Effect of sleep on upper airway dynamics in obese adolescents with obstructive sleep apnea syndrome.

STUDY OBJECTIVES: The biomechanical basis of obstructive sleep apnea syndrome (OSAS) may influence upper airway dynamics. In this study, we investigate dynamic changes during respiration in wakefulness and sleep in obese adolescents with and without OSAS. METHODS: Respiratory-gated dynamic magnetic resonance imaging (MRI) at the retropalatal and retroglossal regions was performed with simultaneous measurement of SpO2 and nasal-oral mask airflow and pressure. Airway cross-sectional area (CSA) was determined using AMIRA. Percent change in CSA was calculated from five continuous tidal breaths in states of wakefulness and sleep. Mixed effects models were used to evaluate interactions between group (OSAS/control), site (retropalatal/retroglossal), and stage (wake/sleep). RESULTS: We studied 24 children with OSAS (mean age 15.49 ± 2.00 years, mean apnea-hypopnea index [AHI] 16.53 ± 8.72 events/h) and 19 controls (mean age 14.86 ± 1.75 years, mean AHI 2.12 ± 1.69 events/h). Groups were similar in age, sex, height, weight, and BMI Z-score. Participants with OSAS had a 48.17% greater increase in percent change of airway CSA during sleep than controls (p < 0.0001), while there was no difference between groups during wakefulness (p = 0.6589). Additionally, participants with OSAS had a 48.80% increase in percent change of airway CSA during sleep as compared with wakefulness (p < 0.0001), whereas no such relationship was observed in controls (p = 0.5513). CONCLUSIONS: This study demonstrates significant effects of sleep on upper airway dynamics in obese children with OSAS. Dynamic MRI with physiological data can potentially provide further insight into the biomechanical basis of OSAS and assist in more effective management.

Airway Inflammation and Lung Function in Sickle Cell Disease.

Rationale: Asthma is a common comorbid condition in sickle cell disease (SCD). However, obstructive lung disease is prevalent in SCD, independent of a diagnosis of asthma. It is speculated that the heightened state of inflammation in SCD, involving pathways distinct from allergic asthma, may underlie the SCD-specific obstructive disease. Objective: The objective of the study was to compare airway and systemic inflammatory markers between SCD patients with pulmonary manifestations and patients with allergic asthma, and correlate the discriminating inflammatory markers with clinical measures of pulmonary disease. Materials and Methods: In a pilot translational study conducted at the Children's Hospital at Montefiore, 15 patients with SCD, and history of asthma, airway obstruction, or airway hyper-reactivity, and 15 control patients with allergic asthma 6-21 years of age were recruited. Inflammatory markers, including peripheral blood T helper cell subsets, serum and exhaled breath condensate (EBC) cytokines and chemokines of the Th-1/Th-17, Th-2, and monocytic pathways, and serum cysteinyl leukotrienes B4 (LTB4), were quantified, compared between the study groups, and correlated with atopic sensitization, pulmonary function tests, and markers of hemolysis. Results: White blood cells (P < 0.05) and monocytes (P < 0.001) were elevated in the SCD group, while atopic characteristics were higher in the control asthma group. Tumor necrosis factor-alpha (P < 0.01), interferon gamma inducible protein (IP)-10 (P < 0.05), and interleukin-4 (P < 0.01) in serum and monocyte chemotactic protein (MCP)-1 in EBC were higher in the SCD group (P ≤ 0.05). Forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) in patients with SCD inversely correlated with serum IP-10 and LTB4 levels. Conclusions: Compared with atopic asthmatic patients, inflammatory markers involving Th-1, Th-2, and monocytic pathways were higher in the SCD group, among which Th-1 measures correlated with pulmonary function deficits.

A physicians survey assessing management of pulmonary airway involvement in sickle cell disease.

BACKGROUND: Airway involvement in patients with sickle cell disease (SCD) involves recurrent episodes of acute chest syndrome (ACS), co-existent asthma, lower airway obstruction (LAO), or airway hyper-responsiveness/ bronchodilator response (AHR/BDR). With increased recognition that sickle cell (SC) airway inflammation may be distinct from asthma, our aim was to study regional and individual practices among pediatric pulmonologists and elucidate the patient characteristics that determine the diagnosis of asthma or SC airway inflammation. METHODS: A cross-sectional web-based survey including 6 case scenarios on diagnosis and management of pulmonary manifestations of pediatric SC airway disease was conducted. The case scenarios, combined different risk factors for airway inflammation: history of recurrent ACS, atopy, family history of asthma, LAO, or AHR/BDR, with possible responses including - diagnosis of asthma, SC airway inflammation, both or neither. RESULTS: Of the 130 responses, 83 were complete. "Asthma" was diagnosed when LAO (OR, 7.96 [4.28, 14.79]; p < 0.001), family history of asthma (OR 18.88 [5.87, 60.7]; p < 0.001), and atopy (OR 3.19 [1.74, 5.8]; p < 0.001) were present. "SC airway inflammation" was diagnosed when ACS (OR 3.95 [2.08, 7.51]; p < 0.001), and restrictive pattern on PFT (OR 3.75 [2.3, 6.09]; p < 0.001) were present in the scenarios. Regardless of the diagnosis, there was a high likelihood of initiating or stepping up inhaled corticosteroid as compared to prescribing montelukast. CONCLUSION: There is variability in the diagnosis and management of SC airway inflammation among pediatric pulmonologists. This study highlights the need for consensus guidelines to improve management of SC airway inflammation.

Allergic sensitization and clinical outcomes in urban children with asthma, 2013-2016.

BACKGROUND: The aim of this study was to examine if food and/or aeroallergen sensitization was associated with worse asthma, pulmonary function tests (PFT), and laboratory markers. METHODS: At our institution, 386 children with asthma were divided into allergic and nonallergic groups based on allergen-specific immunoglobulin E (IgE) testing classes 1-6 versus 0. Asthma severity and/or control, IgE level, eosinophil counts and/or percentages, forced vital capacity (FVC), forced expiratory volume in the first second of expiration (FEV1), and FEV1/FVC, were compared by using bivariate, regression, and subgroup analyses for children who were highly allergic (≥4 allergens). RESULTS: A total of 291 subjects with asthma were allergic, significantly older, and had higher mean IgE levels and eosinophil counts and percentages (all p < 0.001). A total of 203 subjects who were highly allergic had worse obstruction on PFTs. Increasing age predicted allergen sensitization after confounder adjustment, odds ratio (OR) 1.54 (95% confidence interval [CI], 1.18-2.02). Similarly, PFT obstruction was associated with multiple allergen sensitization (OR 0.97 [95% CI, 0.93-1.02]). CONCLUSION: Increasing age predicted allergic sensitization and multiple allergen sensitization. Worse obstruction on PFT also predicted multiple allergen sensitization. Continued surveillance of aeroallergen sensitization and PFT results may be beneficial in asthma management, particularly in older urban children.