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Serotonin-Induced Cortisol Release in CPAP-Treated Obstructive Sleep Apnea Patients FREE TO VIEW

David W. Hudgel; Elizabeth A. Gordon
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From the Department of Medicine, MetroHealth Medical Center and Case Western Reserve University, Cleveland

1997 by the American College of Chest Physicians

Chest. 1997;111(3):632-638. doi:10.1378/chest.111.3.632
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Previously, we demonstrated elevated cortisol production/release in response to the administration of the serotonin precursor, L-5-hydroxytryptophan (L-5-HTP) in untreated patients with obstructive sleep apnea (OSA). We hypothesized that if this elevated cortisol response to L-5-HTP was related to OSA, this finding would not be present in OSA patients treated with nasal continuous positive airway pressure (nCPAP). Eleven OSA patients treated for at least 1 month with nCPAP were studied. On two different days, we measured blood cortisol level every 15 min for 4 h following the ingestion of L-5-HTP, 0.4 mg/kg, or placebo, both given with carbidopa, a peripheral tryptophan decarboxylase inhibitor, used to prevent peripheral L-5-HTP metabolism before brain absorption. For a given subject, the cortisol response was calculated as the difference between the area under the curve of the L-5-HTP and placebo responses. In the nCPAP-treated OSA patients, this net cortisol response, 577±240 min · µg/dL, was less than the value found in the previously studied untreated OSA group, 1,198±227 min · µg/dL (p<0.05) and not different from the previously studied nonapneic control group, 469±154 min · µg/dL. From these results, we speculate that nCPAP treatment reverses the elevated cortisol response to serotonergic stimulation seen in untreated OSA patients.




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