Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine, University Hospital Basel, Basel, Switzerland.
Eur J Endocrinol. 2010 May;162(5):943-9. doi: 10.1530/EJE-09-0930. Epub 2010 Feb 8.
Suppression of the adrenal function after glucocorticoid treatment is common, potentially dangerous, and unpredictable. Identification of patients at risk is of clinical importance. We hypothesized that the dexamethasone suppression test predicts the development of corticosteroid-induced impaired adrenal function.
We included 39 healthy male volunteers. After a 1-microg ACTH test, all participants underwent an overnight 0.5-mg dexamethasone suppression test. Participants then took prednisone, 0.5 mg/kg body weight, for 14-day. After the withdrawal of prednisone, a 1-microg ACTH test was performed and a clinical score was assessed on days 1, 3, 7, and 21.
On days 1, 3, 7, and 21, 100, 50, 26.5 and 32.4% of the participants had a suppressed adrenal function. The risk of developing suppressed adrenal function decreased from 44 to 0% in patients with cortisol levels after the administration of dexamethasone in the lowest and highest quartiles respectively. Receiver operating curve (ROC) analysis performed to predict a suppressed adrenal function on day 7 after the withdrawal of prednisone showed an area under the curve (AUC) of 0.76 (95% confidence interval (CI) 0.58-0.89) for cortisol after the administration of dexamethasone, which was in the range of the AUC of 0.78 (95% CI 0.6-0.9) for pre-intervention cortisol after the administration of ACTH. Basal cortisol before intake of prednisone (AUC 0.62 (95% CI 0.44-0.78)) and the clinical score (AUC 0.64 (95% CI 0.45-0.79)) had significantly lower AUCs.
Circulating cortisol levels after a dexamethasone suppression test and a pre-intervention-stimulated cortisol level are predictive of later development of a suppressed adrenal function after a 14-day course of prednisone, and are superior to a clinical score or basal cortisol levels. This may allow a more targeted concept for the need of stress prophylaxis after cessation of steroid therapy.
糖皮质激素治疗后肾上腺功能抑制很常见，具有潜在危险且不可预测。识别高危患者具有重要的临床意义。我们假设地塞米松抑制试验可预测皮质类固醇引起的肾上腺功能障碍的发生。
我们纳入了 39 名健康男性志愿者。在接受 1μg ACTH 试验后，所有参与者均接受了 1 晚 0.5mg 地塞米松抑制试验。然后，所有参与者接受了为期 14 天的泼尼松治疗，剂量为 0.5mg/kg 体重。在停用泼尼松后，进行了 1μg ACTH 试验，并在第 1、3、7 和 21 天评估临床评分。
在第 1、3、7 和 21 天，100%、50%、26.5%和 32.4%的参与者存在肾上腺功能抑制。地塞米松给药后皮质醇水平处于最低和最高四分位数的患者，发展为肾上腺功能抑制的风险分别从 44%降至 0%。预测泼尼松停药后第 7 天肾上腺功能抑制的受试者工作特征曲线（ROC）分析显示，地塞米松给药后皮质醇的曲线下面积（AUC）为 0.76（95%置信区间（CI）0.58-0.89），与 ACTH 给药后预干预皮质醇的 AUC 0.78（95%CI 0.6-0.9）相当。泼尼松摄入前的基础皮质醇（AUC 0.62（95%CI 0.44-0.78））和临床评分（AUC 0.64（95%CI 0.45-0.79））的 AUC 显著较低。
地塞米松抑制试验后的循环皮质醇水平和预干预刺激后的皮质醇水平可预测泼尼松 14 天后肾上腺功能抑制的发生，且优于临床评分或基础皮质醇水平。这可能为停止类固醇治疗后应激预防的需求提供更有针对性的概念。
