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

David W. Hudgel; Elizabeth A. Gordon
Author and Funding Information

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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Abstract

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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