Oppert M, Reinicke A, Gräf K J, Barckow D, Frei U, Eckardt K U
Department of Nephrology and Medical Intensive Care, Berlin, Germany.
Intensive Care Med. 2000 Dec;26(12):1747-55. doi: 10.1007/s001340000685.
To compare cortisol levels during "low-dose" hydrocortisone therapy to basal and ACTH-stimulated endogenous levels and to assess whether clinical course and the need for catecholamines depend on cortisol levels and/or pretreatment adrenocortical responsiveness.
Prospective observational study in a medical ICU of a university hospital.
Twenty consecutive patients with septic shock and a cardiac index of 3.5 l/min or higher, started on "low-dose" hydrocortisone therapy (100 mg bolus, 10 mg/h for 7 days and subsequent tapering) within 72 h of the onset of shock.
Basal total and free plasma cortisol levels ranged from 203 to 2169 and from 17 to 372 nmol/l. In 11 patients cortisol production was considered "inadequate" because there was neither a response to ACTH of at least 200 nmol/l nor a baseline level of at least 1000 nmol/l. Following the initiation of hydrocortisone therapy total and free cortisol levels increased 4.2- and 8.5-fold to median levels of 3,587 (interquartile range 2,679-5,220) and 1,210 (interquartile range 750-1,846) nmol/l on day 1, and thereafter declined to median levels of 1,310 nmol/l and 345 nmol/l on day 7. Patients with "inadequate" steroid production could be weaned from vasopressor therapy significantly faster, although their plasma free cortisol concentrations during the hydrocortisone treatment period did not differ.
(a) During proposed regimens of "low-dose" hydrocortisone therapy, initially achieved plasma cortisol concentrations considerably exceed basal and ACTH stimulated levels. (b) Cortisol concentrations decline subsequently, despite continuous application of a constant dose. (c) "Inadequate" endogenous steroid production appears to sensitize patients to the hemodynamic effects of a "therapeutic rise" in plasma cortisol levels.
比较“小剂量”氢化可的松治疗期间的皮质醇水平与基础及促肾上腺皮质激素（ACTH）刺激后的内源性皮质醇水平，并评估临床病程及对儿茶酚胺的需求是否取决于皮质醇水平和/或治疗前肾上腺皮质反应性。
在一所大学医院的内科重症监护病房进行的前瞻性观察研究。
20例连续的感染性休克患者，心脏指数为3.5升/分钟或更高，在休克发作后72小时内开始接受“小剂量”氢化可的松治疗（100毫克推注，10毫克/小时，持续7天，随后逐渐减量）。
基础血浆总皮质醇和游离皮质醇水平分别为203至2169纳摩尔/升和17至372纳摩尔/升。11例患者的皮质醇生成被认为“不足”，因为对ACTH的反应未达到至少200纳摩尔/升，且基线水平未达到至少1000纳摩尔/升。氢化可的松治疗开始后，血浆总皮质醇和游离皮质醇水平在第1天分别升高4.2倍和8.5倍，中位数水平分别为3587（四分位数间距2679 - 5220）纳摩尔/升和1210（四分位数间距750 - 1846）纳摩尔/升，此后在第7天降至中位数水平1310纳摩尔/升和345纳摩尔/升。“类固醇生成不足”的患者停用血管升压药治疗的速度明显更快，尽管他们在氢化可的松治疗期间的血浆游离皮质醇浓度并无差异。
（a）在建议的“小剂量”氢化可的松治疗方案期间，最初达到的血浆皮质醇浓度大大超过基础及ACTH刺激水平。（b）尽管持续给予恒定剂量，皮质醇浓度随后仍会下降。（c）“不足的”内源性类固醇生成似乎使患者对血浆皮质醇水平“治疗性升高”的血流动力学效应更为敏感。
