Obstructive sleep apnoea in patients with fibrotic diffuse parenchymal lung disease—characterization and treatment compliance assessment

Abstract

IntroductionRecent studies have reported a high prevalence of obstructive sleep apnoea (OSA) among patients with diffuse parenchymal lung disease (DPLD), mainly idiopathic pulmonary fibrosis (IPF). Effective OSA treatment appears to have a positive impact on morbidity and mortality in these patients. However, poor compliance to positive airway pressure (PAP) treatment in fibrotic DPLD patients has been reported. The aims of our study were to characterize patients with fibrotic DPLD and OSA and to assess their compliance to PAP treatment.MethodsForty-nine patients with fibrotic DPLD underwent level III polysomnography. Auto-adjusting PAP (APAP) treatment was proposed for those patients with moderate-to-severe OSA and those with mild OSA with daytime sleepiness and/or cardiovascular disease. The APAP treatment compliance was assessed after 1 month of therapy.ResultsThe distribution of the 49 fibrotic DPLD patients included was as follows: 21 with chronic hypersensitivity pneumonitis, 12 with IPF, 10 with connective-tissue associated DPLD, 4 with stage IV sarcoidosis, 1 with idiopathic pleuropulmonary fibroelastosis, and 1 with DPLD-associated vasculitis. Thirty-four (69.4%) of the patients presented with OSA; 22 had mild OSA, and 12 had moderate-to-severe OSA. APAP treatment was prescribed in 17 of the patients. After 1 month of therapy, all patients used APAP more than 70% of the nights for more than 4 h per night.ConclusionWe found a high prevalence of OSA among all of the patients with fibrotic DPLD (not only IPF). Despite certain difficulties, it was possible to achieve good APAP compliance in these patients.

Attenuation of intermittent hypoxia-induced apoptosis and fibrosis in pulmonary tissues via suppression of ER stress activation

“…In addition to apoptosis, ER stress activation plays a critical role in the development of pulmonary fibrosis [34,35]. In the clinics, it was found that idiopathic pulmonary fibrosis is a characteristic of OSA patients [18]. It is well known that increased collagen deposition and synthesis are critical contributors of fibrosis [36].…”

“…On the other hand, once ER stress is initiated, it is believed that fibrosis will be induced due to the acceleration of fibroblast proliferation and the expression of extracellular matrix protein, such as transforming growth factor-β1 (TGF-β1) and thrombospondin-1(TSP-1) [16,17]. In the clinics, pulmonary fibrosis was noted in OSA patients [4,18]. However, the major mechanisms underlying the effects of IH treatment on the pathological changes and dysfunction of pulmonary tissue are still largely unknown.…”

Prevalence and impact of comorbid obstructive sleep apnoea in diffuse parenchymal lung diseases

“…The prevalence was not significantly different between patients with and without OSA. Besides, one study [20] reported that pulmonary hypertension was present in 18.2% OSA and 15.3% non-OSA patients, but in another study [13], no significant difference in the calculated systolic pulmonary artery pressure was found in subjects with and without OSA. https://doi.org/10.1371/journal.pone.0246878.g001…”

“…Subgroup analyses were performed to evaluate sources of heterogeneity in the prevalence estimates between studies. The results revealed the prevalence to be higher as 76% (95% CI: 68-83%; I 2 = 69.2%) in the 13 studies enrolling IPF patients [10,[12][13][14][18][19][20][21][22][23][24][25][26] (Fig 2B), whereas in 4 studies including patients with connective tissue associated-ILD or sarcoidosis [20,21,25,26], the pooled prevalence of OSA was much lower (60%, 95% CI: 49-70%; I 2 = 0%), suggesting that the prevalence differed according to the type of DPLDs. Moreover, the prevalence of comorbid OSA in healthy controls and chronic obstructive pulmonary disease (COPD) were examined in two studies, and were found to be less frequent than in IPF (AHI 1.7 ± 1.0 vs 11.6 ± 7.2 [21]; prevalence 44% vs 62% [27]).…”

“…Quality assessment for each study is summarized in S1 Table. Prevalence of OSA in DPLDs Overall, the pooled prevalence of OSA among DPLDs was 72% (95% CI: 65-79%; I 2 = 75.4%), ranging from 45 to 90% (Fig 2A). Based on 12 studies including 546 patients, which reported severity of OSA [10,12,13,[18][19][20][21][22][23][24][25][26], moderate-severe OSA was observed in 40% patients (95% CI: 28-52%; I 2 = 90.8%), ranging from 8 to 68%, and the pooled prevalence of mild OSA was equally high as 36% (95% CI: 23-48%; I 2 = 91.5%), ranging from 6 to 67%.…”