Systemic inflammation and oxidative stress develop because of chronic hypoxia and in response to repetitive intermittent hypoxia during sleep in OSA. One of the main common consequences of these diseases is local and systemic hypoxia. Patients with “overlap syndrome showed an increased risk of death and hospitalization. The term ‘‘overlap syndrome’’ was introduced to describe the association of both conditions in a single patient. COPD and OSA are frequent diseases affecting more than 10% of the adult population each. Treatment with CPAP appears to improve sRAGE levels in patients with OSA who also had COPD.Ĭhronic obstructive pulmonary disease (COPD) is characterized by airflow obstruction and persistent airway inflammation due to the inhalation of noxious gases such as cigarette smoke, whereas obstructive sleep apnoea (OSA) is characterized by periodic collapse of the upper airway during sleep. The levels of sRAGE are reduced in COPD and OSA. Moreover, in patients with OSA and OSA-COPD overlap who were treated with CPAP, sRAGE increased significantly. At follow-up, sRAGE levels did not change significantly in healthy subjects, COPD and OSA or OSA-COPD overlap nontreated with continuous positive airway pressure (CPAP).

There were no differences when comparing sRAGE plasma levels between overlap patients and those with OSA or COPD alone. ResultsĪfter adjusting for age, sex, smoking status and body mass index, sRAGE levels showed a reduction in OSA (− 12.5%, p = 0.005), COPD (− 14.8%, p < 0.001) and OSA-COPD overlap (− 12.3%, p = 0.02) compared with HNS. Plasma levels of sRAGE were measured in 317 subjects at baseline (57 heathy nonsmokers, 84 healthy smokers, 79 OSA, 62 COPD and 35 OSA-COPD overlap patients) and in 294 subjects after one year of follow-up (50 HNS, 74 HS, 77 OSA, 60 COPD and 33 overlap). We assessed sRAGE in patients with hypoxia-related diseases such as COPD, OSA and OSA-COPD overlap.

Hypoxia can reduce the levels of soluble receptor for advanced glycation end-products (sRAGE), a new anti-inflammatory biomarker of COPD.

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