[Obstructive sleep apnoea and oxidative stress]

Untreated obstructive sleep apnoea (OSA) is characterised by elevated systemic and local oxidative stress and inflammation. Non-invasive measurement of metabolites and markers of inflammation in exhaled breath condensate (EBC) is of interest in the interpretation of systemic effects of severe obstructive sleep apnoea. In patients with severe sleep apnoea (AHI ≥ 30 /h) we investigated if CPAP therapy with normalisation of AHI induces changes of H2O2 concentrations in EBC.

Patients with obstructive sleep apnea (AHI ≥ 30 /h) had H2O2 analysis of EBC after native PSG, after the first night and after 6 weeks of CPAP therapy. Only patients with normalisation of AHI (AHI ≤ 10  /h) were included in the further analysis.

23 patients (21 men and 2 women) fulfilled the inclusion criteria. The first night of CPAP therapy led to a significant reduction of AHI, but did not change the H2O2 concentration in EBC. After 6 weeks of CPAP therapy with normalisation of AHI (3 ± 3 /h) H2O2 in EBC showed a significant reduction from 450 ± 163 nmol/L to 294 ± 110 nmol/L. Subgroup analysis showed that in non-smokers and especially in smokers the reduction was less marked than in ex-smokers.

Normalisation of AHI after 6 weeks of CPAP therapy in OSA induces a significant reduction of H2O2 in EBC. This primarily represents a reduction of local inflammation and oxidative stress in the airways, but also indicates a positive effect on elevated oxidative stress in OSA. The influence of smoking status needs further investigations, including subgroup analysis with a sufficient number of patients.