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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