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Effects of CPAP-respiration on markers of glucose metabolism in patients with obstructive sleep apnoea syndrome: a systematic review and meta-analysis

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Author(s): Hecht, Lars | Möhler, Ralph | Meyer, Gabriele

Journal: GMS German Medical Science
ISSN 1612-3174

Volume: 9;
Start page: Doc20;
Date: 2011;
Original page

Keywords: Insulin resistance | continuous positive airway pressure | obstructive sleep apnea | diabetes mellitus type 2 | meta-analysis

ABSTRACT
Background: Obstructive Sleep Apnoea Syndrome (OSAS) is a condition of obstruction, apneas and arousals while sleeping. It has been suggested that OSAS independently influences glucose metabolism. The main treatment for OSAS is continuous positive airways pressure (CPAP). Objectives: To assess the effects of CPAP on insulin resistance and glucose metabolism. Search strategy: We searched Medline, Embase and the Cochrane Controlled Trial Register (January 2010). Selection criteria: We included randomised and non-randomised trials comparing CPAP with inactive control or placebo CPAP in adults with OSAS. Data collection and analysis: Two authors independently assessed trial quality and extracted data. Parallel and crossover group trials were analysed separately. A meta-analysis was carried out. Results: Three parallel group and two cross-over randomised trials and one controlled trial were included investigating 296 participants. Sample sizes ranged from n=13 to n=102 participants, age was 18 to 75 years, mean body mass index (BMI) 27.2 kg/m² to 37.1 kg/m², mean apnoe hypopnoe index (AHI) 29.7 to 39.7 events per hour, mean dips >4% in arterial oxygen saturation per hour of sleep 1 to 42.7 events. The studies’ methodological quality varied. Follow-up ranged from 4 to 12 weeks. Various endpoints were investigated. CPAP did neither influence plasma insulin levels nor HOMA-index, adiponectin levels or HbA1c value. One study reported a significant positive effect on the insulin sensitivity index (1.68%/min, 95% CI 0.3 to 3.06). Conclusion: This systematic review does not support the hypothesis that OSAS independently influences glucose metabolism. Sufficiently powered, long-term randomised controlled trials defining changes of insulin resistance as primary endpoint are needed.

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