Introduction
Sleep-related breathing disorders comprise a range of conditions. Obstructive sleep apnea (OSA) is the most severe and complex sleep-related syndrome. It comprises repeated episodes of airway obstruction leading to apnea (breathing cessation) or hypopnea (a reduction in airflow) during sleep. A person with OSA can suffer from loud snoring, frequent waking, and sleep disruption. Disturbed sleep also results in hypersomnolence (excessive sleep), impaired concentration, and poor quality of life (QoL). The global prevalence of OSA is about five percent in the general population. In India, the prevalence of OSA is around 15 percent, according to different studies. OSA increases with age, particularly in adults older than 60. Obesity, male gender, genetic disorders, smoking, and postmenopausal state in females contribute to OSA. Recent studies have shown a link between asthma and OSA. Further, they have a bidirectional relationship. Hence, asthmatic patients have an increased OSA risk compared to normal individuals.
What Are the Common Risk Factors of Asthma and Obstructive Sleep Apnea?
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Rhinitis: The prevalence of rhinitis (inflammation of the nose) in asthma is around 90 percent. Furthermore, chronic (long-standing) rhinitis is a risk factor for asthma. Rhinitis causes inflammation of the nasal passage, leading to nasal obstruction. The nose is the primary breathing route during sleep. Hence, nasal factors are important determinants of upper-airway patency. Studies show that peak nasal obstruction occurs in the early morning (OSA also peaks during the morning hours). Thus, inflammation in rhinitis and asthma perpetuate each other and could promote the development of OSA (as asthma is also a chronic inflammatory state).
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Gastroesophageal Reflux (GER): Studies report an association between GER (in GER, the stomach acid repeatedly flows back into the esophagus) and OSA. GER is predictive of habitual snoring and high OSA risk in a group of patients with asthma. GER can cause spasms of the upper airway, edema, and mucosal inflammation, promoting OSA. All these factors can also worsen asthma and start a vicious cycle.
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Obesity: Obesity is a risk factor linking asthma with OSA. Studies reveal that it is a significant risk factor for severe asthma. Similarly, asthmatic patients are also at risk for obesity. It is because they are less active during oral corticosteroid therapy, which promotes weight gain. Additionally, fatigue secondary to sleep loss due to asthma favors a sedentary lifestyle and promotes obesity. On the other hand, obesity is also a risk factor for OSA. Obesity changes the structure and function of the upper airway muscles and increases oxygen demand, favoring their collapse.
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Corticosteroid Therapy: Research suggests that steroids may increase upper airway collapse. Long-term inhaled corticosteroid (ICS) therapy in asthma can also modulate hormone secretion (especially growth hormone, GH). OSA is associated with GH excess in children and GH deficiency in adults. As a result, it can cause metabolic and cardiovascular complications that worsen OSA.
What Are the Pathophysiological Links Between OSA and Asthma?
Asthma can predispose to OSA through unique features. Asthma is an inflammatory condition in which chronic inflammation is aggravated by allergic, infectious, and other triggers.
OSA can also contribute to inflammation in asthma. OSA at night has carryover effects on daytime asthma. Recent data shows that OSA alters the asthmatic's inflamed airway.
Studies show that around 90 percent of severe asthma exacerbations are linked to hypoxia (low blood oxygen), which persists for many days. In addition, nocturnal (at night) asthma leads to frequent arousal and poor sleep quality. These observations raise the question of whether these asthma features could contribute to OSA pathogenesis (the disease process). Hence, further studies are needed to investigate these mechanisms.
Inflammatory pathways related to asthma may also sabotage the protective mechanisms of upper airway patency. The site of obstruction in OSA is at the level of the pharyngeal airway (an area extending from the end of the nose to the epiglottis). The region lacks support and is vulnerable to collapse during sleep.
OSA promotes inflammation through hypoxia, hypercapnia (increased carbon dioxide in the blood), and sleep fragmentation. As a result, it leads to a reversible increase in C-reactive protein (CRP, an inflammatory marker). The production of inflammatory cytokines (mediators) is increased in OSA patients. These play an important role in the collapse and re-opening of the airways.
How Does OSA Treatment Affect Asthma Outcomes?
The link between cough or asthma, OSA, rhinitis, and esophageal reflux has been coined “CORE syndrome.” The gold standard for OSA diagnosis is a polysomnogram (PSG, the study used to diagnose sleep disorders). PSG studies report a high prevalence of OSA with severe asthma. PSG is an expensive and time-consuming method. Therefore, it is inconvenient to screen several patients for PSG. Hence, OSA questionnaires in asthmatic populations are beneficial. Further, home sleep apnea testing (HSAT) is better than the questionnaires and can also identify moderate to severe OSA.
OSA patients treated with continuous positive airway pressure (CPAP, a device that delivers continuous pressurized air through a mask while sleeping) have better asthma control, symptoms, and QoL. Therefore, the need to screen asthmatics for OSA is pertinent. CPAP has beneficial effects on the mechanical properties of the upper and lower airways, GER, and local and systemic (body) inflammation. Further, CPAP also restores sleep and controls asthma. Previous studies have shown that PAP treatment is beneficial for sleep disturbances in OSA and asthmatic patients. CPAP treatment also reduces bronchodilator (asthma treatment) use while improving lung function tests. Hence, CPAP represents a useful tool to integrate with corticosteroid treatment. Moreover, animal studies demonstrate that corticosteroids may contract airway smooth muscle, leading to instability and reducing their protective effect on the upper airways during sleep. All these lead to a worsening of OSAS.
Also, bariatric surgery (done to treat obesity) improves asthma control, pulmonary (lung) function, QoL, and OSA. Several studies have shown OSA links to multiple asthma outcomes. In hospitalized patients with severe asthma, an OSA diagnosis is related to poorer outcomes. It is because it leads to invasive respiratory therapy, increased hospital stays, and increased costs.
Conclusion
In conclusion, evidence indicates a relationship between OSA and asthma based on shared risk factors and bidirectional interactions. The science of OSA in asthma is in its infancy. However, the current evidence highlights the need for further studies to elucidate the pathogenesis of OSA in asthma. Further, the role of OSA in asthma variations, gender differences, and responses to medications needs clarification.
