Asthma diagnosis and treatment
Sleep apnea is associated with bronchial inflammation and continuous positive airway pressure–induced airway hyperresponsiveness

https://doi.org/10.1016/j.jaci.2006.11.638Get rights and content

Background

Obstructive sleep apnea syndrome (OSA) is associated with systemic and upper airway inflammation. Pharyngeal inflammation has a potential role in upper airway collapse, whereas systemic inflammation relates to cardiovascular morbidity. However, the presence of an inflammatory involvement of lower airway has been poorly investigated.

Objective

The aim of the study was to demonstrate an inflammatory process at the bronchial level in patients with OSA and to analyze effects of continuous positive airway pressure (CPAP) application and humidification on bronchial mucosa.

Methods

The study was conducted by using sequential induced sputum for cell analysis and IL-8 production, nitric oxide exhalation measurement, and methacholine challenge before and after CPAP.

Results

Bronchial neutrophilia and a high IL-8 concentration were observed in untreated OSA compared with controls (75% ± 20% vs 43% ± 12%, P < .05; and 25.02 ± 9.43 ng/mL vs 8.6 ± 3.7 ng/mL, P < .001, respectively). IL-8 in sputum supernatant was correlated to apnea hypopnea index (P < .01; r = 0.81). After 1 month of CPAP, this inflammatory pattern remained unchanged, and an increase in airway hyperresponsiveness (AHR) was observed (P < .001).

Conclusion

Obstructive sleep apnea syndrome is associated with bronchial inflammation. Our data demonstrate CPAP effect on the development of AHR, possibly facilitated by the pre-existing inflammation. Both issues should be evaluated during long-term CPAP use.

Clinical implications

Results showing a spontaneous bronchial inflammation in OSA and the development of a CPAP-related AHR require a long-term follow-up to evaluate consequences on chronic bronchial obstruction.

Section snippets

Subjects

Fifty-seven consecutive patients (43 males and 14 females) with OSA were included in the study (Table I). OSA was confirmed by using nocturnal polysomnography. Patients were nonsmokers, and none had a previous OSA diagnosis or CPAP therapy. A control group of 13 healthy nonsmoking subjects was simultaneously analyzed. Atopy was investigated by using skin prick tests to a panel of 7 usual aeroallergens. Allergic sensitization was defined by the presence of at least 1 positive skin test (mean

Results

Anthropometric and clinical data are summarized in Table I. Groups were significantly different for body mass index and Epworth index (P < .001 and P < .05, respectively). The prevalences of atopy and allergic medical history were not different between OSA and control groups. In addition, no other inflammatory lung diseases (asthma, chronic bronchitis, systemic diseases) were reported by subjects from either group, and all subjects were nonsmokers. Overall, the subjects had normal pulmonary

Discussion

We demonstrated a neutrophilic bronchial inflammation in a large group of patients with OSA. The associated release of IL-8 in the supernatant of sputum induction was closely related with sleep apnea severity as expressed by the AHI and the amount of oxygen desaturation. This bronchial inflammation was not reversed by 1 month of CPAP use. In addition, we demonstrated for the first time that nasal CPAP induces a sustained increase in nonspecific airway responsiveness.

Severe asthma and COPD are

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    Supported by a grant from the French Committee of Respiratory Diseases (CNMR) and from the Fisher and Paykel Co.

    Disclosure of potential conflict of interest: All of the authors have received grant support from the French Committee of Respiratory Diseases (Comité National Maladies Respiratoires) and Fisher and Paykel Co.

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