Oppert Michael, Schindler Ralf, Husung Claudia, Offermann Katrin, Gräf Klaus-Jürgen, Boenisch Olaf, Barckow Detlef, Frei Ulrich, Eckardt Kai-Uwe
Department of Nephrology and Medical Intensive Care, Charite Universitätsmedizin Berlin, Humboldt University, Berlin, Germany.
Crit Care Med. 2005 Nov;33(11):2457-64. doi: 10.1097/01.ccm.0000186370.78639.23.
To investigate the effect of low-dose hydrocortisone on time to shock reversal, the cytokine profile, and its relation to adrenal function in patients with early septic shock.
Prospective, randomized, double-blind, single-center study.
Medical intensive care unit of a university hospital.
Forty-one consecutive patients with early hyperdynamic septic shock.
After inclusion and a short adrenocorticotropic hormone test, all patients were randomized to receive either low-dose hydrocortisone (50-mg bolus followed by a continuous infusion of 0.18 mg/kg body of weight/hr) or matching placebo. After shock reversal, the dose was reduced to 0.06 mg/kg/hr and afterward slowly tapered. Severity of illness was estimated using Acute Physiology and Chronic Health Evaluation II score and Sequential Organ Failure Assessment score.
Time to cessation of vasopressor support (primary end point) was significantly shorter in hydrocortisone-treated patients compared with placebo (53 hrs vs. 120 hrs, p < .02). This effect was more profound in patients with impaired adrenal reserve. Irrespective of endogenous steroid production, cytokine production was reduced in the treatment group with lower plasma levels of interleukin-6 and a diminished ex vivo lipopolysaccharide-stimulated interleukin-1 and interleukin-6 production. Interleukin-10 levels were unaltered. Adverse events were not more frequent in the treatment group.
Treatment with low-dose hydrocortisone accelerates shock reversal in early hyperdynamic septic shock. This was accompanied by reduced production of proinflammatory cytokines, suggesting both hemodynamic and immunomodulatory effects of steroid treatment. Hemodynamic improvement seemed to be related to endogenous cortisol levels, whereas immune effects appeared to be independent of adrenal reserve.
探讨小剂量氢化可的松对早期脓毒性休克患者休克逆转时间、细胞因子谱及其与肾上腺功能关系的影响。
前瞻性、随机、双盲、单中心研究。
大学医院的医学重症监护病房。
41例连续的早期高动力型脓毒性休克患者。
纳入患者并进行简短促肾上腺皮质激素试验后，所有患者随机分为接受小剂量氢化可的松（50mg静脉推注，随后以0.18mg/kg体重/小时持续输注）或匹配的安慰剂。休克逆转后，剂量减至0.06mg/kg/小时，然后缓慢减量。使用急性生理与慢性健康状况评分系统II和序贯器官衰竭评估评分来评估疾病严重程度。
与安慰剂组相比，氢化可的松治疗组血管升压药支持停止时间（主要终点）显著缩短（53小时对120小时，p < 0.02）。这种效应在肾上腺储备受损的患者中更为显著。无论内源性类固醇产生情况如何，治疗组细胞因子产生减少，血浆白细胞介素-6水平降低，体外脂多糖刺激的白细胞介素-1和白细胞介素-6产生减少。白细胞介素-10水平未改变。治疗组不良事件发生率并未更高。
小剂量氢化可的松治疗可加速早期高动力型脓毒性休克的休克逆转。这伴随着促炎细胞因子产生减少，提示类固醇治疗具有血流动力学和免疫调节作用。血流动力学改善似乎与内源性皮质醇水平有关，而免疫效应似乎与肾上腺储备无关。
