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Chronobiol Med > Volume 6(3); 2024 > Article
Lee and Lee: Exploring the Interaction Between Obstructive Sleep Apnea and Idiopathic Pulmonary Fibrosis

Abstract

Recent evidence suggests that the prevalence of obstructive sleep apnea (OSA) is higher in patients with idiopathic pulmonary fibrosis (IPF) than in the general population, and coexistence of OSA and IPF is associated with a poor prognosis. The relationship between OSA and IPF is complicated and may be bidirectional. This review focuses on recent research about the epidemiology, pathophysiologic links, prognosis, and management of the two disorders. Early recognition and intervention may enhance survival rates, hence better screening methods and appropriate treatment should be further investigated.

INTRODUCTION

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease characterized by fibrotic processes of unknown etiology. Despite the recent use of antifibrotics to slow the progression of the disease, the 3-year survival rate for IPF remains poor at approximately 70% [1,2], and patients with IPF suffer from many respiratory symptoms and have a poor quality of life. In addition to pharmacologic intervention, current guidelines recommend evaluating and treating comorbidities to enhance treatment outcomes, patients’ symptoms, and quality of life [3].
Obstructive sleep apnea (OSA) is one of the most common sleep disorders, with an estimated global prevalence of 22.6% [4]. Furthermore, the incidence of OSA has been reported to be higher in patients with IPF compared to the general population [5]. Emerging evidence suggests that the relationship between OSA and IPF is bidirectional [6]. These two diseases share some similar pathophysiological mechanisms and would exaggerate each other’s development or progression. OSA exposes the lungs to chronic intermittent hypoxia (CIH) and induces oxidative stress [7,8], which might contribute to the development and aggravation of pulmonary fibrosis [9,10]. On the other hand, as IPF progresses, the decrease in lung volume can lead to structural changes in the upper airway and instability, predisposing the patient to developing OSA [6,11].
The aim of this review is to present current evidence and hypotheses on the relationship between OSA and IPF, as well as to emphasize the clinical importance of this relationship.

PREVALENCE OF OSA IN IPF

The prevalence of OSA varies significantly depending on the diagnostic criteria of OSA, manual scoring of hypopnea events, and the characteristics of study populations. Therefore, obtaining an accurate prevalence of OSA is challenging, and the reported prevalences of OSA in IPF vary across studies, ranging 47.2%–88.8% [12-16]. One recent meta-analysis revealed the prevalence of OSA in IPF as 76.4% [5]. A more recent retrospective study in Korea reported a prevalence of 64.7% for OSA in patients with IPF [17]. On the other hand, the prevalence of OSA in the general population is reported to be approximately 25% [4,18], and previous studies have shown a higher prevalence of OSA in IPF compared to the general population [5]. However, old age and male sex, which are mainly affected populations by IPF, are also prevalent for OSA, so caution is needed for interpretation. In fact, one cohort study in the US reported up to 43.2% in men aged 50 to 70 years [19]. Another cohort study reported a higher prevalence of OSA, 53.4% in adults aged 50 to 80 years [20]. Despite the apparent higher prevalence of OSA in the IPF population compared to the general population, we need additional studies that directly compare the two groups with matching key factors like age, sex, and comorbidities to establish strong evidence.

PATHOPHYSIOLOGIC INTERACTIONS BETWEEN OSA AND IPF

Recent studies have proposed a bidirectional link between IPF and OSA, however, the exact mechanisms are not yet fully understood. The main suggested mechanisms by which OSA impacts IPF include CIH-induced oxidative stress, lung injury caused by mechanical stretch, and microaspiration due to gastroesophageal reflux disease (GERD).
OSA accompanies CIH, which more effectively leads to systemic responses than continuous hypoxia, and it eventually makes patients prone to morbidity and mortality [8]. CIH and subsequent re-oxygenation produce reactive oxygen species (ROS) and oxidative stress [7]. After exposure to CIH, the levels of ROS were elevated in lung tissue from patients with interstitial lung disease (ILD) and animal models of pulmonary fibrosis [21,22]. This ROS induces tissue destruction, inflammation, and fibrosis by activating several related proteins, protein kinases, and transcription factors [8,23]. For example, the level of hypoxia-inducible factor-1α (HIF-1α) in lung tissue, a subunit of HIF-1 (an elemental transcription factor for oxygen homeostasis in the body), significantly increased and worsened pulmonary fibrosis in an animal model [22,24]. Transforming growth factor-β is also increased by ROS and contributes to fibrosis [21,25]. The expression of deoxycytidine kinase also increased in hypoxia which induced epithelial cell proliferation and pulmonary fibrosis [9]. In a recent animal study, these processes of fibrosis induced by oxidative stress from CIH were more exaggerated in older groups, which are major concern groups of OSA and IPF [26].
In OSA, resistive inspiration against a closed upper airway is repeated multiple times and may cause alveolar traction injury in peripheral lung [27]. During inspiration, the lung compliance is relatively low, so it becomes more predisposed to tractional injury [27,28]. Tractional injury has been proposed as a key pathogenic mechanism that leads to alveolar epithelial injuries and fibrosis in IPF [27].
Moreover, OSA is known to be associated with an increased prevalence of GERD [29]. One study reported that OSA causes gastroesophageal reflux by inducing frequent transient lower esophageal sphincter relaxation [30]. GERD, also very common in IPF, has been raised as having a major role in pathogenesis of IPF. One study investigated the prevalence of GERD between OSA and non-OSA individuals with fibrotic ILD, and there was no difference between the two groups, nor was OSA a risk factor for GERD in fibrotic ILD [31]. However, given the cross-sectional nature of this study, a longitudinal cohort study is necessary to determine the causative relationship among these three diseases.
The exact mechanism by which IPF affects OSA is also still unclear. One hypothesis is that a reduction in lung volume from progression of IPF may increase resistance of pharynx due to decreased traction on the upper airway, and as a result, it may reduce upper airway instability and provoke collapse [32]. This instability aggravates especially during REM sleep, as skeletal muscle atonia occurs and functional residual capacity is further reduced [6,33]. Skeletal muscle dysfunction in patients with IPF is also common, and it may also contribute to upper airway collapse, but further study is required.
The low respiratory arousal threshold, which means numerous arousals even by minimal stimulations and leads to sleep fragmentation, is an important contributor to the pathogenesis of OSA. Sleep fragmentation prevents progression from shallow stages to deeper sleep stages, and prevents the stabilization of respiratory drive and synchronization with pharyngeal dilatator muscles [5]. Similarly, in patients with IPF, sleep fragmentation and shallow sleep stages are common [16]. This predisposition may relate to development of OSA, but further research is required.

THE IMPACT OF OSA ON QUALITY OF LIFE, PROGNOSIS, AND SURVIVAL IN IPF

Patients with IPF commonly suffer from decreased quality of life due to sleep. One study found that patients with IPF experience poor sleep quality, as measured by their self-reported Pittsburgh Sleep Quality Index. This poor sleep quality was also correlated with a lower health-related quality of life to the Short-Form 36 Health Survey (SF-36) [34]. A later study demonstrated that quality of life was notably reduced in patients with IPF or sarcoidosis, especially in the domains related to physical health and the level of independence [35]. In addition, the presence of OSA further reduced the quality of life in patients with IPF. One study in 2021 showed that patients with IPF and OSA exhibited more significant functional impairments in questionnaire assessments, particularly in the domains of general health component of the SF-36 [36]. Another study with newly diagnosed IPF found that those with OSA and nocturnal hypoxemia had a poorer health-related quality of life, as measured by the St. George’s Respiratory Questionnaire when compared with those without OSA [37].
Patients with IPF and OSA showed poor prognosis in terms of mortality and clinical deterioration, compared to IPF without OSA [38]. Particularly, intermittent desaturations during sleep seem to be associated with poorer survival. In a study of 31 patients with IPF, maximum difference in SpO2 between wakefulness and sleep was correlated with survival, dyspnea, estimated right ventricular systolic pressure, and inversely correlated with diffusing capacity [39]. This intermittent hypoxemia has also been linked to a poor prognosis for IPF with OSA, possibly due to a predisposition to the development of pulmonary hypertension (PH) [40]. The exact mechanism of development of PH in IPF is not well understood, but nocturnal hypoxemia in IPF was associated with advanced PH and right ventricular dysfunction [41]. OSA in patients with IPF additionally contributes to nocturnal hypoxemia and promotes pulmonary hypoxic vasoconstriction and the development of PH [42]. One recent study that analyzed the cardiopulmonary exercise test results of IPF without and with sleep related breathing disorders (SRBD) showed that pulmonary vascular limitations are significantly worse in the SRBD subgroup [43].

SCREENING AND DIAGNOSIS OF OSA IN PATIENTS WITH IPF

Even though OSA is common in IPF, there are no well-validated screening tools for use in IPF. Some questionnaires, such as the STOP-Bang questionnaire, the Epworth Sleepiness Scale (ESS), and the Berlin Questionnaire, have been developed for screening OSA, but previous studies identifying their roles in IPF showed low positive and negative predictive values [13]. Symptoms expressed by patients with IPF are somewhat distinct from those of the general population [6]. Patients with both IPF and OSA frequently reported daytime fatigue, sleep onset, and maintenance insomnia, but excessive daytime sleepiness was less common, and they scored normal on the ESS [44]. One study suggested that the STOP-Bang scores with cut-off scores of <3 points and >6 points for rule-out and rule-in respectively, could improve their predictive value in patients with ILD. Nevertheless, the optimal screening for OSA in patients with IPF has yet to be established, necessitating evaluation with overnight polysomnography (PSG), which is the gold standard diagnostic test for OSA. Even in the absence of OSA, patients with IPF can develop nocturnal hypoxemia as a result of decreased ventilation and deterioration in gas exchange during sleep [10,45]. Therefore, among the four types of sleep studies, type 1 (in-laboratory overnight) PSG remains the gold standard for the diagnosis of OSA in patients with IPF [6].

TREATMENT OF CONCOMITANT OSA AND IPF

Data is limited regarding treatment options for patients with both IPF and OSA, but managing OSA in IPF seems to improve the quality of life and prognosis [36,44,46]. Continuous positive airway pressure (CPAP) therapy remains an effective therapy for concomitant IPF and OSA. There are controversial results regarding mortality rates among patients with IPF coexisting with OSA. A recent retrospective multicenter study of 131 patients with ILD and OSA showed that adherence to CPAP was not related to improvement in all-cause mortality or progression-free survival, even after adjustment for confounding factors [47]. On the other hand, a cohort study of IPF with OSA in Greece revealed that patients with good CPAP compliance showed significantly better overall survival at 24 months after CPAP initiation compared with poor CPAP compliance group [44]. Regarding quality of life, previous studies similarly reported that CPAP therapy improves overall life and sleep quality [36,44,46].
Maintaining compliance with CPAP in patients with IPF is often challenging due to many reasons, such as an irritating cough, claustrophobia, and insomnia. One study suggested that the intensive follow-up by the CPAP clinic staff can be helpful to improve compliance [44]. The major problem, an irritating cough, can be managed with the use of heated, humidified air [46]. Another problem is claustrophobia, which may be attributed to the rapid and shallow breathing patterns of patients with IPF. This can be solved by having an acclimatization period with low CPAP pressures and intense follow-up [46].

CONCLUSION

The interaction between IPF and OSA is complex and significant, affecting both the prognosis and quality of life of patients. The bidirectional relationship between these two conditions, driven by mechanisms such as CIH, mechanical strain on lung tissue, and instability in upper airway, suggests that managing both OSA and IPF is crucial. Despite the lack of well-validated screening tools for OSA in IPF, overnight in-laboratory PSG remains the gold standard for diagnosis. The evidence indicates that treating OSA with CPAP can improve quality of life and potentially increase survival, although compliance with CPAP therapy poses challenges. Intensive follow-up and fine adjustment for individuals to address common issues such as cough and claustrophobia are essential to enhance adherence to CPAP therapy. Further research should focus on optimizing screening and treatment protocols for OSA in IPF patients, with the goal of improving clinical outcomes and quality of life in this population.

NOTES

Conflicts of Interest

Sang Haak Lee, a contributing editor of Chronobiology in Medicine, was not involved in the editorial evaluation or decision to publish this article. The remaining author has declared no conflicts of interest.

Availability of Data and Material

Data sharing not applicable to this article as no datasets were generated or analyzed during the study.

Author Contributions

Conceptualization: Bora Lee, Sang Haak Lee. Supervision: Sang Haak Lee. Writing—original: Bora Lee. Writing—review & editing: Sang Haak Lee.

Funding Statement

None

Acknowledgments

None

REFERENCES

1. Kaunisto J, Salomaa ER, Hodgson U, Kaarteenaho R, Kankaanranta H, Koli K, et al. Demographics and survival of patients with idiopathic pulmonary fibrosis in the FinnishIPF registry. ERJ Open Res 2019;5:00170–2018.
crossref pmid pmc
2. Margaritopoulos GA, Trachalaki A, Wells AU, Vasarmidi E, Bibaki E, Papastratigakis G, et al. Pirfenidone improves survival in IPF: results from a reallife study. BMC Pulm Med 2018;18:177.
crossref pmid pmc pdf
3. Raghu G, Remy-Jardin M, Richeldi L, Thomson CC, Inoue Y, Johkoh T, et al. Idiopathic pulmonary fibrosis (an update) and progressive pulmonary fibrosis in adults: an official ATS/ERS/JRS/ALAT clinical practice guideline. Am J Respir Crit Care Med 2022;205:e18–e47.
pmid pmc
4. Lechat B, Naik G, Reynolds A, Aishah A, Scott H, Loffler KA, et al. Multinight prevalence, variability, and diagnostic misclassification of obstructive sleep apnea. Am J Respir Crit Care Med 2022;205:563–569.
crossref pmid pmc
5. Karuga FF, Kaczmarski P, Szmyd B, Białasiewicz P, Sochal M, Gabryelska A. The association between idiopathic pulmonary fibrosis and obstructive sleep apnea: a systematic review and meta-analysis. J Clin Med 2022;11:5008.
crossref pmid pmc
6. Khor YH, Ryerson CJ, Landry SA, Howard ME, Churchward TJ, Edwards BA, et al. Interstitial lung disease and obstructive sleep apnea. Sleep Med Rev 2021;58:101442.
crossref pmid
7. Pialoux V, Hanly PJ, Foster GE, Brugniaux JV, Beaudin AE, Hartmann SE, et al. Effects of exposure to intermittent hypoxia on oxidative stress and acute hypoxic ventilatory response in humans. Am J Respir Crit Care Med 2009;180:1002–1009.
crossref pmid
8. Prabhakar NR, Kumar GK. Oxidative stress in the systemic and cellular responses to intermittent hypoxia. Biol Chem 2004;385:217–221.
crossref pmid
9. Weng T, Poth JM, Karmouty-Quintana H, Garcia-Morales LJ, Melicoff E, Luo F, et al. Hypoxia-induced deoxycytidine kinase contributes to epithelial proliferation in pulmonary fibrosis. Am J Respir Crit Care Med 2014;190:1402–1412.
crossref pmid pmc
10. Troy LK, Young IH, Lau EMT, Wong KKH, Yee BJ, Torzillo PJ, et al. Nocturnal hypoxaemia is associated with adverse outcomes in interstitial lung disease. Respirology 2019;24:996–1004.
crossref pmid pdf
11. Bradley TD, Brown IG, Grossman RF, Zamel N, Martinez D, Phillipson EA, et al. Pharyngeal size in snorers, nonsnorers, and patients with obstructive sleep apnea. N Engl J Med 1986;315:1327–1331.
crossref pmid
12. Gille T, Didier M, Boubaya M, Moya L, Sutton A, Carton Z, et al. Obstructive sleep apnoea and related comorbidities in incident idiopathic pulmonary fibrosis. Eur Respir J 2017;49:1601934.
crossref pmid
13. Lancaster LH, Mason WR, Parnell JA, Rice TW, Loyd JE, Milstone AP, et al. Obstructive sleep apnea is common in idiopathic pulmonary fibrosis. Chest 2009;136:772–778.
crossref pmid pmc
14. Lee JH, Park CS, Song JW. Obstructive sleep apnea in patients with interstitial lung disease: prevalence and predictive factors. PLoS One 2020;15:e0239963.
crossref pmid pmc
15. Tabaj GC, Visentini D, Malamud P, Ginestet CG, Ernst G, Rando G, et al. Prevalence of obstructive sleep apnoea in patients with idiopathic pulmonary fibrosis. Open Access Libr J 2015;2:1–8.
crossref
16. Mermigkis C, Stagaki E, Tryfon S, Schiza S, Amfilochiou A, Polychronopoulos V, et al. How common is sleep-disordered breathing in patients with idiopathic pulmonary fibrosis? Sleep Breath 2010;14:387–390.
crossref pmid pdf
17. Lee JH, Jang JH, Park JH, Lee S, Kim JY, Ko J, et al. Prevalence and clinical impacts of obstructive sleep apnea in patients with idiopathic pulmonary fibrosis: a single-center, retrospective study. PLoS One 2023;18:e0291195.
crossref pmid pmc
18. Gottlieb DJ, Punjabi NM. Diagnosis and management of obstructive sleep apnea: a review. JAMA 2020;323:1389–1400.
crossref pmid
19. Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol 2013;177:1006–1014.
crossref pmid pmc
20. Johnson DA, Guo N, Rueschman M, Wang R, Wilson JG, Redline S. Prevalence and correlates of obstructive sleep apnea among African Americans: the Jackson Heart Sleep Study. Sleep 2018;41:zsy154.
crossref pmid pmc
21. Kang HH, Kim IK, Yeo CD, Kim SW, Lee HY, Im JH, et al. The effects of chronic intermittent hypoxia in bleomycin-induced lung injury on pulmonary fibrosis via regulating the NF-κB/Nrf2 signaling pathway. Tuberc Respir Dis (Seoul) 2020;83(Supple 1): S63–S74.
crossref pmid pmc pdf
22. Xiong M, Zhao Y, Mo H, Yang H, Yue F, Hu K. Intermittent hypoxia increases ROS/HIF-1α 'related oxidative stress and inflammation and worsens bleomycin-induced pulmonary fibrosis in adult male C57BL/6J mice. Int Immunopharmacol 2021;100:108165.
crossref pmid
23. Berggren-Nylund R, Ryde M, Löfdahl A, Ibáñez-Fonseca A, Kåredal M, Westergren-Thorsson G, et al. Effects of hypoxia on bronchial and alveolar epithelial cells linked to pathogenesis in chronic lung disorders. Front Physiol 2023;14:1094245.
crossref pmid pmc
24. da Rosa DP, Forgiarini LF, Baronio D, Feijó CA, Martinez D, Marroni NP. Simulating sleep apnea by exposure to intermittent hypoxia induces inflammation in the lung and liver. Mediators Inflamm 2012;2012:879419.
pmid pmc
25. Bellocq A, Azoulay E, Marullo S, Flahault A, Fouqueray B, Philippe C, et al. Reactive oxygen and nitrogen intermediates increase transforming growth factor-beta1 release from human epithelial alveolar cells through two different mechanisms. Am J Respir Cell Mol Biol 1999;21:128–136.
crossref pmid
26. Lee H, Kim IK, Im J, Jin BS, Kim HH, Kim SW, et al. Effects of aging on accompanying intermittent hypoxia in a bleomycin-induced pulmonary fibrosis mouse model. Korean J Intern Med 2023;38:934–944.
crossref pmid pmc pdf
27. Leslie KO. Idiopathic pulmonary fibrosis may be a disease of recurrent, tractional injury to the periphery of the aging lung: a unifying hypothesis regarding etiology and pathogenesis. Arch Pathol Lab Med 2012;136:591–600.
crossref pmid pdf
28. Toumpanakis D, Kastis GA, Zacharatos P, Sigala I, Michailidou T, Kouvela M, et al. Inspiratory resistive breathing induces acute lung injury. Am J Respir Crit Care Med 2010;182:1129–1136.
crossref pmid
29. Emilsson ÖI, Aspelund T, Janson C, Benediktsdottir B, Juliusson S, Maislin G, et al. Nocturnal gastro-oesophageal reflux and respiratory symptoms are increased in sleep apnoea: comparison with the general population. BMJ Open Respir Res 2024;11:e002192.
crossref pmid pmc
30. Kuribayashi S, Kusano M, Kawamura O, Shimoyama Y, Maeda M, Hisada T, et al. Mechanism of gastroesophageal reflux in patients with obstructive sleep apnea syndrome. Neurogastroenterol Motil 2010;22:611–e172.
crossref pmid
31. Pillai M, Olson AL, Huie TJ, Solomon JJ, Fernandez-Perez ER, Brown KK, et al. Obstructive sleep apnea does not promote esophageal reflux in fibrosing interstitial lung disease. Respir Med 2012;106:1033–1039.
crossref pmid pmc
32. Kairaitis K, Byth K, Parikh R, Stavrinou R, Wheatley JR, Amis TC. Tracheal traction effects on upper airway patency in rabbits: the role of tissue pressure. Sleep 2007;30:179–186.
crossref pmid
33. Bouloukaki I, Fanaridis M, Testelmans D, Pataka A, Schiza S. Overlaps between obstructive sleep apnoea and other respiratory diseases, including COPD, asthma and interstitial lung disease. Breathe (Sheff) 2022;18:220073.
crossref pmid pmc
34. Krishnan V, McCormack MC, Mathai SC, Agarwal S, Richardson B, Horton MR, et al. Sleep quality and health-related quality of life in idiopathic pulmonary fibrosis. Chest 2008;134:693–698.
crossref pmid
35. Mavroudi M, Papakosta D, Kontakiotis T, Domvri K, Kalamaras G, Zarogoulidou V, et al. Sleep disorders and health-related quality of life in patients with interstitial lung disease. Sleep Breath 2018;22:393–400.
crossref pmid pdf
36. Papadogiannis G, Bouloukaki I, Mermigkis C, Michelakis S, Ermidou C, Mauroudi E, et al. Patients with idiopathic pulmonary fibrosis with and without obstructive sleep apnea: differences in clinical characteristics, clinical outcomes, and the effect of PAP treatment. J Clin Sleep Med 2021;17:533–544.
crossref pmid pmc
37. Bosi M, Milioli G, Parrino L, Fanfulla F, Tomassetti S, Melpignano A, et al. Quality of life in idiopathic pulmonary fibrosis: the impact of sleep disordered breathing. Respir Med 2019;147:51–57.
crossref pmid
38. Bosi M, Milioli G, Fanfulla F, Tomassetti S, Ryu JH, Parrino L, et al. OSA and prolonged oxygen desaturation during sleep are strong predictors of poor outcome in IPF. Lung 2017;195:643–651.
crossref pmid pdf
39. Kolilekas L, Manali E, Vlami KA, Lyberopoulos P, Triantafillidou C, Kagouridis K, et al. Sleep oxygen desaturation predicts survival in idiopathic pulmonary fibrosis. J Clin Sleep Med 2013;9:593–601.
crossref pmid pmc
40. Milioli G, Bosi M, Poletti V, Tomassetti S, Grassi A, Riccardi S, et al. Sleep and respiratory sleep disorders in idiopathic pulmonary fibrosis. Sleep Med Rev 2016;26:57–63.
crossref pmid
41. Pitsiou G, Bagalas V, Boutou A, Stanopoulos I, Argyropoulou-Pataka P. Should we routinely screen patients with idiopathic pulmonary fibrosis for nocturnal hypoxemia? Sleep Breath 2013;17:447–448.
crossref pmid pdf
42. Myall KJ, West A, Kent BD. Sleep and interstitial lung disease. Curr Opin Pulm Med 2019;25:623–628.
crossref pmid
43. Hagmeyer L, Herkenrath SD, Treml M, Pietzke-Calcagnile A, Anduleit N, Randerath W. Sleep-related breathing disorders in idiopathic pulmonary fibrosis are frequent and may be associated with pulmonary vascular involvement. Sleep Breath 2023;27:961–971.
crossref pmid pdf
44. Mermigkis C, Bouloukaki I, Antoniou K, Papadogiannis G, Giannarakis I, Varouchakis G, et al. Obstructive sleep apnea should be treated in patients with idiopathic pulmonary fibrosis. Sleep Breath 2015;19:385–391.
crossref pmid pdf
45. Aydoğdu M, Ciftçi B, Firat Güven S, Ulukavak Ciftçi T, Erdoğan Y. [Assessment of sleep with polysomnography in patients with interstitial lung disease]. Tuberk Toraks 2006;54:213–221.Turkish.
pmid
46. Mermigkis C, Bouloukaki I, Antoniou KM, Mermigkis D, Psathakis K, Giannarakis I, et al. CPAP therapy in patients with idiopathic pulmonary fibrosis and obstructive sleep apnea: does it offer a better quality of life and sleep? Sleep Breath 2013;17:1137–1143.
crossref pmid pdf
47. Adegunsoye A, Neborak JM, Zhu D, Cantrill B, Garcia N, Oldham JM, et al. CPAP adherence, mortality, and progression-free survival in interstitial lung disease and OSA. Chest 2020;158:1701–1712.
crossref pmid pmc


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