Han Yong Y, Doughty Lesley A, Kofos Danny, Sasser Howell, Carcillo Joseph A
Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Pediatr Crit Care Med. 2003 Jan;4(1):21-5. doi: 10.1097/00130478-200301000-00004.
To examine the relationships between procalcitonin, bacterial infection, sepsis-induced multiple organ failure, and mortality rate in children.
Cohort study.
A multidisciplinary, tertiary-care pediatric intensive care unit.
Seventy-eight children meeting criteria for sepsis or septic shock and 12 critically ill children without sepsis.
Venous or arterial blood sampling.
Demographic, epidemiologic, and outcome data were recorded. Plasma from children with sepsis were collected on days 1 and 3, and procalcitonin concentrations were measured by immunoluminometric assay. Organ failure index scores were determined, and multiple organ failure was defined as organ failure index > or = 3. Persistent multiple organ failure was defined by presence of multiple organ failure on day 3. Procalcitonin concentrations (median [25th percentile-75th percentile]) were increased among children with sepsis on day 1 (2.4 ng/mL [0.2-24.2], p < .01) but not on day 3 (0.8 ng/mL [0.1-8.1], p = nonsignificant) vs. controls (0.2 ng/mL [0.1-0.5]). This increase in procalcitonin concentration was particularly robust among children with bacterial sepsis on day 1 (7.1 ng/mL [0.9-44.8], p < .001) and on day 3 (2.9 ng/mL [0.1-32.4], p < .05). Procalcitonin concentrations were not increased among children with fungal, viral, or culture-negative sepsis vs. controls. Procalcitonin concentrations were persistently increased over time among patients with bacterial sepsis who had persistent multiple organ failure (p < .05) and who died (p < .01) but not among patients with nonbacterial sepsis.
Procalcitonin is persistently increased among children with poor outcome from bacterial sepsis. Further study is needed to better delineate this differential procalcitonin response to bacterial vs. nonbacterial sepsis and to characterize any mechanistic role that procalcitonin might play in the development of bacterial sepsis-induced multiple organ failure and mortality.
探讨儿童降钙素原、细菌感染、脓毒症诱导的多器官功能衰竭及死亡率之间的关系。
队列研究。
一家多学科的三级护理儿科重症监护病房。
78名符合脓毒症或脓毒性休克标准的儿童以及12名无脓毒症的危重症儿童。
静脉或动脉采血。
记录人口统计学、流行病学及转归数据。在第1天和第3天采集脓毒症患儿的血浆，采用免疫发光分析法测定降钙素原浓度。确定器官功能衰竭指数评分，将多器官功能衰竭定义为器官功能衰竭指数≥3。持续性多器官功能衰竭定义为第3天存在多器官功能衰竭。脓毒症患儿第1天的降钙素原浓度（中位数[第25百分位数 - 第75百分位数]）升高（2.4 ng/mL [0.2 - 24.2]，p < 0.01），但第3天未升高（0.8 ng/mL [0.1 - 8.1]，p = 无统计学意义），而对照组为（0.2 ng/mL [0.1 - 0.5]）。降钙素原浓度的这种升高在第1天的细菌性脓毒症患儿中尤为显著（7.1 ng/mL [0.9 - 44.8]，p < 0.001），第3天也是如此（2.9 ng/mL [0.1 - 32.4]，p < 0.05）。真菌性、病毒性或血培养阴性脓毒症患儿的降钙素原浓度与对照组相比未升高。在患有持续性多器官功能衰竭（p < 0.05）和死亡（p < 0.01）的细菌性脓毒症患者中，降钙素原浓度随时间持续升高，但在非细菌性脓毒症患者中未升高。
细菌性脓毒症预后不良的儿童降钙素原持续升高。需要进一步研究以更好地阐明降钙素原对细菌性与非细菌性脓毒症的不同反应，并确定降钙素原在细菌性脓毒症诱导的多器官功能衰竭和死亡发生过程中可能发挥的任何机制作用。
