Asthma Linked to New-Onset Sleep Apnea

Diana Phillips

January 14, 2015

Adults with asthma are at increased risk for new-onset obstructive sleep apnea (OSA), according to a new study.

Furthermore, the longer the duration of asthma, the more likely an individual is to develop the potentially serious sleep disorder, in which breathing repeatedly stops and starts, report Mihaela Teodorescu, MD, from the University of Wisconsin School of Medicine and Public Health, Madison, and colleagues in an article published in the January 13 issue of JAMA.

Although accumulating evidence suggests a bidirectional relationship between asthma and OSA, "[n]o studies, to our knowledge, have evaluated the prospective relationship of asthma with incident polysomnographically OSA," the authors note.

To test the hypothesis that preexistent asthma is a risk factor for later development of OSA, the investigators examined the relationship between the two conditions in the population-based, prospective Wisconsin Sleep Cohort Study.

Study participants include a random sample of Wisconsin state employees who were recruited beginning in 1998 to attend overnight polysomnography studies at 4-year intervals, during which asthma and covariate information were assessed through March 2013. The final sample for the current analysis included 547 participants with a total of 1105 sets of 4-year intervals, including 211 participants with one set, 173 with two sets, 105 with 3 sets, 57 with 4 sets, and 1 with 5 sets, the authors write.

Of 81 participants with asthma, 22 (27%; 95% confidence interval [CI], 17% - 37%) developed incident OSA during their first observed 4-year interval compared with 75 (16%; 95% CI, 13% - 19%) of 466 participants without asthma, the authors report. When the investigators analyzed all available 4-year intervals, those with asthma experienced 45 incident OSA cases over the course of 167 4-year intervals (27%; 95% CI, 20% - 34%) compared with 160 incident cases over the course of 938 4-year intervals in participants without asthma (17%; 95% CI, 15% - 19%; P difference = .007). "These differences in OSA risk were observed even though there were similar average [body mass index] changes among those with and without asthma during 4-year follow-up intervals," the authors write.

In regression modeling controlling for sex, age, baseline and change in body mass index, and other factors, the corresponding relative risk for development of OSA for participants with asthma compared with those who were asthma-free was 1.39 (95% CI, 1.06 - 1.82).

The authors also examined OSA with concomitant sleepiness "because OSA in the presence of sleepiness is of particular clinical interest," they write, noting that excessive daytime sleepiness is frequently used as a diagnostic criterion for clinically significant OSA. The adjusted relative risk for incident OSA with habitual sleepiness for those with asthma compared with asthma-free participants was 2.72 (95% CI, 1.26 - 5.89). "However, our findings do not distinguish a direct association between asthma and sleepiness vs an association between asthma and sleepiness mediated by OSA," they state.

Reiteration of the regression models based on asthma duration showed the highest risk for long asthma duration (more than 10 years) compared with no asthma. Specifically, the long-duration relative risks were 1.65 (95% CI, 1.21 - 2.25) for incident OSA and 3.36 (95% CI, 1.49 - 7.56) for OSA with habitual sleepiness. "For both OSA and OSA with habitual sleepiness, there were significant trends in [relative risks] with longer duration asthma category," the authors report.

The study findings, together with others reported in the literature, "lend further support to a potential causal role of asthma in OSA development," the authors write, noting several plausible pathways, including alterations to pharyngeal airway patency, upper airway compromise, and inflammatory mechanisms.

"Studies investigating the mechanisms underlying this association and the value of periodic OSA evaluation in patients with asthma are warranted," they conclude.

This work was funded by the National Institutes of Health; additional resources were from the William S. Middleton Memorial VA Hospital in Madison, Wisconsin. The authors have no relevant financial relationships to disclose.

JAMA. 2015;313:156-164. Abstract


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