Airway inflammation in obstructive sleep apnea: is leptin the missing link?
BACKGROUND
Local and systemic inflammation is implicated in the pathophysiology of Obstructive Sleep Apnea (OSA). Exhaled breath condensate (EBC) is a non-invasive sampling method for the lower airways. However, it is important to consider the potential effect of the systemic origin whereas systemic inflammation is significantly elevated. This prospective study was designed to investigate whether airway inflammation is significantly related to plasma leptin levels in OSA patients. Simultaneously, it was designed to investigate whether inflammatory variables predict parameters expressing disease severity and finally whether smoking habit affect the above measurements.


METHODS
About 45 OSA patients (mean AHI 40+/-25, 28 smokers) and 25 healthy controls (AHI<5, 15 smokers) were studied and underwent overnight diagnostic polysomnography. We measured pH, 8-isoprostane, TNF-alpha and IL-6 in EBC and leptin in plasma. Plausible associations between leptin and inflammatory parameters were analyzed after adjustment for proper variables. Similar associations between inflammatory variables and parameters of disease severity were also performed.


RESULTS
An increased level of leptin and respective increase of inflammatory variables was found. No significant association was observed between parameters of EBC and plasma leptin levels. A part of the parameters of disease severity is significantly associated with pH and 8-isoprostane. Smoking did not seem to be a critical confounding factor for evaluation of the above measurements.


CONCLUSIONS
Increased levels of leptin were not associated with the observed airway inflammation in OSA. The observed airway inflammation seemed to be independent of smoking habit with limited association with disease severity.
Antonopoulou
Sofia
S
Sleep Laboratory, 1st Respiratory Medicine Dept, Medical School, University of Mesogeion 152, 15669, Athens, Greece. santonod@hotmail.com
Loukides
Stelios
S
Papatheodorou
Georgios
G
Roussos
Charis
C
Alchanatis
Manos
M
D000328:Adult; D015415:Biomarkers / Q000032:analysis; D001944:Breath Tests; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D015237:Dinoprost / Q000031:analogs & derivatives / Q000032:analysis; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D006863:Hydrogen-Ion Concentration; D015850:Interleukin-6 / Q000032:analysis; D020738:Leptin / Q000097:blood*; D016014:Linear Models; D008168:Lung / Q000276:immunology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D017286:Polysomnography; D020181:Sleep Apnea, Obstructive / Q000276:immunology* / Q000503:physiopathology; D012907:Smoking / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014797:Vital Capacity
D015415:Biomarkers; D015850:Interleukin-6; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; C075750:8-epi-prostaglandin F2alpha; D002097:C-Reactive Protein; D015237:Dinoprost