Immunological Consequences of Obstructive Sleep Apnea
Obstructive sleep apnea (OSA) is a medical problem whose importance is increasing in recognition and awareness. OSA is associated with the development of hypertension and other cardiovascular diseases (1,2). OSA has pathophysiologic characteristics that are known to negatively impact immune function. Both sleep deprivation and hypoxia, hallmarks of OSA, impair immune responses (6,8,11). In addition, patients with OSA are frequently obese and obesity may be associated with increased chance of infections and immune impairment (14,15). Adipose cells are known to secrete cytokines and hormones that are involved in the immune response such as leptin, tumor necrosis factor alpha and interleukin-6 (16-19). Thus, it seems very likely that OSA may impact antigen-specific immune responses. Although it is known that characteristics of OSA impact immune function, it is not known what effects clinical OSA has on immunity.
The central hypothesis of this application is that that patients with obstructive sleep apnea will have attenuated cell-mediated and humoral immune responses to influenza vaccine compared to matched control subjects. Our hypothesis has been formulated on the basis that patients with OSA are sleep deprived and experience repeated hypoxemia that negatively impact both humoral and cell-mediated immune responses.
|Study Design:||Allocation: Non-Randomized
Intervention Model: Parallel Assignment
Masking: Open Label
|Official Title:||Influence of Obstructive Sleep Apnea on Humoral and Cell-Mediated Vaccine Responses|
- The primary outcome variable will be mean lymphocyte interferon- ÿ (IFN- ÿ) production at 14 days (measured by ELISA)
- Mean influenza antibody concentrations (pre- and post-immunization) with standard deviations will be calculated and compared between sleep apnea and control patients.
|Study Start Date:||October 2004|
|Study Completion Date:||June 2006|
|Primary Completion Date:||June 2006 (Final data collection date for primary outcome measure)|
Please refer to this study by its ClinicalTrials.gov identifier: NCT00214071
|United States, Wisconsin|
|University of Wisconsin|
|Madison, Wisconsin, United States, 53719|
|Principal Investigator:||John M Dopp, PharmD||University of Wisconsin, Madison|