TREATMENT WITH CONTINUOUS POSITIVE AIRWAY PRESSURE AND CHANGES IN GLUCOSE METABOLISM AND INSULIN RESISTANCE IN PATIENTS WITH SLEEP APNEA-HYPOPNEA SYNDROME

Objective: To assess the effect of continuous positive airway pressure (CPAP) therapy on glucose metabolism and insulin resistance in patients with sleep apnea-hypopnea syndrome (AHS). Design and method: We prospectively included 30 consecutive patients recently diagnosed of AHS with an apnea-hypopnea index of 15 or higher and without prior treatment with CPAP. Patients were evaluated before and after 3-month CPAP therapy. There was no change on drug treatment during the study. Fasting blood glucose (FBG), insulin and HbA1c were measured. Beta-cell function, insulin sensitivity (IS) and insulin resistance index (IR) were estimated using the Homeostasis Model Assessment (HOMA) equations. Results: Mean (SD) age was 51.7 ± 11.5 years, and mean AHI: 56.3 ± 25.5. 63.3% were males. 23.3% had type 2 diabetes mellitus and 56.7% hypertension. Body mass index, FBG and HbA1c at baseline were 35.8 ± 6.5 kg/m2, 108.8 ± 26.5 mg/dL and 6.1 ± 0.7%, respectively, and they remained unchanged at the end of follow-up (p = 0,939, p = 0.300 and p = 0.307, respectively). At baseline, AHI correlated with IS (r = -0.45, p = 0.017) and IR (r = 0.43, p = 0.022). 3-month treatment with CPAP significantly decreased insulin levels (microU/ml, baseline: 23.5 ± 23.9; postCPAP therapy: 16.9 ± 11.6; p = 0.008) and IR (baseline: 2.5 ± 1.4; post-CPAP therapy: 2.2 ± 1,56; p = 0.024). Changes in IS (baseline 54,2 ± 30,0; postCPAP therapy: 60,0 ± 26,5; p = 0.055) and beta-cell function (%, baseline 137,8 ± 70,1; postCPAP therapy: 121,7 ± 48,9; p = 0.060) tended to be significant. Conclusions: Our results suggest that more severe AHS is related to an impaired IS and higher IR, and that treatment with CPAP may improve the insulin resistance syndrome.