Rhinitis and Sleep Apnea Maria T. Staevska, MD, Mariana A. Mandajieva, MD, and Vasil D. Dimitrov, MD, PhD Address Clinic of Asthma, Allergology, and Clinical Immunology, Medical University–Sofia, University Hospital “Alexandrovska”, 1, St. George Sofiisky str., 1431, Sofia, Bulgaria. E-mail: marista@rtb-mu.com Current Allergy and Asthma Reports 2004, 4:193–199 Current Science Inc. ISSN 1529-7322 Copyright © 2004 by Current Science Inc. Introduction Allergic rhinitis (AR), the most prevalent allergic disorder, and nonallergic rhinitis affect more than 25% of the popu- lation [1]. AR is characterized by local symptoms, such as nasal obstruction, itching, sneezing, rhinorrhea, and post- nasal drip, as well as daytime sleepiness, fatigue, head- aches, and malaise [1]. The latter systemic symptoms are especially related to poor performance and concentration at school and work, and to overall impairment of quality of life. It is generally accepted that complaints of sleepi- ness, fatigue, and malaise are secondary to the action of high levels of inflammatory mediators, such as tumor necrosis factor (TNF)- α, interferon (IFN)- γ , and other cytokines on the hypothalamus [2]. There is an increasing body of evidence, however, that the disabilities might be partially due to nasal congestion and sleep-disordered breathing [3–5]. Obstructive sleep apnea syndrome (OSAS) is character- ized by: 1) complete or partial collapse of the upper air- ways during sleep, with consequent cessation of breathing, despite ongoing respiratory effort; and 2) coexistent day- time somnolence. OSAS is an important health problem, given its associated adverse consequences and its preva- lence of least 4%. Two kinds of clinical sequelae are associ- ated with the disorder. Neuropsychiatric complications include sleepiness; depression; cognitive dysfunction; dis- ruption of professional, family, and social life; and inatten- tion that can result in road and industrial accidents. Cardiovascular complications include pulmonary and sys- temic hypertension due to chronic sleep-related hypoventi- lation, congestive heart failure, coronary heart disease, myocardial infarction, and stroke [6]. Obesity, increased neck circumference, aging, male sex, acromegaly, hypothyroidism, and relatively rare craniofa- cial abnormalities are strong risk factors for sleep-disor- dered breathing (SDB). Currently, the most important clinical risk factors are those of high prevalence that poten- tially can be modified [7]. Rhinitis meets these criteria, because it is a syndrome of high and increasing prevalence with relatively easily modified nasal congestion as a major contributing factor. Although earlier studies failed to dem- onstrate a linear correlation between nasal resistance and the severity of OSA [7–9], in 2000, Lofaso et al. [10••] used stepwise multiple regression analysis to show that daytime nasal obstruction represented an independent risk factor for OSAS. Rhinitis had a weaker correlation than cephalo- metric landmarks, obesity, and male sex, but was stronger than age. Recently, several reviews discussing the role of nasal obstruction in the genesis of SDB have been pub- lished [11,12•,13]. Finally, OSA might be a chronic inflammatory condi- tion characterized by high levels of cytokines and inflam- matory mediators that are similar to those of allergic rhinitis and asthma. Asthma might be more severe and dif- ficult to control if OSA is present. Nasal continuous posi- tive airway pressure (nCPAP) therapy can improve both the OSA and asthma [14,15]. The inflammatory mediators generated by OSA could possibly account for the cardiovas- cular and asthmatic complications [16•]. The cause of the OSA-related inflammation and its role in rhinitis are still open to debate. Scope of Sleep-disordered Breathing Sleep-disordered breathing is a large entity encompassing a variety of conditions of sleep-related regular respiratory The nose and pharynx begin the upper airway system and represent a continuum. This is the biologic basis for the mutual influences of rhinitis and obstructive sleep apnea (OSA). Sleep-disordered breathing has a large differential diagnosis that includes snoring, upper airway resistance syndrome, and severe OSA. Nasal obstruction is an inde- pendent risk factor for OSA, but there is no correlation of daytime nasal resistance with the severity of OSA. How- ever, nasal resistance was an independent predictor of apnea–hypopnea index in a recent study of nonobese OSA patients. Rhinitis alone is associated with mild OSA, but commonly causes microarousals and sleep fragmentation. Reduction of nasal inflammation with topical treatment improves sleep quality and subsequent daytime sleepiness and fatigue. Patient compliance with the nasal continuous positive airway pressure (nCPAP) device is relatively low, in part due to adverse nasal effects.