Relación entre apnea del sueño y cáncer

In the light of relationships reported between hypoxemia (tissue hypoxia) and cancer, Abrams et al. concluded in 2008 that sleep apnea-hypopnea syndrome (SAHS) and its main consequence, intermittent hypoxia, could be related with increased susceptibility to cancer or poorer prognosis of a pre-existing tumor. This pathophysiological association was confirmed in animal studies. Two large independent historical cohort studies subsequently found that the degree of nocturnal hypoxia in patients with SAHS was associated with higher cancer incidence and mortality. This finding has been confirmed in almost all subsequent studies, although the retrospective nature of some requires that they be considered as hypothesis-generating only. The relationship between sleep apnea and cancer, and the pathophysiological mechanisms governing it, could be clarified in the near future in a currently on-going study in a large group of melanoma patients.     

Síndrome de apneas-hipopneas del sueño y diabetes tipo 2. ¿Una relación de ida y vuelta?

Epidemiological data suggest that sleep apnea-hypopnea syndrome (SAHS) is independently associated with the development of insulin resistance and glucose intolerance. Moreover, despite significant methodological limitations, some studies report a high prevalence of SAHS in patients with type 2 diabetes mellitus (DM2). A recent meta-analysis shows that moderate-severe SAHS is associated with an increased risk of DM2 (relative risk = 1.63 [1.09 to 2.45]), compared to the absence of apneas and hypopneas.Common alterations in various pathogenic pathways add biological plausibility to this relationship. Intermittent hypoxia and sleep fragmentation, caused by successive apnea-hypopnea episodes, induce several intermediate disorders, such as activation of the sympathetic nervous system, oxidative stress, systemic inflammation, alterations in appetite-regulating hormones and activation of the hypothalamic-pituitary-adrenal axis which, in turn, favor the development of insulin resistance, its progression to glucose intolerance and, ultimately, to DM2.Concomitant SAHS seems to increase DM2 severity, since it worsens glycemic control and enhances the effects of atherosclerosis on the development of macrovascular complications. Furthermore, SAHS may be associated with the development of microvascular complications: retinopathy, nephropathy or diabetic neuropathy in particular. Data are still scant, but it seems that DM2 may also worsen SAHS progression, by increasing the collapsibility of the upper airway and the development of central apneas and hypopneas.