1Department of Pediatrics, Medical University of South Carolina, Charleston, SC. 2Department of Pediatric Emergency Medicine, Akron Children's Hospital, Akron, OH. 3Department of Medicine, Division of Biostatistics and Epidemiology, Medical University of South Carolina, Charleston, SC. 4Department of Clinical Psychology, University of Massachusetts, Boston, MA. 5Department of Pediatrics, Eastern Virginia Medical School, Norfolk, VA. 6Department of Pediatrics, University of Virginia, Charlottesville, VA. 7Department of Pediatrics, Albany Medical Center, Albany, NY. 8Department of Pediatrics, Brooklyn Hospital Center, Brooklyn, NY. 9Department of Pediatrics, University of Saskatchewan, Saskatoon, SK, Canada. 10Department of Pediatrics, University of Alberta, Edmonton, AB, Canada.
Pediatr Crit Care Med. 2013 Oct;14(8):786-95. doi: 10.1097/PCC.0b013e3182975cc9.
To determine systemic hypothermia's effect on circulating immune cells and their corresponding chemokines after hypoxic ischemic encephalopathy in neonates.
In our randomized, controlled, multicenter trial of systemic hypothermia in neonatal hypoxic ischemic encephalopathy, we measured total and leukocyte subset and serum chemokine levels over time in both hypothermia and normothermia groups, as primary outcomes for safety.
Neonatal ICUs participating in a Neurological Disorders and Stroke sponsored clinical trial of therapeutic hypothermia.
Sixty-five neonates with moderate to severe hypoxic ischemic encephalopathy within 6 hours after birth.
Patients were randomized to normothermia of 37°C or systemic hypothermia of 33°C for 48 hours.
Complete and differential leukocyte counts and serum chemokines were measured every 12 hours for 72 hours. The hypothermia group had significantly lower median circulating total WBC and leukocyte subclasses than the normothermia group before rewarming, with a nadir at 36 hours. Only the absolute neutrophil count rebounded after rewarming in the hypothermia group. Chemokines, monocyte chemotactic protein-1 and interleukin-8, which mediate leukocyte chemotaxis as well as bone marrow suppression, were negatively correlated with their target leukocytes in the hypothermia group, suggesting active chemokine and leukocyte modulation by hypothermia. Relative leukopenia at 60-72 hours correlated with an adverse outcome in the hypothermia group.
Our data are consistent with chemokine-associated systemic immunosuppression with hypothermia treatment. In hypothermic neonates, persistence of lower leukocyte counts after rewarming is observed in infants with more severe CNS injury.
确定全身低温对新生儿缺氧缺血性脑病后循环免疫细胞及其相应趋化因子的影响。
在我们对新生儿缺氧缺血性脑病进行全身低温的随机、对照、多中心试验中，我们测量了低温和正常体温组中随时间推移的总白细胞亚群和血清趋化因子水平，作为安全性的主要结果。
参与神经障碍和中风赞助的治疗性低温临床试验的新生儿 ICU。
出生后 6 小时内患有中度至重度缺氧缺血性脑病的 65 名新生儿。
患者随机分为正常体温 37°C 或全身低温 33°C 组，持续 48 小时。
每 12 小时测量一次完整和差异白细胞计数和血清趋化因子，持续 72 小时。在复温前，低温组的循环总白细胞和白细胞亚群中位数明显低于正常体温组，最低值出现在 36 小时。只有低温组的绝对中性粒细胞计数在复温后反弹。趋化因子，单核细胞趋化蛋白-1 和白细胞介素-8，作为白细胞趋化因子以及骨髓抑制的介质，与低温组的靶白细胞呈负相关，表明低温积极调节趋化因子和白细胞。低温组 60-72 小时的相对白细胞减少与不良预后相关。
我们的数据与低温治疗相关的趋化因子相关的全身免疫抑制一致。在低温新生儿中，在中枢神经系统损伤更严重的婴儿中，复温后白细胞计数持续较低。
