title: Pituitary reactivity, androgens and catecholamines in obstructive sleep apnoea. Effects of continuous positive airway pressure treatment (CPAP).
abstract: We studied the effects of chronic nocturnal hypoxaemia due to obstructive sleep apnoea syndrome (OSAS) on the hypothalamic-pituitary-thyroid and hypothalamic-pituitary-testicular axes and on catecholamine and cortisol secretion. We investigated whether hormones other than catecholamines may serve as markers for chronic hypoxic stress and the possible effects of nasal continuous positive airway pressure (nCPAP) treatment on endocrine status. Nocturnal oximetry was performed in 16 male patients with OSAS diagnosed by polysomnography, immediately before nCPAP treatment and in 11 of the patients the oximetry was repeated after 7 months of nCPAP therapy. Plasma and urinary catecholamines, luteinizing hormone (LH) testosterone, cortisol, thyroid stimulating hormone (TSH), prolactin (PRL), and the response of TSH and PRL to a thyroid releasing hormone (TRH) challenge test were measured immediately before and after 7 months of nCPAP treatment. Subnormal LH and TSH and elevated serum cortisol as well as increased nocturnal urinary norepinephrine levels were found in patients prior to treatment; otherwise endocrine values were normal. There was a significant correlation between low pretreatment nocturnal arterial oxygen saturation and high plasma and urinary norepinephrine levels. The nCPAP treatment caused significant reduction in serum prolactin and TSH, and significant reduction in plasma epinephrine and urinary norepinephrine. The reduction in serum TSH and urinary norepinephrine was most pronounced in the subjects with the worst pretreatment nocturnal hypoxaemia. No other significant changes were found in basal hormone levels. The response to TRH challenge was normal before and after treatment and was not influenced by CPAP therapy. OSAS is associated with elevated catecholamine and cortisol and decreased TSH and LH levels but a normal response to TRH challenge and a normal androgen status. Apart from catecholamines, none of the hormones studied is likely to serve as a specific marker for chronic hypoxic stress.
authors.affiliation: Department of Respiratory and Allergic Diseases, Huddinge University Hospital, Karolinska Institute, Sweden.
authors.forename: T
authors.initials: T
authors.lastname: Bratel
authors.forename: A
authors.initials: A
authors.lastname: Wennlund
authors.forename: K
authors.initials: K
authors.lastname: Carlström
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000652:urine; D010092:Oximetry; D010902:Pituitary Gland / Q000503:physiopathology*; D011175:Positive-Pressure Respiration; D012891:Sleep Apnea Syndromes / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D018709:Statistics, Nonparametric; D013972:Thyrotropin / Q000097:blood; D013973:Thyrotropin-Releasing Hormone
chemical_list: D015415:Biomarkers; D013973:Thyrotropin-Releasing Hormone; D007986:Luteinizing Hormone; D013972:Thyrotropin; D006854:Hydrocortisone; D009638:Norepinephrine