Briegel J, Kellermann W, Forst H, Haller M, Bittl M, Hoffmann G E, Büchler M, Uhl W, Peter K
Institut für Anaesthesiologie, Ludwig-Maximilians-Universität München, Klinikum Grosshadern, Germany.
Clin Investig. 1994 Oct;72(10):782-7. doi: 10.1007/BF00180547.
There is increasing evidence that the hypercortisolemia in inflammatory diseases suppresses the elaboration of proinflammatory cytokines, thus protecting the host from its own defence reactions. In severe sepsis and septic shock cortisol levels are usually elevated, but some patients may have relative adrenal insufficiency. This may contribute to the overwhelming systemic inflammatory response syndrome. We evaluated the impact of low-dose hydrocortisone infusion (10 mg/h) on the course of the systemic inflammatory response syndrome. This dose corresponds to a maximum secretory rate of cortisol achieved in corticotropin-stimulated healthy humans. In a prospective observational study 57 surgical patients with severe sepsis or septic shock were studied, of which in addition to the conventional treatment 12 patients were infused with low-dose hydrocortisone, and 45 were treated without any corticosteroid. In the longitudinal analysis the systemic inflammatory response--as judged by body temperature, cardiovascular response, and kinetics of inflammatory mediators such as phospholipase A2, C-reactive protein, and neutrophil elastase--started to differ in favor of the hydrocortisone-treated patients after 2 days of treatment (P < 0.05, Mann-Whitney U test). The difference disappeared after withdrawal of exogenous cortisol. Shock reversal was achieved in all patients treated with low-dose hydrocortisone. The data provide evidence that low-dose hydrocortisone infusion attenuates the systemic inflammatory response in human septic shock. From an immunological point of view a relative cortisol deficiency may contribute to the amplified immune response in systemic inflammatory diseases. A randomized clinical trial must clarify the impact of low-dose hydrocortisone infusion on the clinical course and outcome of septic shock patients.
越来越多的证据表明，炎症性疾病中的高皮质醇血症会抑制促炎细胞因子的产生，从而保护宿主免受自身防御反应的影响。在严重脓毒症和脓毒性休克中，皮质醇水平通常会升高，但一些患者可能存在相对肾上腺功能不全。这可能导致压倒性的全身炎症反应综合征。我们评估了低剂量氢化可的松输注（10毫克/小时）对全身炎症反应综合征病程的影响。该剂量相当于促肾上腺皮质激素刺激的健康人中皮质醇达到的最大分泌率。在一项前瞻性观察研究中，对57例患有严重脓毒症或脓毒性休克的外科患者进行了研究，其中除常规治疗外，12例患者接受了低剂量氢化可的松输注，45例患者未接受任何皮质类固醇治疗。在纵向分析中，通过体温、心血管反应以及炎症介质如磷脂酶A2、C反应蛋白和中性粒细胞弹性蛋白酶的动力学判断的全身炎症反应，在治疗2天后开始有利于接受氢化可的松治疗的患者（P<0.05，曼-惠特尼U检验）。停用外源性皮质醇后，差异消失。所有接受低剂量氢化可的松治疗的患者均实现了休克逆转。数据表明，低剂量氢化可的松输注可减轻人类脓毒性休克中的全身炎症反应。从免疫学角度来看，相对皮质醇缺乏可能导致全身炎症性疾病中免疫反应的放大。一项随机临床试验必须阐明低剂量氢化可的松输注对脓毒性休克患者临床病程和结局的影响。
