Influence of nCPAP on Metabolic Consequences Associated With OSAS
|Obstructive Sleep Apnea Syndrome Obesity||Procedure: nasal continuous positive airway pressure|
|Study Design:||Allocation: Non-Randomized
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Basic Science
|Official Title:||Improvement in Hypothalamic-Pituitary-Adrenal Axis Function After Continuous Positive Airway Pressure Therapy in Obstructive Sleep Apnea Syndrome|
- To explore the interactive mechanisms of HPA axis, sympathetic nervous system activation, inflammatory cytokines, insulin resistance and hypertension in patients with and without sleep apnea, excluding the interference of the degree of fat accumulation. [ Time Frame: one day ]
- To evaluate low-dose dexamethasone-induced cortisol suppression and circadian rhythm of cortisol secretion in severe obese patients with sleep apnea in response to treatment with continuous positive airway pressure. [ Time Frame: three months ]
|Study Start Date:||October 2004|
|Study Completion Date:||March 2006|
Active Comparator: A
10 patients with severe OSAS (Apnea Hypopnea Index of more than 30 events per hour of sleep) were treated with nCPAP for three months and all mentioned measurements above were repeated.
Procedure: nasal continuous positive airway pressure
After an average interval of three months, 10 patients with severe OSAS (AHI of more than 30 events per hour of sleep) treated with a mean nCPAP pressure of 11.2 ± 0.7 cm of H2O were reassessed and all mentioned measurements above were repeated
Background: There is evidence that obstructive sleep apnea syndrome (OSAS) increases the risk of cardiovascular events. Sympathetic nervous system and hypothalamic-pituitary-adrenal (HPA) axis activation may be the mechanism of this relationship. We evaluate HPA axis and metabolic consequences in obese patients with and without OSAS and we determine if continuous positive airway pressure therapy (nCPAP) influenced responses.
Methods: Plasma inflammatory cytokines, insulin resistance index, 24-hour ambulatory blood pressure monitoring and overnight cortisol suppression test with 0.25 mg of dexamethasone were performed in 22 severe obese patients with OSAS and 23 obese controls. Ten patients with severe apnea were re-evaluated three months after nCPAP therapy.
Results: Body mass index, abdominal circumference, blood pressure levels and insulin resistance indexes of OSAS patients and obese controls were very similar. In OSAS patients, adiponectin (p<0.05) and salivary cortisol suppression pos DEX (p<0.05) were lower, while heart rate (p<0.05) and TNF-alpha levels (p<0.05) were higher compared with obese controls. After nCPAP therapy, patients showed a reduction in heart rate (p=0.036) and a higher cortisol suppression after dexamethasone (p=0.001) and there were no differences in insulin resistance (HOMA p=0.139), arterial blood pressure (p=0.183) and adipokines compared with baseline. Cortisol suppression was positively correlated with the improvement of apnea hypopnea index while on nCPAP therapy (r= 0.799, p=0.010).
Conclusions: Patients with OSAS present nocturnal hypercortisolism, hyperactivity of sympathetic central nervous system, a higher degree of inflammation and hypoadiponectinemia independent of the body mass index. Furthermore, hyperactivity of HPA axis and sympathetic nervous system are recovered by nCPAP.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00435643
|Universidade Federal de Sao Paulo|
|Sao Paulo, SP, Brazil, 04023-062|
|Principal Investigator:||Gláucia Carneiro, MD||UNIFESP-EPM|