Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2010, Article ID 675320, 6 pages
Research Article

Inflammatory Markers in Middle-Aged Obese Subjects: Does Obstructive Sleep Apnea Syndrome Play a Role?

1Department of Pneumonology, Medical School, Democritus University of Thrace, 68100 Alexandroupolis, Greece
2Sleep Unit, Second Chest Department, General Hospital “George Papanikolaou”, 57010 Thessaloniki, Greece
3Outpatient Clinic of Obesity, Diabetes and Metabolism, Second Department of Internal Medicine, Democritus University of Thrace, 68100 Alexandroupolis, Greece
4Immunology Laboratory, General Hospital “George Papanikolaou”, 57010 Thessaloniki, Greece

Received 16 December 2009; Accepted 11 April 2010

Academic Editor: Oreste Gualillo

Copyright © 2010 Paschalis Steiropoulos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Obstructive Sleep Apnea Syndrome (OSAS) is associated with inflammation, but obesity may be a confounding factor. Thus, the aim of this study was to explore differences in serum levels of inflammation markers between obese individuals with or without OSAS. Methods. Healthy individuals ( ) from an outpatient obesity clinic were examined by polysomnography and blood analysis, for measurement of TNF- , IL-6, CRP, and fibrinogen levels. According to Apnea-Hypopnea Index (AHI), participants were divided into two BMI-matched groups: controls (AHI < 15/h, ) and OSAS patients (AHI   15/h, ). Results. OSAS patients had significantly higher TNF- levels ( ) while no other difference in the examined inflammation markers was recorded between groups. Overall, TNF- levels were correlated with neck circumference ( ), AHI ( ), and Oxygen Desaturation Index ( ). Conclusions. Obese OSAS patients have elevated TNF- levels compared to BMI-matched controls, suggesting a role of OSAS in promoting inflammation, possibly mediated by TNF-a.