Bronchial hyperreactivity and airway wall thickening in obstructive sleep apnea patients
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Hypoxia/reoxygenation episodes in obstructive sleep apnea (OSA) results in the alteration of the oxidative balance, leading to the development of inflammation. Airway wall thickening and inflammatory changes are suggested as a primary cause of the airway hyperresponsiveness in asthmatics. Bronchial hyperreactivity (BH) may also occur in patients with OSA. We investigated the presence of BH and airway wall thickness in OSA and correlations with inflammatory markers. Sixteen OSA patients and ten controls without allergic diseases were prospectively studied. Plasma pro-B-type natriuretic peptide (pro-BNP), fibrinogen, D-dimer, alpha 1-antitrypsin, and high-sensitive C-reactive protein levels were measured. Airway wall thickness was evaluated with high-resolution CT, and BH was assessed by giving each subject a methacholine challenge test. In OSA patients, bronchial wall thickness, fibrinogen, D-dimer, alpha 1-antitrypsin, high sensitive C-reactive protein, and pro-BNP levels were significantly greater than those in control subjects. Among the 16 patients, three had BH on methacholine challenge. Bronchial wall thickness(mm) was positively correlated with apnea-hypopnea index (AHI: number of apneas + hypopneas/hour of sleep), BMI, respiratory arousal index, nocturnal oxygen desaturation (NOD) duration (time in minutes with a nocturnal arterial oxygen saturation of < 90% during sleep), and alpha 1-antitrypsin levels. NOD duration also correlated with pro-BNP and fibrinogen levels. In OSA patients, walls of central airways were thicker than normal subjects. BH may have occurred in OSA patients. NOD duration correlated with inflammatory parameters and oxygen desaturation index 3% had an effect on the thickness of bronchial walls. But overall, AHI was found to be the only independent predictor of bronchial wall thickness.