Venkatesh Bala, Cohen Jeremy, Hickman Ingrid, Nisbet Janelle, Thomas Peter, Ward Gregory, Hall Jonathan, Prins John
Department of Intensive Care, Princess Alexandra and Wesley Hospitals, University of Queensland, 4102, Queensland, Australia.
Intensive Care Med. 2007 Oct;33(10):1746-53. doi: 10.1007/s00134-007-0727-7. Epub 2007 Jun 9.
Changes in cortisol metabolism due to altered activity of the enzyme 11beta-hydroxysteroid dehydrogenase (11beta-HSD) have been implicated in the pathogenesis of hypertension, obesity and the metabolic syndrome. No published data exist on the activity of this enzyme in critical illness.
To investigate cortisol metabolism in critically ill patients utilising plasma cortisol: cortisone ratio as an index of 11beta-HSD activity.
Tertiary level intensive care unit.
Three cohorts of critically ill patients: sepsis (n = 13); multitrauma (n = 20); and burns (n = 19).
Serial plasma cortisol: cortisone ratios.
Plasma total cortisol cortisone ratios were determined serially after admission to the intensive care unit. As compared with controls, the plasma cortisol:cortisone ratio was significantly elevated in the sepsis and trauma cohorts on day 1 (22 +/- 9, p = 0.01, and 23 +/- 19, p = 0.0003, respectively) and remained elevated over the study period. Such a relationship was not demonstrable in burns. The ratio was significantly correlated with APACHE II (r = 0.77, p = 0.0008) and Simplified Acute Physiology Score (r = 0.7, p = 0.003) only on day 7 and only in the burns cohort. There were no significant correlations observed between total plasma cortisol or cortisone and sickness severity in the sepsis and trauma cohorts.
In critically ill patients, there is evidence of altered cortisol metabolism due to an increase in 11beta-HSD activity as demonstrated by an elevation of plasma cortisol: cortisone ratios. Further studies with larger sample sizes specifically designed to examine altered tissue 11beta-HSD activity and its clinical significance and correlation with outcome are warranted.
11β-羟类固醇脱氢酶（11β-HSD）活性改变导致的皮质醇代谢变化与高血压、肥胖症及代谢综合征的发病机制有关。目前尚无关于该酶在危重病中活性的已发表数据。
利用血浆皮质醇：可的松比值作为11β-HSD活性指标，研究危重病患者的皮质醇代谢情况。
三级重症监护病房。
三组危重病患者：脓毒症（n = 13）；多发伤（n = 20）；烧伤（n = 19）。
连续测定血浆皮质醇：可的松比值。
入住重症监护病房后连续测定血浆总皮质醇：可的松比值。与对照组相比，脓毒症组和创伤组在第1天血浆皮质醇：可的松比值显著升高（分别为22±9，p = 0.01；23±19，p = 0.0003），且在研究期间一直保持升高。烧伤组未表现出这种关系。仅在第7天且仅在烧伤组中，该比值与急性生理与慢性健康状况评分系统II（APACHE II，r = 0.77，p = 0.0008）和简化急性生理学评分（r = 0.7，p = 0.003）显著相关。在脓毒症组和创伤组中，未观察到血浆总皮质醇或可的松与疾病严重程度之间存在显著相关性。
在危重病患者中，血浆皮质醇：可的松比值升高表明存在因11β-HSD活性增加导致的皮质醇代谢改变。有必要进行进一步研究，采用更大样本量，专门研究组织11β-HSD活性改变及其临床意义以及与预后的相关性。
