Evaluating the impact of adenotonsillectomy for pediatric sleep-disordered breathing on parental sleep.


  • 影响因子:2.32
  • DOI:10.1002/lary.27806
  • 作者列表:"Ernst H","Dzioba A","Glicksman J","Paradis J","Rotenberg B","Strychowsky J
  • 发表时间:2020-01-01

OBJECTIVES/HYPOTHESIS:To evaluate the impact of adenotonsillectomy for pediatric sleep-disordered breathing (SDB) on parental sleep quality, daytime sleepiness, and child quality of life. STUDY DESIGN:Prospective cohort study. METHODS:Pediatric patients aged 2 to 10 years with SDB and suspected obstructive sleep apnea (OSA) requiring adenotonsillectomy were identified at a single tertiary-care pediatric otolaryngology hospital. Parental daytime sleepiness and quality of sleep were evaluated pre- and postoperatively using the Epworth Sleepiness Scale (ESS) and Pittsburg Sleep Quality Index (PSQI), respectively. Child quality of life, in the context of suspected OSA, was evaluated by the Obstructive Sleep Apnea Quality of Life Survey (OSA-18), pre- and postoperatively. Paired-samples t tests were conducted to analyze data. RESULTS:Forty-seven patients with a mean (standard deviation [SD]) age of 4.9 (2.2) years, participated. Mean (SD) parental age was 35.5 (4.6) years. Statistically significant decreases of 2.1 points were observed between preoperative and postoperative parental mean global ESS (P = .007; 95% confidence interval [CI]: 0.6-3.6) and mean total PSQI (P = .001; 95% CI: 0.9-3.1) scores. A statistically significant improvement (41.6 points) was observed between preoperative and postoperative on mean OSA-18 scores (P < .0001; 95% CI: 35.7-47.6). CONCLUSIONS:Adenotonsillectomy performed in the pediatric population for SDB, with suspected OSA, can positively impact parental daytime sleepiness and sleep quality in addition to pediatric quality of life. LEVEL OF EVIDENCE:2 Laryngoscope, 130:232-237, 2020.


目的/假设: 评估腺样体扁桃体切除术治疗儿童睡眠呼吸障碍 (SDB) 对父母睡眠质量、白天嗜睡和儿童生活质量的影响。 研究设计: 前瞻性队列研究。 方法: 在一家三级保健儿童耳鼻喉科医院确定了 2 ~ 10 岁 SDB 和疑似阻塞性睡眠呼吸暂停 (OSA) 需要腺样体扁桃体切除术的儿童患者。分别采用 Epworth 嗜睡量表 (ESS) 和匹兹堡睡眠质量指数 (PSQI) 评价父母白天嗜睡和睡眠质量。在疑似 OSA 的情况下,通过阻塞性睡眠呼吸暂停生活质量调查 (OSA-18) 评估术前和术后的儿童生活质量。进行配对样本 t检验分析数据。 结果: 47 例患者的平均 (标准差 [SD]) 年龄为 4.9 (2.2) 岁,参与。平均 (SD) 父母年龄为 35.5 (4.6) 岁。在术前和术后父母平均整体 ESS 之间观察到 2.1 分的统计学显著下降 (P =。007; 95% 置信区间 [CI]: 0.6-3.6) 和平均总 PSQI (P = .001; 95% CI: 0.9-3.1) 分。在术前和术后的平均 OSA-18 评分之间观察到统计学显著改善 (41.6 分) (P < .0001; 95% CI: 35.7-47.6)。 结论: 在疑似 OSA 的 SDB 儿童人群中进行的腺样体扁桃体切除术除了对儿童生活质量有积极影响外,还能对父母白天嗜睡和睡眠质量产生积极影响。 证据级别: 2 喉镜,130:232-237,2020。



作者列表:["De Cunto G","Brancaleone V","Riemma MA","Cerqua I","Vellecco V","Spaziano G","Cavarra E","Bartalesi B","D'Agostino B","Lungarella G","Cirino G","Lucattelli M","Roviezzo F"]

METHODS:BACKGROUND AND PURPOSE:A critical role for sphingosine kinase/sphingosine-1-phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD). EXPERIMENTAL APPROACH:C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed. KEY RESULTS:Cigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K2 , and S1P receptors (S1P2 and S1P3 ) has been detected in the lung of smoking mice. Sphingosine kinases inhibition reversed the increased cholinergic response in airways of smoking mice. CONCLUSIONS AND IMPLICATIONS:S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.

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作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

METHODS::The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.

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作者列表:["Zaragosi LE","Deprez M","Barbry P"]

METHODS::The respiratory tract is lined by a pseudo-stratified epithelium from the nose to terminal bronchioles. This first line of defense of the lung against external stress includes five main cell types: basal, suprabasal, club, goblet and multiciliated cells, as well as rare cells such as ionocytes, neuroendocrine and tuft/brush cells. At homeostasis, this epithelium self-renews at low rate but is able of fast regeneration upon damage. Airway epithelial cell lineages during regeneration have been investigated in the mouse by genetic labeling, mainly after injuring the epithelium with noxious agents. From these approaches, basal cells have been identified as progenitors of club, goblet and multiciliated cells, but also of ionocytes and neuroendocrine cells. Single-cell RNA sequencing, coupled to lineage inference algorithms, has independently allowed the establishment of comprehensive pictures of cell lineage relationships in both mouse and human. In line with genetic tracing experiments in mouse trachea, studies using single-cell RNA sequencing (RNAseq) have shown that basal cells first differentiate into club cells, which in turn mature into goblet cells or differentiate into multiciliated cells. In the human airway epithelium, single-cell RNAseq has identified novel intermediate populations such as deuterosomal cells, 'hybrid' mucous-multiciliated cells and progenitors of rare cells. Novel differentiation dynamics, such as a transition from goblet to multiciliated cells have also been discovered. The future of cell lineage relationships in the respiratory tract now resides in the combination of genetic labeling approaches with single-cell RNAseq to establish, in a definitive manner, the hallmarks of cellular lineages in normal and pathological situations.

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