Original articleCorrelates of daytime sleepiness in patients with asthma
Introduction
Daytime sleepiness is a particularly frequent complaint in patients with asthma [1], [2]. Daytime sleepiness has a negative impact on quality of life, work performance, and risk for motor vehicle crashes or work-related accidents [3]. In general, daytime sleepiness is often the result of poor sleep quality, and asthmatics do commonly complain about difficulty with initiation [1], [4] and maintenance of sleep, especially in the early morning [1], [5]. Such sleep disturbances become more frequent with increased nocturnal asthma symptoms [1]. Nocturnal wakefulness correlates with daytime airways obstruction, as measured by forced expiratory volume in one second as percent of predicted value (FEV1%) [1]. Sleep studies in asthmatics have provided some objective evidence of poor sleep quality as evidenced by a reduced sleep time, delayed latency to sleep, frequent awakenings after sleep onset, early morning arousals and reduced slow wave sleep [4], [6]. Therefore, daytime sleepiness in asthma is often thought to be the consequence of a direct effect of nocturnal asthma on sleep quality.
Both increased subjective sleepiness and poor sleep quality scores were documented recently in a large population of asthmatics [7], but two therapeutic strategies for asthma failed to improve subjective sleepiness and sleep quality scores [8]. These results suggest that other possible reasons for daytime sleepiness in asthmatics also should be considered. Excessive daytime sleepiness (EDS) is one of the most common presenting symptoms of obstructive sleep apnea (OSA), in itself a common and frequently unrecognized condition [9], [10]. Snoring is frequent in both OSA patients and asthmatics [2], [11], [12]. Recently, in a sample of 22 difficult-to-control asthmatics, daytime sleepiness was reported by 20 (90.9%) of the subjects and OSA was demonstrated by polysomnography in 21 (95.5%) of them [13]. Furthermore, asthma frequently coexists with allergic rhinitis and chronic sinusitis [14], gastroesophageal reflux disease (GERD) [15], obesity [16], and psychopathology such as anxiety, depression and panic disorders [17], [18], all of which are known to be associated with daytime sleepiness [3], [5], [19], [20]. The medications commonly used to treat asthma tend to have stimulating, anxiety-provoking or mood-depressing properties [5], [21], [22] that could interfere with sleep quality and exacerbate daytime sleepiness.
Previous studies of sleepiness in asthma have been limited by reliance on patient-reported asthma diagnosis or have not included information on comorbid conditions and medications that could influence sleepiness. We therefore studied a sample of medically well-characterized asthmatics with validated survey measures to examine possible reasons for EDS. In particular, we hypothesized that unrecognized OSA is an important contributor to EDS in asthmatics.
Section snippets
Subjects
This study was approved by the Institutional Review Board and conducted between May 2004 and February 2005. Clinic rosters were used to identify patients returning for routine asthma follow-up visits at the University of Michigan Pulmonary Clinics and Briarwood Asthma-Airways Center. Patients completed the screening questionnaires if they were 18–75 years old, able to provide informed consent, and willing and able to complete the survey. Patients at the clinics for urgent asthma-related visits
Subjects' characteristics
Among 156 consecutive asthmatics who were approached between May 2004 and February 2005, 150 completed the informed consent and survey. Additional lung diseases (such as chronic obstructive pulmonary disease, bronchiectasis, sarcoidosis, interstitial lung disease, and hypersensitivity pneumonitis) were present in 15 subjects, who were excluded from the present analysis. Forty (30%) of the remaining subjects had a prior diagnosis of SDB, and half of them were being treated at the time of survey
Acknowledgements
The authors thank Jack D. Kalbfleisch, PhD and Yining Ye, MS for their expert statistical support, and Radu C. Nistor and Jesica M. Pedroza for assistance with administration of screening questionnaires and entry of data. The authors thank the physicians at the University of Michigan Pulmonary Clinics and Briarwood Asthma-Airways Center for their help in identification of subjects for this study. This work was supported by University of Michigan General Clinical Research Center (MO1 RR00042)
Conflict of interest disclosures
The following authors: M Teodorescu, WF Bria, MJ Coffey, MS McMorris, KJ Weatherwax, J Palmisano, CM Senger and RD Chervin have nothing to disclose. Dr FB Consens and A Durance RN have received speaker's honoraria (each under $10,000 in the last year) from GlaxoSmithKline, and from Novartis Pharma and Genentech, respectively.
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