The relationships between intermittent hypoxia and oxidative stress in patients with sleep apnea syndrome

Intermittent hypoxia in sleep apnea syndrome (SAS) patients increases the oxidative stress and can cause serious cardiovascular diseases such as hypertension or atherosclerotic diseases through endothelial dysfunction. The evaluation of risk caused by oxidative stress, however, is not easy in a clinical setting. Thus, we intended to evaluate the changes in oxidative stress by SAS treatment using a simple method that can be easily used in the clinical testing. We enrolled 42 consecutive newly diagnosed severe SAS patients (30 men). Reactive oxygen species metabolites (d-ROMs) for oxidative stress and biological antioxidant (BAP) in blood samples were estimated using FREE Carrio Duo^® before and 3 months after continuous positive airway pressure (CPAP) treatment. SAS parameters were obtained by polysomnography before CPAP and endothelial function was measured twice as well. The body mass index and apnea hypopnea index (AHI) were 29.1 ± 5.3 and 57.9 ± 19.7/h. The d-ROMs and BAP were 317.4 ± 71.8 CARR U and 2121.2 ± 299.6 μmol/L. Although no significant correlation was found between hypoxia parameters and d-ROMs or BAP before CPAP treatment, we found a significant negative correlation between basal AHI or basal oxygen desaturation index representing intermittent hypoxia and the change in d-ROMs (r = − 0.31, p = 0.046/r = − 0.33, p = 0.03) and between the change in SpO₂ < 90% duration (min) representing continuous hypoxia and the change in BAP (r = − 0.35, p = 0.03) after CPAP treatment. The changes in d-ROM and BAP might reflect the different kind of reduction of oxidative stress by CPAP treatment and, thus, can be used as handy indicators of the treatment effect.