AVAPS-AE versus ST mode: A randomized controlled trial in patients with obesity hypoventilation syndrome.

BACKGROUND AND OBJECTIVE: Average volume-assured pressure support-automated expiratory positive airway pressure (AVAPS-AE) combines an automated positive expiratory pressure to maintain upper airway patency to an automated pressure support with a targeted tidal volume. The aim of this study was to compare the effects of 2-month AVAPS-AE ventilation versus pressure support (ST) ventilation on objective sleep quality in stable patients with OHS. Secondary outcomes included arterial blood gases, health-related quality of life, daytime sleepiness, subjective sleep quality and compliance to NIV. METHODS: This is a prospective multicentric randomized controlled trial. Consecutive OHS patients included had daytime Pa CO2 > 6 kPa, BMI ≥ 30 kg/m2 , clinical stability for more than 2 weeks and were naive from home NIV. PSG were analysed centrally by two independent experts. Primary endpoint was sleep quality improvement at 2 months. RESULTS: Among 69 trial patients, 60 patients had successful NIV setup. Baseline and follow-up PSG were available for 26 patients randomized in the ST group and 30 in the AVAPS-AE group. At baseline, Pa CO2 was 6.94 ± 0.71 kPa in the ST group and 6.61 ± 0.71 in the AVAPS-AE group (P = 0.032). No significant between-group difference was observed for objective sleep quality indices. Improvement in Pa CO2 was similar between groups with a mean reduction of -0.87 kPa (95% CI: -1.12 to -0.46) in the ST group versus -0.87 kPa (95% CI: -1.14 to -0.50) in the AVAPS-AE group (P = 0.984). Mean NIV use was 6.2 h per night in both groups (P = 0.93). NIV setup duration was shorter in the AVAPS-AE group (P = 0.012). CONCLUSION: AVAPS-AE and ST ventilation for 2 months had similar impact on sleep quality and gas exchange.

A Telemedicine Intervention to Ensure the Correct Usage of Inhaler Devices.

Background: Chronic obstructive pulmonary disease and asthma patients' use of inhalers is error prone. Introduction: This study evaluated telemedicine to improve the use of inhalers. Materials and Methods: Prospective, single-center pilot study in 50 patients with long-term prescription of inhaled medicine and ongoing home health care visits. In an initial telemedicine intervention, tablet devices were used by the patient to record inhaler use at home in the real-time remote presence of a physician. Errors were identified, explained to the patient, and corrected remotely. When necessary, further telemedicine interventions were scheduled at 24-48 h intervals. Follow-up interventions were performed during routine outpatient visits. Patient satisfaction was evaluated on a scale of 0 (completely unsatisfied) to 10 (completely satisfied). Results: An initial telemedicine intervention was conducted for 42 of the 50 patients included. In these patients, 96 initial inhaler medicine administration telemedicine interventions were performed, of which 94 were usable. In the initial interventions, 71 errors were identified, of which 22 (31%) were considered critical. In 81 follow-up interventions in 39 patients (median delay 256 days), 32 errors were identified (p < 0.001 vs. initial 71 errors), of which 7 were critical (p = 0.0017 vs. initial 22 errors). Discussion: This paves the way for future studies testing putative benefits of telemedicine regarding inhaled drug delivery, treatment adherence, disease control, quality of life, and health care burden and costs. Conclusions: A telemedicine intervention aimed at improving the administration of inhaled medication by adult patients at home is feasible, highly appreciated by patients, and effective at correcting medicine administration errors.

Cystic fibrosis airway epithelium remodelling: involvement of inflammation.

Chronic inflammation is a hallmark of cystic fibrosis (CF) lung disease and airway epithelium damage and remodelling are important components of lung pathology progression in CF. Whether this remodelling is secondary to deleterious infectious and inflammatory mediators, or to alterations of CF human airway epithelial (HAE) cells, such as their hyper inflammatory phenotype or their basic cystic fibrosis transmembrane conductance regulator (CFTR) default, remains debated. In this study, we evaluated the involvement of alterations of CF HAE cells in airway epithelium remodelling. HAE cells from non-CF and CF patients were cultured in an air-liquid interface, with and without inflammatory stimulation, along the regeneration process, and the remodelling of the reconstituted epithelium was analysed. We confirmed that CF HAE cells showed a hyperinflammatory phenotype which was lost with time. In comparison to non-CF epithelium, CF epithelium regeneration in the absence of exogenous inflammation was higher and exhibited basal cell hyperplasia. This remodelling was mimicked by inflammatory stimulation of non-CF cells and was absent when CF HAE cells were no longer hyperinflamed. Moreover, the number of goblet cells was similar in non-CF and CF cultures and increased equally under inflammatory stimulation. Finally, whatever the inflammatory environment, CF cultures showed a delay in ciliated cell differentiation. In conclusion, alterations of CF HAE cells partly regulate airway epithelium remodelling following injury and regeneration. This remodelling, together with goblet cell hyperplasia induced by exogenous inflammation and alteration of ciliated cell differentiation, may worsen mucociliary clearance impairment, leading to injury.