Lower Airway Disease in Asthmatics with and without Rhinitis

STUDY OBJECTIVES: The purpose of this study was to determine if asthma with rhinitis and asthma without rhinitis represent distinct forms of disease. DESIGN: We performed a prospective cross-sectional study. PARTICIPANTS: The study included healthy controls, participants with asthma without rhinitis, and participants with both asthma and rhinitis. Interventions We compared lung function and airway inflammation between the three groups of participants. RESULTS: We recruited 32 participants: 12 normals, 8 asthmatics without rhinitis, and 12 with rhinitis. Compared to asthmatics with rhinitis, asthmatics without rhinitis had more severe airflow limitation (FEV(1)/FVC = 60.6% [IQR = 22.8] vs. 74.8% [IQR = 7.8] and fewer induced sputum eosinophils (2.8 [IQR = 5.8] and 9.6 [IQR = 23.8], respectively). Sputum interleukin-6 correlated inversely with lung function measured by postbronchodilator FEV(1) in the study cohort (Spearman correlation coefficient = -0.55, p < 0.01). CONCLUSIONS: Asthmatics without rhinitis tend to have lower lung function and less eosinophilic inflammation in the lung. This small study suggests that asthmatics without rhinitis represent a distinct phenotype of asthma in which low lung function is dissociated from eosinophilic cellular inflammation, and it suggests that larger studies addressing this phenotype are warrented.     

Effect of nasal obstruction on upper airway muscle activation in normal subjects

It is not known whether nasal occlusion produces obstructive sleep apnea (OSA) by decreasing upper airway muscle activation via nasal reflexes or by increasing upper airway resistance and hence lowering the pressure in the pharnyx. The purpose of this study was to determine the effect of nasal occlusion on upper airway muscle activation. We studied seven men and measured alae nasi (AN) and genioglossal (GG) electromyograms (EMGs) during two nights of sleep, one with their nose open and the other with their nose occluded. Nasal occlusion produced OSA in all subjects and also increased the percentage of time during sleep in which phasic AN and GG EMG activity was present. Apneas tended to occur at the nadirs of EMG activity. This suggests that nasal occlusion generally increases respiratory drive to upper airway muscles during sleep and that it does not cause OSA by merely decreasing respiratory drive to these muscles.     

Changes in breathing and the pharynx after weight loss in obstructive sleep apnea

The effect of weight loss following dietary restriction on disordered breathing on the pharyngeal airway is controversial in patients with obstructive sleep apnea (OSA). We therefore prospectively studied eight patients before and after dietary-induced weight loss. Mean weight loss was 20.6 kg +/- 12.8 SD. After weight loss there were significant improvements in PO2 and PCO2 measured during wakefulness, and in the number of desaturation episodes per hour of sleep, average desaturation per episode, and number of movement arousals. The number of apneas and hypopneas significantly decreased in six of eight patients. There was a significant correlation between body mass index and number of disordered breathing events. Nasopharyngeal collapsibility and pulse flow resistance decreased in awake patients after weight loss. We conclude that moderate weight loss in obese patients with OSA improves oxygenation during both sleep and wakefulness, decreases the number of disordered breathing events in many patients, decreases the collapsibility of the nasopharyngeal airway.     

Prolonged relaxation rate of inspiratory muscles in patients with sleep apnea

To evaluate whether inspiratory muscle function is impaired in patients with sleep apnea, we measured inspiratory muscle strength and relaxation rate before and after sleep in 13 patients. The sleep apnea group was composed of eight patients with severe obstructive sleep apnea, and the non-apnea group was composed of five patients without significant sleep apnea. We chose the time constant of relaxation (TauR) as an index of impaired inspiratory muscle contractility, and in subsets of each group, we measured the inspiratory pressure-time index as an indicator of a fatiguing breathing pattern. In patients with sleep apnea, presleep TauR was 79 +/- 22 ms (SD), longer than that of normal subjects (normal, 59 +/- 7 ms) (p less than 0.05). TauR increased by 21 +/- 16 ms during sleep (p less than 0.01). In patients without apnea, presleep TauR was 67 +/- 7 ms and it did not change after sleep. Maximal inspiratory and expiratory pressures were unchanged after sleep. We conclude that patients with sleep apnea do not develop overt inspiratory muscle failure but do have impaired contractility. We speculate that hypoxemia as well as increased work load was responsible.