Weight Loss Ameliorates Markers of Systemic Inflammation and Endothelial Dysfunction in Obstructive Sleep Apnea Obese Patients| Stephy Publishers

 


SOJ Diabetes and Endocrinology Care - (SOJDEC)| Stephy Publishers


Abstract

Background: Obstructive sleep apnea (OSA) is the most common sleep disorder in clinical practice. Its growing worldwide prevalence may be due to the rising incidence of obesity in the public. OSA has been increasingly recognized as a major public health issue, as it has a significant influence on the incidence and prognosis of cardiovascular diseases. Although, these abnormalities could be modulated with weight reduction, there is limitation in clinical studies have addressed the beneficial effects of weight reduction in modulating biomarkers of endothelial dysfunction and cytokines for obesity associated with OSA.

Objective: This study was designed to detect the effects of weight loss on the inflammatory cytokines and adhesive molecules in obese patients with obstructive sleep apnea.

Methods: Seventy obese patients with moderate to severe OSA (the apnea-hypopnea index (AHI)>15 events/hour), their age ranged from 36-50 years and their body mass index ranged from 26-31kg/m2 were equally assigned into two groups: the weight reduction group received aerobic exercises, diet regimen, where the control group received no intervention for 12 weeks.

Results: The mean values of body mass index (BMI), apnea-hypopnea index (AHI), tumor necrosis factor –alpha (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), inter-cellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1) and E-selectin were significantly decreased in the training group, however the results of the control group were not significant. In addition, there were significant differences between both groups at the end of the study.

Conclusion: Weight loss ameliorates inflammatory cytokines and adhesive molecules among obese patients with obstructive sleep apnea.

Keywords

Obstructive sleep apnea, Obesity, Adhesive molecules, Cytokines, Weight reduction

Introduction

Obstructive sleep apnea (OSA) is a clinical condition characterized by recurrent episodes of obstruction (apnea or hypopnea) of the upper airway, which can lead to intermittent hypoxia, hypercapnia and significant negative intrathoracic pressure during sleep.1,2 Obstructive sleep apnea is common and affects 3%-7% of the general population.3 OSA is quantified based on the apnea-hypopnea index (AHI), which represents the average number of apneas and hypopneas per hour of sleep. The diagnosis of OSA is made when AHI is >five events/hour of sleep and its severity can be classified according to the AHI into mild (>5 and <15 events/hour), moderate (≥15 and ≤30 events/hour) and severe (>30 events/hour).4 OSA affects all age groups and is prevalent across different populations globally.5 In the Wisconsin Sleep Cohort Study, the prevalence of undiagnosed OSA in adults was 9% for women and 24% for men6 and 13% and 6%, respectively, have moderate-to-severe disease.7

Obesity is an important risk factor for OSA8 and their shared pathways of oxidative stress and inflammation make discerning independent roles in cardiovascular disease difficult.9 Obesity stimulates an inflammatory state, as adipose tissue has resident macrophages and is a rich source of pro-inflammatory cytokines.10 An increased prevalence of OSA has been associated with some risk factors including age, male sex, and obesity.11 Obesity is one of the strongest risk factors and mild to moderate obesity has been associated with markedly increased sleep apnea prevalence.12 Obesity promotes enlargement of soft tissue structures within, and surrounding, the airway, thereby contributing significantly to pharyngeal airway narrowing and to the development of OSA.13

OSA is associated with an increased risk of cardiovascular events and mortality.14,15 Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular disease (CVD). In addition, obese individuals OSA is independently associated with inflammation and insulin resistance.16 However, it remains debated whether this relationship is independent of confounding factors such as age, sex, and obesity. The mechanisms responsible for the development of atherosclerosis triggered by OSA are not completely known. Several pathogenic factors are proposed as intermediate mechanisms linking OSA with cardiovascular disease (CVD). There is evidence that sleep apnea mainly by chronic intermittent hypoxia is associated with sympathetic activation, oxidative stress, systemic inflammation, hypercoagulability, endothelial dysfunction, and metabolic dysregulation.17 These mechanisms are closely interrelated and are observed in individuals with excessive body weight.



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