Bratel T, Wennlund A, Carlström K
Department of Respiratory and Allergic Diseases, Huddinge University Hospital, Karolinska Institute, Sweden.
Respir Med. 1999 Jan;93(1):1-7. doi: 10.1016/s0954-6111(99)90068-9.
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.
我们研究了阻塞性睡眠呼吸暂停综合征（OSAS）所致慢性夜间低氧血症对下丘脑 - 垂体 - 甲状腺轴和下丘脑 - 垂体 - 睾丸轴以及儿茶酚胺和皮质醇分泌的影响。我们调查了除儿茶酚胺以外的激素是否可作为慢性低氧应激的标志物，以及鼻持续气道正压通气（nCPAP）治疗对内分泌状态的可能影响。对16例经多导睡眠图诊断为OSAS的男性患者在nCPAP治疗前立即进行夜间血氧饱和度测定，其中11例患者在nCPAP治疗7个月后重复进行血氧饱和度测定。在nCPAP治疗7个月前后立即测定血浆和尿儿茶酚胺、促黄体生成素（LH）、睾酮、皮质醇、促甲状腺激素（TSH）、催乳素（PRL）以及TSH和PRL对促甲状腺激素释放激素（TRH）激发试验的反应。治疗前患者发现LH和TSH低于正常、血清皮质醇升高以及夜间尿去甲肾上腺素水平增加；其他内分泌值正常。治疗前夜间动脉血氧饱和度低与血浆和尿去甲肾上腺素水平高之间存在显著相关性。nCPAP治疗使血清催乳素和TSH显著降低，血浆肾上腺素和尿去甲肾上腺素显著降低。血清TSH和尿去甲肾上腺素的降低在治疗前夜间低氧血症最严重的受试者中最为明显。基础激素水平未发现其他显著变化。治疗前后对TRH激发试验的反应正常，且不受CPAP治疗影响。OSAS与儿茶酚胺和皮质醇升高以及TSH和LH水平降低有关，但对TRH激发试验反应正常且雄激素状态正常。除儿茶酚胺外，所研究的激素均不太可能作为慢性低氧应激的特异性标志物。
