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West et al are to be commended for the laborious study of the impact of continuous positive airway pressure (CPAP) on insulin resistance and glycaemic control in males with obstructive sleep apnoea syndrome (OSAS) and type 2 diabetes (Thorax 2007;62:969–74). The authors did not demonstrate an improvement in insulin sensitivity and glycaemic control in obese patients after 3 months of therapeutic CPAP compared with placebo CPAP. The presentation of the apnoea–hypopnoea index (AHI) results (shown as mean (SD, 0–100% range)) suggests some patients had a relatively low AHI. It is noteworthy that the impact of the severity of OSAS on insulin resistance and a possible therapeutic approach by CPAP remains to be clarified. The effect of chronic glucose toxicity in patients with poor glycaemic control has to be considered. The HbA1c between 8.5% and 8.4% remained unchanged and accounts for mean blood glucose levels of about 190 mg/dl.
We could not demonstrate changes in insulin sensitivity in our study in 40 non-diabetic OSAS patients (AHI 43.1 (SD11.4)), in the subgroup with a body mass index (BMI) ⩾30 kg/m2,1 and also no early effect in nine well controlled diabetic patients with OSAS (BMI 37.3 (SD5.6) kg/m2).2 These findings underline the enormous impact of obesity on insulin resistance in OSAS patients, whether or not they have diabetes.
Therapeutic CPAP improved glycaemic control after 3 months in our subjects with diabetes. Changes in body composition may play a role. Unfortunately, bioelectrical impedance analysis, as used in all studies, has its limitations.3
It would be very interesting to know whether there is an effect of CPAP therapy on insulin sensitivity in less obese diabetic subjects as we demonstrated a rapid improvement in insulin sensitivity in our study in the non-diabetic OSAS group in those with a BMI <30 kg/m2. That this early effect of CPAP may be related to acclimatisation to the conditions of the sleep laboratory and the clamp procedure is questionable as our studies were done under exactly the same conditions and there is no reason to postulate a higher stress sensitivity in leaner patients.
Although we could not measure plasma catecholamines, we were able to re-measure serum cortisol as another marker of sympathetic stimulation in 20 individuals in our study,1 and could not find significant differences before (mean 19.18 (SD 3.52) μg/dl) and 2 days after (19.35 (3.27) μg/dl) onset of CPAP therapy (p = 0.59).
Competing interests: None.
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