Abstract
Background: In recent years, sleep apnea syndrome (SAS) has been widely considered to be a cardiovascular disease (CVD) risk factor. Although several plausible mechanisms have been put forth to explain such association in patients with SAS, oxidative stress has been suggested to play a major role. In patients with SAS, the repetitive ischemia-reperfusion state causes excessive production of oxygen free radicals and may subsequently lead to oxidative injury of various biomolecules. Due to the high prevalence of SAS in dialysis patients, this possible uremia-specific CVD risk factor may definitely need more medical attention. Methods: We, therefore, performed a case control study to investigate the relationship between oxidative stress and SAS in a group of dialysis patients, using some well-established oxidative biomarkers. Results: Our results showed that plasma nitrotyrosine, protein carbonyl and malonaldehyde levels were significantly elevated in patients with SAS. Markers of endothelial activation such as soluble CD40 ligand were also increased in this subgroup of patients. However, there was no significant difference in serum C-reactive protein levels between these groups. Conclusions: Our results indicate that patients with SAS manifest evidence for higher oxidative stress and endothelial activation. Thus, intermittent hypoxia represents a form of oxidative stress and low-grade chronic inflammatory state that may be associated with increased cardiovascular disease in these patients.