Putative associations between inflammatory biomarkers, obesity, and obstructive sleep apnea.

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From: Annals of Thoracic Medicine(Vol. 16, Issue 4)
Publisher: Medknow Publications and Media Pvt. Ltd.
Document Type: Article
Length: 4,253 words
Lexile Measure: 1660L

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Byline: Siraj. Wali, Md. Manzar, Mohammed. Abdelaziz, Ranya. Alshomrani, Faris. Alhejaili, Jamil. Al-Mughales, Wail. Alamoudi, David. Gozal

BACKGROUND: Previous studies have reported increased levels of inflammatory mediators in patients with obstructive sleep apnea (OSA), but their relation with the severity of OSA is controversial. OBJECTIVE: To address potential relationships between OSA-related inflammatory markers, namely, C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a), and fibrinogen, with different oxygenation parameters and with BMI. METHODS: All eligible patients with suspected OSA newly referred to the Sleep Medicine Research Center at King Abdulaziz University Hospital, Jeddah, were evaluated demographically and anthropometrically, and underwent overnight polysomnography. Fasting morning blood samples were collected to measure serum levels of CRP, fibrinogen, TNF-a, and IL-6. Potential correlations between these inflammatory mediators and severity measures of OSA and body mass index (BMI) were explored. RESULTS: Sixty-four patients completed the study (40 with OSA and 24 without OSA). Significantly increased levels of CRP, fibrinogen, IL-6, and TNF-a emerged in patients with OSA compared to non-OSA. Significant associations between log CRP and log fibrinogen levels emerged with increasing BMI. However, there was no significant association between any of the inflammatory markers and the severity of OSA based on the apnea/hypopnea index or oxyhemoglobin saturation-derived parameters. CONCLUSIONS: OSA patients exhibit increased levels of inflammatory mediators that do not appear to be associated with polysomnographic measures, but exhibit positive correlation with the degree of adiposity.

Obstructive sleep apnea syndrome (OSAS) is a highly prevalent disease associated with significant cardiovascular and cerebrovascular morbidity, as well as organ-specific and overall mortality.[1],[2],[3] There is evolving evidence that inflammatory processes resulting in endothelial dysfunction play a critically important role in OSA-associated morbidities.[4] Fleming et al .[5] reported that several biomarkers are more likely affected by the presence of OSA, and that these biomarker signatures of the disorder may assist in the initial screening of patients with suspected OSA, as well as in their follow-up responses to therapy.

Prototypic biomarkers serving as indicators of systemic inflammation include erythrocyte sedimentation rate, C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a), and fibrinogen.[6],[7],[8],[9],[10],[11],[12] CRP has been widely studied in OSA, and is frequently reported to be increased, particularly among those patients with concurrent obesity, dyslipidemia, diabetes, and cardiovascular diseases.[13],[14],[15],[16] TNF-a, on the other hand, is a key modulator of systemic inflammation,[17],[18],[19] and TNF inhibition has been shown to ameliorate the progression of OSA[20] or ameliorate some of its important manifestations, such as excessive daytime sleepiness.[21],[22] Moreover, Li and Zheng[23] found that TNF-a was significantly higher in patients with OSA than in controls, and this difference was more prominent with the severity of OSA, indicating again that TNF-a might be a circulating biomarker favorable for the development of OSA. Similarly, significant elevations in serum levels of interleukin 1 ß and IL-6 have been observed in patients with OSA.[22],[24] In a recent open-label controlled trial, we reported the presence of an augmented inflammatory state among patients recently diagnosed with OSA, as reflected by significant increases in the levels of circulating TNF-a...

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Gale Document Number: GALE|A680637882