Obstructive apneas during sleep in patients with seasonal allergic rhinitis
ABSTRACT The possible role of high nasal airway resistance in the pathogenesis of obstructive sleep apnea has been examined in 7 patients with seasonal (ragweed) allergic rhinitis, a naturally occurring model of reversible nasal obstruction. Measurements of nasal resistance and overnight polysomnographic studies were performed during the ragweed season when the patients complained of nasal obstruction; and 6 to 8 wk later when the symptoms had subsided (control study). During the symptomatic phase, mean (+/- SE) nasal resistance was 4.9 +/- 0.8 cm H2O/L/s, and the patients experienced 1.7 +/- 0.3 obstructive apneas per hour of sleep. In contrast, at the time of the control study, nasal resistance had decreased to 2.5 +/- 0.3 cm H2O/L/s (p less than 0.01); and the rate of obstructive apneas had decreased to 0.7 +/- 0.4 per hour of sleep (p less than 0.005). The duration of these apneas had also decreased from 15.5 +/- 0.8 s to 6.1 +/- 2.9 s (p less than 0.01). Apneas were rarely associated with significant O2 desaturation and were fewer in number than typically seen in a clinically significant sleep apnea syndrome. In male patients there was a direct relationship (r = 0.9) between the change in nasal resistance from symptomatic to control studies and the corresponding change in frequency of obstructive sleep apneas. Coincident with these respiratory changes at the time of the control study was an increase in the amount of slow-wave sleep (p = 0.05) and a small reduction in the frequency of arousals during sleep (p = NS). We conclude that in patients with allergic rhinitis, obstructive sleep apneas are longer and more frequent during a period of symptomatic nasal obstruction than when symptoms are absent. The results support the concept that a high nasal resistance may be a contributing factor in the pathogenesis of obstructive sleep apneas in general.
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- "In addition, upper airway structure and function are altered in patients with OSAS     . With recurrent obstruction and reopening of the upper airways during sleep, mucosal congestion in the airway can further increase local inflammation and oxidative stress   . Elevation of levels of serum biomarkers for inflammation and oxidative stress were consistently reported in OSAS patients   . "
ABSTRACT: Relationships between exhaled breath condensate (EBC) and serum cytokines and apnea-hypopnea index (AHI) in patients with excessive daytime sleepiness and loud snoring were evaluated for their potential to predict the severity of obstructive sleep apnea syndrome (OSAS). Non-smoking patients with suspected OSAS who had undergone polysomnography (PSG) were selected until 22 non-OSAS, and 22 mild, 22 moderate and 24 severe OSAS cases based on AHI were achieved. Ten healthy smokers served as a smoker control group. Interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-alpha), and 8-isoprostane were measured in EBC and serum on the morning after PSG and related to OSAS severity using linear discriminant analysis (LDA) and logistic regression (LR). Biomarker levels, in both EBC and serum, differed significantly across the four groups. Classification by LDA using IL-10 in EBC showed the highest agreement with AHI classification (kappa=0.88). LR distinguished moderate and severe OSAS from mild OSAS and non-OSAS perfectly using IL-6 in EBC and almost perfectly using IL-10 in EBC (area under the ROC curve=0.997). The levels of biomarkers among smokers overlapped with mild to severe OSAS patients. Among non-smoker OSAS suspects, EBC IL-6 and IL-10 have potential to predict severity of OSAS.Sleep Medicine 02/2008; 10(1):95-103. DOI:10.1016/j.sleep.2007.11.013 · 3.10 Impact Factor
Article: Obstructive Sleep Apnea in Children[Show abstract] [Hide abstract]
ABSTRACT: Obstructive sleep apnea (OSA) is a common condition of childhood, and is associated with significant morbidity. Prevalence of the condition peaks during early childhood, due in part to adenoidal and tonsillar enlargement within a small pharyngeal space. The lymphoid tissues regress after 10 years of age, in the context of ongoing bony growth, and there is an associated fall in the prevalence of OSA. Obstruction of the nasopharynx by adenoidal enlargement promotes pharyngeal airway collapse during sleep, and the presence of large tonsils contributes to airway obstruction. Administration of systemic corticosteroids leads to a reduction in the size of lymphoid tissues due to anti-inflammatory and lympholytic effects. However, a short course of systemic prednisone has been demonstrated not to have a significant effect on adenoidal size or the severity of OSA, and adverse effects preclude the long-term use of this therapy. Intranasal corticosteroids are effective in relieving nasal obstruction in allergic rhinitis, and allergic sensitization is more prevalent among children who snore than among those who do not snore. Intranasal corticosteroids have also been demonstrated to reduce adenoidal size, independent of the individual’s atopic status. There is preliminary evidence of an improvement in the severity of OSA in children treated with intranasal corticosteroids, but further studies are needed before such therapy can be routinely recommended. Prescribing clinicians should take into account the potential benefits to the patient, the age of the child, the presence of comorbidities such as allergic rhinitis, the agent used, and the dose and duration of treatment when considering such therapy.American journal of respiratory medicine: drugs, devices, and other interventions 06/2012; 1(3). DOI:10.1007/BF03256605
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ABSTRACT: Patients with allergic rhinitis frequently present with symptoms of nasal congestion, runny nose, sneezing, daytime somnolence and fatigue associated with decreased cognitive performance and impaired quality of life. Recent research has suggested that daytime somnolence in allergic rhinitis can be attributed to chronic inflammation of the nasal mucosa leading to nasal congestion and obstructed nasal passageways resulting in disturbed sleep. Treating daytime somnolence due to allergic rhinitis requires a reduction in obstruction caused by nasal congestion. Currently available therapy for allergic rhinitis includes topical corticosteroids, sedating and non-sedating antihistamines, topical cromolyn sodium (sodium cromoglycate), decongestants, immunotherapy and topical ipratropium bromide. The effectiveness of antihistamines in patients with allergic rhinitis has long been established. However, results of placebo-controlled trials investigating the effects of azelastine on sleep and daytime somnolence have produced conflicting results. Sleep improved with azelastine therapy, but there was a lack of evidence that azelastine significantly affected daytime sleepiness, sleep severity and nasal congestion. Sedating antihistamines exacerbate daytime somnolence and should be avoided in patients with allergic rhinitis. In a separate study, desloratadine failed to benefit sleep, but did not worsen daytime somnolence. Topical nasal cromolyn sodium is inconvenient to use and is unlikely to have a major effect on nasal congestion. Decongestants do decrease nasal congestion but the effect this has on sleep has not been adequately studied. Recent research has shown that topical corticosteroids are an effective treatment for alleviating nasal congestion secondary to allergic rhinitis. However, few studies have assessed the effect of topical corticosteroids on daytime fatigue and sleep. In 20 patients with allergic rhinitis and symptoms of daytime sleepiness, flunisolide significantly improved sleep quality and congestion but daytime sleepiness was not significantly improved. A similar study with fluticasone propionate showed improvement in nasal congestion and sleep but there was no significant change in objective sleep measurements recorded on polysomnography. Further research involving objective measures of sleep quality is necessary to determine the efficacy of medications in the treatment of allergic rhinitis associated with fatigue and daytime somnolence.American journal of respiratory medicine: drugs, devices, and other interventions 06/2012; 1(3). DOI:10.1007/BF03256609