4.3 Article

Pro-atherogenic cytokine profile of patients with suspected obstructive sleep apnea

期刊

SLEEP AND BREATHING
卷 13, 期 4, 页码 391-395

出版社

SPRINGER HEIDELBERG
DOI: 10.1007/s11325-009-0259-1

关键词

Sleep apnea; Inflammation; Cytokine; Cardiovascular disease

资金

  1. BC
  2. CIHR/HSFC IMPACT
  3. Michael Smith Foundation for Health Research
  4. CIHR/BC Lung Association
  5. University British Columbia
  6. Michael Smith Foundation for Health Research Unit

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Purpose Systemic inflammation is important in the pathogenesis of cardiovascular disease (CVD). We sought to characterize the systemic inflammatory profile associated with obstructive sleep apnea (OSA). Methods Adult patients referred for suspected OSA at the University of British Columbia Hospital Sleep Disorders Program were recruited for our study. Patients using HMG CoA inhibitors or a history of CVD were excluded. Fasting serum samples were obtained the morning after their diagnostic polysomnograms. Samples were tested for the following circulating inflammatory mediators: interferon gamma; interleukins 1B, 6, and 8; intercellular and vascular cell adhesion molecules (sICAM-1 and sVCAM-1); and leptin using a multiplex Luminex System. Results There were 176 patients; 68% were male, mean age=50+/-(SD) 11 years, mean apnea/hyponea index (AHI)=22.9+/-22/h, mean desaturation (i.e. % of sleep time spent below an oxyhemoglobin saturation of 90%)=5.4%+15, and mean body mass index (BMI)=32.2+8 kg/m(2). In univariate analyses, only leptin, sVCAM-1, and sICAM-1 were significantly associated with indices of OSA severity (i.e. AHI and/or desaturation). In multivariate linear regression analyses that controlled for BMI, gender, age, and current smoking; desaturation persisted as a significant independent predictor for elevated sVCAM-1 and leptin. Conclusions We did not find significant associations between OSA and markers of activated innate immunity (IL-1B, 6, and 8). However, OSA severity was independently associated with serum levels of sVCAM-1 and leptin; these may represent mechanisms involved in the pathogenesis of OSA-related CVD.

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