title: Influence of CPAP treatment on airway and systemic inflammation in OSAS patients.
abstract: OBJECTIVE
  Obstructive sleep apnea syndrome (OSAS) is characterized by recurrent respiratory disorders in the upper airways during sleep. Although continuous positive airway pressure (CPAP) has been accepted to be the most effective treatment for OSAS, its role on inflammation remains debatable. In this study, our aim was to examine the influence of 3 months of CPAP treatment on tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), 8-isoprostane, and peroxynitrite levels in exhaled breathing condensates (EBC) and serum.
  
  
  METHODS
  Thirty-five patients who were newly diagnosed as moderate or severe OSAS with full night polysomnography and used CPAP therapy regularly for 3 months were included in the study. Polysomnography, spirometric tests, fasting blood samples, and EBC were ascertained on entry into the study and after 3 months of treatment. All patients were assessed monthly for treatment adherence and side effects.
  
  
  RESULTS
  We found that all polysomnographic parameters were normalized after CPAP therapy in the control polysomnogram. Also, all markers in EBC and nitrotyrosine and 8-isoprostane levels in serum were decreased significantly with CPAP treatment. Sedimentation rate, C-reactive protein, IL-6, and TNF-α remained unchanged in serum after treatment. We found that baseline nitrotyrosine levels were significantly correlated with apnea-hypopnea index, oxygen desaturation index, and percent time in SpO2 < 90 % (p < 0.01).
  
  
  CONCLUSIONS
  CPAP therapy has primarily a relevant impact on airways, and nitrotyrosine levels correlated well with severity of OSAS. This treatment decreases both inflammation and oxidative stress levels in airways in OSAS patients. Also, this treatment helps to decrease systemic oxidative stress levels in serum.
authors.affiliation: Department of Respiratory Medicine, Fatih University Medical School, Ankara, Turkey.
authors.forename: Harun
authors.initials: H
authors.lastname: Karamanlı
authors.forename: Duygu
authors.initials: D
authors.lastname: Özol
authors.forename: K Serife
authors.initials: KS
authors.lastname: Ugur
authors.forename: Zeki
authors.initials: Z
authors.lastname: Yıldırım
authors.forename: Ferah
authors.initials: F
authors.lastname: Armutçu
authors.forename: Bulent
authors.initials: B
authors.lastname: Bozkurt
authors.forename: Ramazan
authors.initials: R
authors.lastname: Yigitoglu
mesh_terms: D000328:Adult; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D045422:Continuous Positive Airway Pressure; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000628:therapy; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D030421:Peroxynitrous Acid / Q000097:blood; D017286:Polysomnography; D011446:Prospective Studies; D020181:Sleep Apnea, Obstructive / Q000276:immunology* / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D030421:Peroxynitrous Acid; C075750:8-epi-prostaglandin F2alpha; D002097:C-Reactive Protein; D015237:Dinoprost