scholarly journals Role of nocturnal oxygen therapy in interstitial lung disease with obstructive sleep apnoea syndrome

2006 ◽  
Vol 1 (1) ◽  
pp. 41-44
Author(s):  
D. V. Shah ◽  
J. M. Joshi
Respirology ◽  
2010 ◽  
Vol 15 (2) ◽  
pp. 377-379 ◽  
Author(s):  
Stanley D.W. MILLER ◽  
Senan F. GLYNN ◽  
John L. KIELY ◽  
Walter T. McNICHOLAS

2012 ◽  
Vol 11 (5) ◽  
pp. 11-17
Author(s):  
V. V. Rostorotskaya ◽  
I. A. Elgardt ◽  
A. P. Ivanov ◽  
N. S. Sdobnyakova

Aim. To study the role of obstructive sleep apnoea syndrome (OSAS) in the development of treatment resistance in patients with arterial hypertension (AH). To assess the effects of autonomic nervous system (ANS) dysfunction, as one of the potential pathophysiological mechanisms of inadequate blood pressure (BP) reduction in patients with AH and OSAS. Material and methods. The study included 365 ambulatory AH patients: 194 with OSAS and 161 with resistance to antihypertensive therapy after 6-15 months. The 24-hour BP monitoring (BPM) and 24-hour cardio-respiratory monitoring of electrocardiogram (ECG), with heart rate variability (HRV) analysis, were performed. Results. Among patients with AH and OSAS, most individuals had low antihypertensive therapy compliance. All parameters of 24-hour BPM in this group were lower than in OSAS-free hypertensives, and this difference was more pronounced in patients with lower treatment compliance, particularly for pulse BP and HR. HRV parameters correlated with apnoea-hypopnoea index (AHI) and BP levels during 24-hour BPM. However, in multivariate analyses, these correlations were observed only for HRV parameters and AHI. Conclusion. In AH patients, OSAS aggravates the clinical course of the disease. ANS dysfunction could be one of the mechanisms underlying the development of antihypertensive treatment resistance.


2014 ◽  
Vol 23 (3) ◽  
pp. 291-299 ◽  
Author(s):  
Giovanni Tarantino ◽  
Vincenzo Citro ◽  
Carmine Finelli

Non-alcoholic fatty liver disease (NAFLD) and obstructive sleep apnoea syndrome (OSAS) are common conditions, frequently encountered in patients with obesity and/or metabolic syndrome. NAFLD and OSAS are complex diseases that involve an interaction of several intertwined factors. Several lines of evidence lend credence to an immune system derangement in these patients, i.e. the low grade chronic inflammation status, reckoned to be the most important factor in causing and maintaining these two illnesses. Furthermore, it is emphasized the main role of spleen involvement, as a novel mechanism. In this review the contribution of the visceral adiposity in both NAFLD and OSAS is stressed as well as the role of intermittent hypoxia. Finally, a post on the prevention of systemic inflammation is made.Abbreviations: ALT: alanine aminotransferase; BMI: body mass index; CCR2: chemokine (C-C motif) receptor 2; CRP: C-reactive protein; CPAP: continuous positive airway pressure; FFA: free fatty acid; IGF-I: insulin-like growth factor; IR: insulin resistance; IL-6: interleukin-6; IH: intermittent hypoxia; IKK-β: IκB kinase β; LPS: lipopolysaccharide; MCP-1: monocyte chemoattractant protein-1; NAFLD: non-alcoholic fatty liver disease; NASH: nonalcoholic steatohepatitis; NEFA: non-esterified fatty acid; NF-κB: nuclear factor-κB; OSAS: obstructive sleep apnoea syndrome; PAI-1: plasminogen activator inhibitor-1; ROS: reactive oxygen species; TNF-α: tumor necrosis factor-α; T2D: type 2 diabetes.


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