BACKGROUND: The aim of the present study was to evaluate the effect of untreated sleep apnea syndrome (SAS) on glycemic control, evaluated by HbA1c, in patients with type 2 diabetes (T2D). METHODS: The study sample consisted of 100 consecutive adult (≥18 years) patients with T2D without a prior diagnosis of sleep apnea recruited from an outpatient diabetes clinic. All patients underwent an in-hospital cardiorespiratory study using a three-channel portable sleep diagnostic tool; 64 were found to have sleep apnea, 36 were not. Information on medical history, body weight, height, sleep apnea symptoms, Epworth Sleepiness Scale scores, and HbA1c and fasting plasma glucose levels were recorded. RESULTS: After adjusting for factors known to affect HbA1c (gender, age, diabetes duration, diabetes treatment, body mass index [BMI], and waist circumference), HbA1c was higher in patients with than without SAS (8.4 % vs 7.6 %, respectively; P = 0.04). A positive correlation was found between the presence of sleep apnea and HbA1c (r = 0.24; P = 0.02). After adjusting for confounding factors (including BMI), only mean and lowest O2 saturation during sleep were significantly associated with HbA1c (β = -0.23 [P = 0.03] and β = -0.24 [P = 0.007], respectively). After further adjusting for waist circumference, only lowest O2 saturation during recording remained independently associated with HbA1c (β = -0.21; P = 0.05). CONCLUSIONS: The presence of sleep apnea is associated with poorer glycemic control in patients with T2D. In patients with sleep apnea and T2D, greater levels of oxygen desaturation are associated with poorer glycemic control.
BACKGROUND: The aim of the present study was to evaluate the effect of untreated sleep apnea syndrome (SAS) on glycemic control, evaluated by HbA1c, in patients with type 2 diabetes (T2D). METHODS: The study sample consisted of 100 consecutive adult (≥18 years) patients with T2D without a prior diagnosis of sleep apnea recruited from an outpatientdiabetes clinic. All patients underwent an in-hospital cardiorespiratory study using a three-channel portable sleep diagnostic tool; 64 were found to have sleep apnea, 36 were not. Information on medical history, body weight, height, sleep apnea symptoms, Epworth Sleepiness Scale scores, and HbA1c and fasting plasma glucose levels were recorded. RESULTS: After adjusting for factors known to affect HbA1c (gender, age, diabetes duration, diabetes treatment, body mass index [BMI], and waist circumference), HbA1c was higher in patients with than without SAS (8.4 % vs 7.6 %, respectively; P = 0.04). A positive correlation was found between the presence of sleep apnea and HbA1c (r = 0.24; P = 0.02). After adjusting for confounding factors (including BMI), only mean and lowest O2 saturation during sleep were significantly associated with HbA1c (β = -0.23 [P = 0.03] and β = -0.24 [P = 0.007], respectively). After further adjusting for waist circumference, only lowest O2 saturation during recording remained independently associated with HbA1c (β = -0.21; P = 0.05). CONCLUSIONS: The presence of sleep apnea is associated with poorer glycemic control in patients with T2D. In patients with sleep apnea and T2D, greater levels of oxygen desaturation are associated with poorer glycemic control.
Authors: Tamara S Hannon; Sara E Watson; Hasnaa E Jalou; Sangeeta Chakravorty; Kieren J Mather; Silva A Arslanian Journal: Front Endocrinol (Lausanne) Date: 2018-06-01 Impact factor: 5.555