James B. Skatrud Pulmonary/Sleep Research Laboratory, Medical Service, William S. Middleton Memorial Veteran's Hospital, Madison, WI ; Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI ; Center for Sleep Medicine and Sleep Research/Wisconsin Sleep, University of Wisconsin School of Medicine and Public Health, Madison, WI.
Population Health Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI.
J Clin Sleep Med. 2014 Feb 15;10(2):183-93. doi: 10.5664/jcsm.3450.
Obstructive sleep apnea is prevalent among people with asthma, but underlying mechanisms remain unknown. Inhaled corticosteroids may contribute. We tested the effects of orally inhaled fluticasone propionate (FP) on upper airway (UAW) during sleep and wakefulness.
16-week single-arm study.
18 (14 females, mean [ ± SD] age 26 ± 6 years) corticosteroid-naïve subjects with mild asthma (FEV1 89 ± 8% predicted).
High dose (1,760 mcg/day) inhaled FP.
(1) UAW collapsibility (passive critical closing pressure [Pcrit]); (2) tongue strength (maximum isometric pressure-Pmax, in KPa) and endurance-time (in seconds) able to maintain 50% Pmax across 3 trials (Ttot)-at anterior and posterior locations; (3) fat fraction and volume around UAW, measured by magnetic resonance imaging in three subjects.
Pcrit overall improved (became more negative) (mean ± SE) (-8.2 ± 1.1 vs. -12.2 ± 2.2 cm H2O, p = 0.04); the response was dependent upon baseline characteristics, with older, male gender, and worse asthma control predicting Pcrit deterioration (less negative). Overall, Pmax increased (anterior p = 0.02; posterior p = 0.002), but Ttot generally subsided (anterior p = 0.0007; posterior p = 0.06), unrelated to Pcrit response. In subjects studied with MRI, fat fraction and volume increased by 20.6% and 15.4%, respectively, without Pcrit changes, while asthma control appeared improved.
In this study of young, predominantly female, otherwise healthy subjects with well-controlled asthma and stiff upper airways, 16-week high dose FP treatment elicited Pcrit changes which may be dependent upon baseline characteristics, and determined by synchronous and reciprocally counteracting local and lower airway effects. The long-term implications of these changes on sleep disordered breathing severity remain to be determined.
阻塞性睡眠呼吸暂停在哮喘患者中较为常见，但具体的发病机制仍不明确。吸入性皮质类固醇可能是其中的一个影响因素。我们检测了口服氟替卡松丙酸酯（FP）对睡眠和清醒时上呼吸道（UAW）的影响。
为期 16 周的单臂研究。
18 名（14 名女性，平均[±SD]年龄 26±6 岁）皮质类固醇初治的轻中度哮喘患者（FEV1 占预计值的 89%±8%）。
高剂量（1760μg/天）吸入 FP。
（1）UAW 的塌陷性（被动临界闭合压力[Pcrit]）；（2）舌肌力量（最大等长压-Pmax，单位为千帕）和耐力时间（以秒计，在 3 次试验中维持 50%Pmax 的时间-Ttot-在前部和后部位置）；（3）UAW 周围的脂肪分数和体积，在 3 名受试者中通过磁共振成像测量。
总的来说，Pcrit 变得更负（mean±SE）（-8.2±1.1 比-12.2±2.2cmH2O，p=0.04）；这种反应依赖于基线特征，年龄较大、男性、哮喘控制较差的患者的 Pcrit 恶化（更负）。总的来说，Pmax 增加（前部 p=0.02；后部 p=0.002），但 Ttot 通常减少（前部 p=0.0007；后部 p=0.06），与 Pcrit 反应无关。在接受 MRI 检查的受试者中，脂肪分数和体积分别增加了 20.6%和 15.4%，而 Pcrit 没有变化，同时哮喘控制似乎有所改善。
在这项研究中，16 周的高剂量 FP 治疗对年轻、以女性为主、其他健康的、上气道僵硬的哮喘控制良好的患者的 Pcrit 产生了影响，其变化可能取决于基线特征，并由局部和下气道的同步和相互抵消的作用决定。这些变化对睡眠呼吸障碍严重程度的长期影响仍有待确定。
