Sarcoidosis and Obstructive Sleep Apnoea: An Intriguing Relationship

Sarcoidosis is a systemic granulomatous disorder of unknown etiology, most commonly affecting the lungs but potentially involving multiple organs. Fatigue and Excessive Daytime Sleepiness (EDS) represent highly prevalent and disabling symptoms, often persisting despite stable systemic disease. Growing evidence indicates an increased prevalence of Obstructive Sleep Apnoea (OSA) among patients with sarcoidosis, suggesting a complex and multifactorial association. Several mechanisms contribute to this link. Shared inflammatory pathways promote systemic inflammation and vascular dysfunction. Corticosteroid therapy, although central to sarcoidosis management, indirectly predisposes to OSA through weight gain, fat redistribution, and myopathy. Direct upper airway involvement (sarcoidosis of the upper respiratory tract, SURT) may cause mechanical obstruction, while restrictive pulmonary disease reduces lung volumes and increases pharyngeal collapsibility. Clinical studies consistently report a higher prevalence of OSA in sarcoidosis compared with the general population, even in non-obese and treatment-naïve patients. While OSA contributes to fatigue and EDS, these symptoms are also influenced by immune dysregulation, chronic inflammation, and treatment side effects. Continuous Positive Airway Pressure (CPAP) therapy has demonstrated efficacy in reducing apnoea burden and improving both fatigue and quality of life, underscoring the importance of systematic OSA screening in sarcoidosis patients with persistent sleep-related symptoms. Despite increasing recognition, current evidence is limited by small sample sizes, heterogeneous diagnostic methods, and confounding effects of corticosteroid therapy. Future studies should clarify pathophysiological mechanisms, evaluate the impact of OSA treatment on sarcoidosis outcomes, and investigate wake-promoting agents such as solriamfetol and pitolisant as potential adjunctive therapies in patients with residual EDS.