Asthma and Obstructive Sleep Apnea Overlap: What Has the Evidence Taught Us?

Abstract

Obstructive sleep apnea (OSA) and asthma are highly prevalent chronic respiratory disorders. Beyond their frequent coexistence arising from their high prevalence and shared risk factors, these disorders feature a reciprocal interaction whereby each disease impacts the severity of the other. Emerging evidence implicates airway and systemic inflammation, neuroimmune interactions, and effects of asthma-controlling medications (corticosteroids) as factors that predispose patients with asthma to OSA. Conversely, undiagnosed or inadequately treated OSA adversely affects asthma control, partly via effects of intermittent hypoxia on airway inflammation and tissue remodeling. In this article, we review multiple lines of recently published evidence supporting this interaction. We provide a set of recommendations for clinicians involved in the care of adults with asthma, and identify critical gaps in our knowledge about this overlap.

Keywords: asthma; continuous positive airway pressure; obstructive sleep apnea; overlap; pathophysiology.

Figure 1.

Schematic of mechanisms bidirectionally linking asthma and obstructive sleep apnea (OSA), as suggested by currently available data. In each direction, shared risk factors and specific features of each disease (asthma or OSA) may also underlie the interaction. See text for details. GER = gastroesophageal reflux.

Figure 2.

Disease-specific features known to contribute to the asthma/obstructive sleep apnea (OSA) overlap. Asthma commences early in life, traditionally as an eosinophilic airway disease, and has been shown to lead to incident OSA, with a new set of symptoms overlapping those of asthma. Asthma’s pathognomonic features, notably airway and systemic inflammation, could destabilize peripheral and central breathing and upper-airway control mechanisms. In conjunction with anatomical effects of long-term inhaled corticosteroid (ICS) therapy on the pharyngeal airway, it sets the stage for upper-airway collapse during sleep and OSA. Once established, OSA, through its features, notably chronic intermittent hypoxia, has been shown to shift the airway inflammatory profile away from T-helper cell type 2 (Th2) pathways, which leads to lung remodeling and airway dysfunction, in a pattern that is less responsive to ICS therapy. Without addressing OSA, achieving asthma control would likely require a step-up in ICS dose and repeated steroid bursts, further raising the risk for or the severity of OSA with its consequences for asthma, accelerating this vicious cycle and translating into irreversible airway dysfunction. See text for additional details.