Fernandez E F, Montman R, Watterberg K L
Division of Neonatology, Department of Pediatrics, University of New Mexico, Albuquerque, NM 87131, USA.
J Perinatol. 2008 Dec;28(12):797-802. doi: 10.1038/jp.2008.190. Epub 2008 Nov 6.
To determine cortisol and adrenocorticotropic hormone (ACTH) responses to critical illness in term and late preterm newborns and examine the relationship of these values to measures of clinical illness, including markers of cardiovascular dysfunction.
In this prospective observational study, we measured ACTH, baseline cortisol and ACTH-stimulated cortisol concentrations in mechanically ventilated infants >or=34 weeks gestational age and <5 postnatal days. ACTH-stimulated cortisol concentrations were also measured in a comparison group of non-critically ill, non-mechanically ventilated infants. The relationship of these values to measures of severity of illness including SNAP (score for neonatal acute physiology) scores, blood pressure and vasopressor initiation was examined.
Concentrations are presented as median (25th to 75th percentile). Baseline cortisol values in critically ill infants (n=35) were 4.6 microg per 100 ml (3.0 to 16.2); 26 (74%) of these were <15 microg per 100 ml. ACTH-stimulated cortisol values were not significantly different from the comparison group (41 microg per 100 ml (30.3 to 51.8) vs 34.2 microg per 100 ml (25.2 to 43.3)). ACTH concentrations in ill infants (n=10) were 12 pgml(-1) (5.5 to 19.2). None of baseline cortisol, stimulated cortisol and ACTH increased significantly with increasing severity of illness. Of the ill infants, 71% received vasopressor therapy for hypotension. Cortisol concentrations in these infants were similar to those infants who did not receive vasopressor therapy.
The majority of these critically ill newborns had very low cortisol and ACTH values without the expected increase in response to critical illness; however, their response to exogenous ACTH was normal. These results demonstrate that the inadequate response to critical illness in these newborns does not result from adrenal dysfunction. We therefore hypothesize that this is a secondary insufficiency arising from inadequate stimulation of the adrenal gland.
确定足月儿和晚期早产儿危重症时皮质醇和促肾上腺皮质激素（ACTH）的反应，并研究这些值与临床疾病指标（包括心血管功能障碍标志物）之间的关系。
在这项前瞻性观察研究中，我们测量了胎龄≥34周且出生后<5天的机械通气婴儿的ACTH、基础皮质醇和ACTH刺激后的皮质醇浓度。还测量了非危重症、非机械通气婴儿对照组的ACTH刺激后的皮质醇浓度。研究了这些值与疾病严重程度指标（包括SNAP（新生儿急性生理学评分）、血压和血管升压药使用起始情况）之间的关系。
浓度以中位数（第25至75百分位数）表示。危重症婴儿（n = 35）的基础皮质醇值为每100 ml 4.6 μg（3.0至16.2）；其中26例（74%）<每100 ml 15 μg。ACTH刺激后的皮质醇值与对照组无显著差异（每100 ml 41 μg（30.3至51.8）对每100 ml 34.2 μg（25.2至43.3））。患病婴儿（n = 10）的ACTH浓度为12 pg/ml（5.5至19.2）。基础皮质醇、刺激后皮质醇和ACTH均未随疾病严重程度增加而显著升高。患病婴儿中，71%因低血压接受血管升压药治疗。这些婴儿的皮质醇浓度与未接受血管升压药治疗的婴儿相似。
这些危重症新生儿大多数皮质醇和ACTH值极低，对危重症无预期的反应增加；然而，他们对外源性ACTH的反应正常。这些结果表明，这些新生儿对危重症反应不足并非肾上腺功能障碍所致。因此，我们推测这是肾上腺刺激不足引起的继发性功能不全。
