Abstract

It seems paradoxical to observe how obstructive sleep apnoea (OSA) has been associated with a large number of systemic diseases, and is even recognized as a risk factor for some of them [1–4], but is nevertheless, strictly speaking, basically a local mechanical problem resulting from intermittent collapses of the upper airway during sleep. The explanation for this phenomenon is that these repetitive airway obstructions trigger several pathophysiological mechanisms that have an overall systemic effect. Thus, sympathetic activation, periodical hypoxaemias–normoxaemias, hypercapnia, arousals and changes in intrathoracic pressure induced by OSA lead to the activation of some pathophysiological pathways similar to those observed in several cardiovascular diseases [5]. This explains why OSA has been associated with the onset, poor control and worsened prognosis of some of the most prevalent cardiovascular diseases, such as arterial hypertension [6], cardiac arrhythmias [7], and cerebral and cardiovascular events [3, 4]. One aspect that has been far less studied to date is the relationship between OSA and systemic inflammation. In this respect, OSA has recently been associated with diseases with a great inflammatory burden, such as psoriasis [8] and other autoimmune disorders [9]. The relative scientific youthfulness of OSA means that new action mechanisms and previously unknown associations with other diseases are now being increasingly discovered. One particular piece of news was sprung on the scientific community at recent international congresses, creating quite a stir: some studies in both animals [10–12] and humans [13–15], undertaken almost simultaneously, had found an association between OSA and cancer. There have been reports of a relationship between different aspects of nonapnoeic sleep disorders, particularly sleep duration, and cancer. Specifically, some studies have shown an association between …

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