NEURO-ENDOCRINE DYSFUNCTION IN SLEEP-APNEA - REVERSAL BY CONTINUOUS POSITIVE AIRWAYS PRESSURE THERAPY

NEURO-ENDOCRINE DYSFUNCTION IN SLEEP-APNEA - REVERSAL BY CONTINUOUS POSITIVE AIRWAYS PRESSURE THERAPY
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DOI:
10.1210/jcem-68-2-352
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发表时间:
1989-02-01
影响因子:
5.8
通讯作者:
SULLIVAN, CE
SULLIVAN, CE
中科院分区:
医学2区
文献类型:
--
作者:
GRUNSTEIN, RR;HANDELSMAN, DJ;SULLIVAN, CE

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我们研究了睡眠呼吸暂停对神经内分泌功能的影响,对22名连续接受睡眠研究的男性进行了横断面研究,并对43名患有严重阻塞性睡眠呼吸暂停的男性进行了纵向研究,用鼻腔持续正压消除上呼吸道阻塞的方法成功治疗了3个月。于清醒后0600-0630h采血测定血浆胰岛素样生长因子-I(IGF-I)、总睾酮和游离睾酮、性激素结合球蛋白(SHBG)、黄体生成素(LH)、促卵泡刺激素(FSH)、催乳素(PRL)、T4、T4结合球蛋白和皮质醇。分析血浆激素水平与睡眠呼吸暂停严重程度的关系,通过减饱和指数(动脉血氧减饱和发作的每小时频率和稳定基线的4%)和减饱和发作期间的平均最低氧饱和度来表示。在这项横断面研究中,血浆IGF-I、游离和总睾酮以及SHBG水平与睡眠呼吸暂停的严重程度相关,而血浆LH、FSH、PRL、T4、T4结合球蛋白和皮质醇水平与睡眠呼吸暂停程度无关。协方差分析表明,血浆IGF-I、总睾酮和游离睾酮的降低与年龄和肥胖的影响无关。在纵向研究中,鼻腔持续正压治疗3个月后,血浆IGF-I、总睾酮和SHBG显著升高,而游离睾酮无显著升高。我们得出结论,睡眠呼吸暂停导致男性可逆性神经内分泌功能障碍,表现为血浆、IGF-I、睾酮和SHBG水平下降。这种神经内分泌功能障碍与睡眠呼吸暂停的严重程度有关,如动脉血氧密度的最低水平和减饱和发作的比率所示。这些激素测量可能为睡眠呼吸暂停的严重程度及其对治疗干预的反应提供生化标记物。此外,睡眠呼吸暂停可能是一个以前未被认识到的神经内分泌与衰老相关的混杂因素。
We studied the effects of sleep apnea on neuroendocrine function in a cross-sectional study of 22 consecutive men undergoing sleep studies and in a longitudinal study of 43 men with severe obstructive sleep apnea before and after 3 months of successful treatment with nasal continuous positive airways pressure to eliminate upper airways obstruction. Blood samples were collected at 0600-0630 h on awakening for measurement of plasma insulin-like growth factor I (IGF-I), total and free testosterone, sex hormone-binding globulin (SHBG), LH, FSH, PRL, T4, T4-binding globulin, and cortisol. The plasma hormone levels were analyzed in relation to the severity of sleep apnea, as indicated by the desaturation index (the hourly rate of episodes of arterial oxygen desaturation > 4% of the stable baseline) and the mean minimal oxygen saturation during the desaturation episodes. In the cross-sectional study plasma IGF-I, free and total testosterone, and SHBG levels were significantly lower in relation to the severity of sleep apnea, whereas plasma LH, FSH, PRL, T4, T4-binding globulin, and cortisol were not. The decreases in plasma IGF-I and total and free testosterone were independent of the effects of aging and adiposity by covariance analysis. In the longitudinal study plasma IGF-I, total testosterone, and SHBG, but not free testosterone, significantly increased after 3 months of nasal continuous positive airways pressure treatment. We conclude that sleep apnea causes reversible neuroendocrine dysfunction in men, which is manifested by decreased plasma, IGF-I, testosterone, and SHBG levels. This neuroendocrine dysfunction is related to the severity of the sleep apnea, as indicated by the nadir levels of arterial oxygen densaturation and the rate of desaturation episodes. These hormonal measurements may provide biochemical markers for both the severity of sleep apnea and its response to therapeutic intervention. In addition, sleep apnea may be a previously unrecognized confounder of the neuroendocrine correlates of aging.