobin saturation is associated with worse glucose regulation in children with CF. Further studies are needed to determine whether lower saturation negatively impacts glucose regulation or, alternatively, whether abnormalities in glucose metabolism are an early sign of pulmonary dysfunction.
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