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Obstructive Sleep Apnea and Inflammation: Proof of Concept Based on Two Illustrative Cytokines
by
Gozal, David
, Kheirandish-Gozal, Leila
in
Biomarkers
/ Cytokines
/ Disease
/ Hypoxia
/ Inflammation
/ Metabolism
/ Morbidity
/ Obesity
/ Pediatrics
/ Review
/ Sleep apnea
/ Tumor necrosis factor-TNF
2019
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Obstructive Sleep Apnea and Inflammation: Proof of Concept Based on Two Illustrative Cytokines
by
Gozal, David
, Kheirandish-Gozal, Leila
in
Biomarkers
/ Cytokines
/ Disease
/ Hypoxia
/ Inflammation
/ Metabolism
/ Morbidity
/ Obesity
/ Pediatrics
/ Review
/ Sleep apnea
/ Tumor necrosis factor-TNF
2019
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While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Obstructive Sleep Apnea and Inflammation: Proof of Concept Based on Two Illustrative Cytokines
by
Gozal, David
, Kheirandish-Gozal, Leila
in
Biomarkers
/ Cytokines
/ Disease
/ Hypoxia
/ Inflammation
/ Metabolism
/ Morbidity
/ Obesity
/ Pediatrics
/ Review
/ Sleep apnea
/ Tumor necrosis factor-TNF
2019
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Obstructive Sleep Apnea and Inflammation: Proof of Concept Based on Two Illustrative Cytokines
Journal Article
Obstructive Sleep Apnea and Inflammation: Proof of Concept Based on Two Illustrative Cytokines
2019
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Overview
Obstructive sleep apnea syndrome (OSAS) is a markedly prevalent condition across the lifespan, particularly in overweight and obese individuals, which has been associated with an independent risk for neurocognitive, behavioral, and mood problems as well as cardiovascular and metabolic morbidities, ultimately fostering increases in overall mortality rates. In adult patients, excessive daytime sleepiness (EDS) is the most frequent symptom leading to clinical referral for evaluation and treatment, but classic EDS features are less likely to be reported in children, particularly among those with normal body-mass index. The cumulative evidence collected over the last two decades supports a conceptual framework, whereby sleep-disordered breathing in general and more particularly OSAS should be viewed as low-grade chronic inflammatory diseases. Accordingly, it is assumed that a proportion of the morbid phenotypic signature in OSAS is causally explained by underlying inflammatory processes inducing end-organ dysfunction. Here, the published links between OSAS and systemic inflammation will be critically reviewed, with special focus on the pro-inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), since these constitute classical prototypes of the large spectrum of inflammatory molecules that have been explored in OSAS patients.
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