A Pilot Double-Blind Placebo-Controlled Randomized Clinical Trial to Investigate the Effects of Early Enteral Nutrients in Sepsis.
A Pilot Double-Blind Placebo-Controlled Randomized Clinical Trial to Investigate the Effects of Early Enteral Nutrients in Sepsis.
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DOI：
10.1097/cce.0000000000000550
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发表时间：
2021-10
影响因子：
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通讯作者：
McVerry BJ
中科院分区：
文献类型：
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作者：
Shah FA;Kitsios GD;Yende S;Dunlap DG;Scholl D;Chuan B;Al-Yousif N;Zhang Y;Nouraie SM;Morris A;Huang DT;O'Donnell CP;McVerry BJ
补充数字内容可在文本中找到。我们实验室的临床前研究证明了肠内葡萄糖给药在脓毒症急性期的治疗效果，由肠源性肠促胰岛素激素葡萄糖依赖性胰岛素肽介导。本研究探讨了早期肠内葡萄糖输注对危重脓毒症患者全身炎症和葡萄糖代谢的影响。单中心、双盲、安慰剂对照随机先导临床试验（NCT03454087）。宾夕法尼亚州匹兹堡的三级医疗中心。危重成人患者在48小时内败血症诊断和建立肠内通路。参与者按1:1随机分组，接受连续水（安慰剂）或肠内葡萄糖输注（50%葡萄糖，0.5 g/mL），每小时10 mL，持续24小时。我们在2018年6月至2020年1月期间随机分配了58名参与者（安慰剂：n = 29，葡萄糖：n = 29）。方案依从性高，安慰剂组（中位持续时间，24小时[四分位数间距，20.9-24小时]）和葡萄糖组（23.9小时[23-24小时]）的研究输注时间相似（p = 0.59）。葡萄糖组（中位数为32 pg/mL [19-79 pg/mL]）和安慰剂组（24 pg/mL [9-59 pg/mL]; p = 0.13）在输注末期循环白介素-6的主要结局没有差异，在其他系统性宿主免疫反应的测量中也有类似的结果。与临床前研究一致的安慰剂相比，肠内葡萄糖增加了循环葡萄糖依赖性胰岛素肽（增加76%，95% CI [35-119], p < 0.01）和胰岛素（增加53% [17-88]，p < 0.01），但也增加了24小时输注期间的血糖（153 mg/dL[119-223]对116 mg/dL [91-140]， p < 0.01）。呕吐的发生、ICU和住院时间以及30天死亡率在安慰剂组和肠内葡萄糖组之间没有差异。危重症脓毒症患者早期低水平肠内葡萄糖输注可增加胰岛素和促肠促胰岛素激素葡萄糖依赖性胰岛素肽的循环水平，但不能减少全身炎症。
Supplemental Digital Content is available in the text. Preclinical studies from our laboratory demonstrated therapeutic effects of enteral dextrose administration in the acute phase of sepsis, mediated by the intestine-derived incretin hormone glucose-dependent insulinotropic peptide. The current study investigated the effects of an early enteral dextrose infusion on systemic inflammation and glucose metabolism in critically ill septic patients. Single-center, double-blind, placebo-controlled randomized pilot clinical trial (NCT03454087). Tertiary-care medical center in Pittsburgh, PA. Critically ill adult patients within 48 hours of sepsis diagnosis and with established enteral access. Participants were randomized 1:1 to receive a continuous water (placebo) or enteral dextrose infusion (50% dextrose; 0.5 g/mL) at 10 mL per hour for 24 hours. We randomized 58 participants between June 2018 and January 2020 (placebo: n = 29, dextrose: n = 29). Protocol adherence was high with similar duration of study infusion in the placebo (median duration, 24 hr [interquartile range, 20.9–24 hr]) and dextrose (23.9 hr [23–24 hr]) groups (p = 0.59). The primary outcome of circulating interleukin-6 at end-infusion did not differ between the dextrose (median, 32 pg/mL [19–79 pg/mL]) and placebo groups (24 pg/mL [9–59 pg/mL]; p = 0.13) with similar results in other measures of the systemic host immune response. Enteral dextrose increased circulating glucose-dependent insulinotropic peptide (76% increase; 95% CI [35–119]; p < 0.01) and insulin (53% [17–88]; p < 0.01) compared with placebo consistent with preclinical studies, but also increased blood glucose during the 24-hour infusion period (153 mg/dL [119–223] vs 116 mg/dL [91–140]; p < 0.01). Occurrence of emesis, ICU and hospital length of stay, and 30-day mortality did not differ between the placebo and enteral dextrose groups. Early infusion of low-level enteral dextrose in critically ill septic patients increased circulating levels of insulin and the incretin hormone glucose-dependent insulinotropic peptide without decreasing systemic inflammation.