Brian D Kent1, Ludger Grote2, Silke Ryan1, Jean-Louis Pépin3, Maria R Bonsignore4, Ruzena Tkacova5, Tarja Saaresranta6, Johan Verbraecken7, Patrick Lévy3, Jan Hedner2, Walter T McNicholas8. 1. School of Medicine and Medical Science, University College Dublin and Pulmonary and Sleep Disorders Unit, St. Vincent's University Hospital, Dublin, Ireland. 2. Department of Sleep Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden. 3. Université Grenoble Alpes, Institut National de la Santé et de la Recherche Médicale, and Centre Hospitalier Universitaire de Grenoble, Grenoble, France. 4. Biomedical Department of Internal & Specialist Medicine, University of Palermo and National Research Council Institute of Biomedicine and Molecular Immunology, Palermo, Italy. 5. Department of Respiratory Medicine, Pavol Jozef Šafárik University in Košice and Louis Pasteur University Hospital, Kosice, Slovakia. 6. Division of Medicine, Department of Pulmonary Diseases, Turku University Hospital and Sleep Research Unit, Department of Physiology, University of Turku, Turku, Finland. 7. Department of Pulmonary Medicine, Antwerp University Hospital and University of Antwerp, Antwerp, Belgium. 8. School of Medicine and Medical Science, University College Dublin and Pulmonary and Sleep Disorders Unit, St. Vincent's University Hospital, Dublin, Ireland. Electronic address: Walter.mcnicholas@ucd.ie.
Abstract
BACKGROUND: OSA is associated with an increased risk of cardiovascular morbidity. A driver of this is metabolic dysfunction and in particular type 2 diabetes mellitus (T2DM). Prior studies identifying a link between OSA and T2DM have excluded subjects with undiagnosed T2DM, and there is a lack of population-level data on the interaction between OSA and glycemic control among patients with diabetes. We assessed the relationship between OSA severity and T2DM prevalence and control in a large multinational population. METHODS: We performed a cross-sectional analysis of 6,616 participants in the European Sleep Apnea Cohort (ESADA) study, using multivariate regression analysis to assess T2DM prevalence according to OSA severity, as measured by the oxyhemoglobin desaturation index. Patients with diabetes were identified by previous history and medication prescription, and by screening for undiagnosed diabetes with glycosylated hemoglobin (HbA1c) measurement. The relationship of OSA severity with glycemic control was assessed in diabetic subjects. RESULTS: T2DM prevalence increased with OSA severity, from 6.6% in subjects without OSA to 28.9% in those with severe OSA. Despite adjustment for obesity and other confounding factors, in comparison with subjects free of OSA, patients with mild, moderate, or severe disease had an OR (95% CI) of 1.33 (1.04-1.72), 1.73 (1.33-2.25), and 1.87 (1.45-2.42) (P < .001), respectively, for prevalent T2DM. Diabetic subjects with more severe OSA had worse glycemic control, with adjusted mean HbA1c levels 0.72% higher in patients with severe OSA than in those without sleep-disordered breathing (analysis of covariance, P < .001). CONCLUSIONS: Increasing OSA severity is associated with increased likelihood of concomitant T2DM and worse diabetic control in patients with T2DM.
BACKGROUND: OSA is associated with an increased risk of cardiovascular morbidity. A driver of this is metabolic dysfunction and in particular type 2 diabetes mellitus (T2DM). Prior studies identifying a link between OSA and T2DM have excluded subjects with undiagnosed T2DM, and there is a lack of population-level data on the interaction between OSA and glycemic control among patients with diabetes. We assessed the relationship between OSA severity and T2DM prevalence and control in a large multinational population. METHODS: We performed a cross-sectional analysis of 6,616 participants in the European Sleep Apnea Cohort (ESADA) study, using multivariate regression analysis to assess T2DM prevalence according to OSA severity, as measured by the oxyhemoglobin desaturation index. Patients with diabetes were identified by previous history and medication prescription, and by screening for undiagnosed diabetes with glycosylated hemoglobin (HbA1c) measurement. The relationship of OSA severity with glycemic control was assessed in diabetic subjects. RESULTS: T2DM prevalence increased with OSA severity, from 6.6% in subjects without OSA to 28.9% in those with severe OSA. Despite adjustment for obesity and other confounding factors, in comparison with subjects free of OSA, patients with mild, moderate, or severe disease had an OR (95% CI) of 1.33 (1.04-1.72), 1.73 (1.33-2.25), and 1.87 (1.45-2.42) (P < .001), respectively, for prevalent T2DM. Diabetic subjects with more severe OSA had worse glycemic control, with adjusted mean HbA1c levels 0.72% higher in patients with severe OSA than in those without sleep-disordered breathing (analysis of covariance, P < .001). CONCLUSIONS: Increasing OSA severity is associated with increased likelihood of concomitant T2DM and worse diabetic control in patients with T2DM.
Authors: Ari Shechter; Gary D Foster; Wei Lang; David M Reboussin; Marie-Pierre St-Onge; Gary Zammit; Anne B Newman; Richard P Millman; Thomas A Wadden; John M Jakicic; Elsa S Strotmeyer; Rena R Wing; F Xavier Pi-Sunyer; Samuel T Kuna Journal: J Sleep Res Date: 2017-05-31 Impact factor: 3.981