Groneck P, Reuss D, Götze-Speer B, Speer C P
Department of Pediatrics, Children's Hospital of the City of Cologne, Germany.
J Pediatr. 1993 Jun;122(6):938-44. doi: 10.1016/s0022-3476(09)90024-5.
To evaluate the effects of dexamethasone on pulmonary inflammation and permeability in preterm infants at high risk for chronic lung disease (birth weight < 1200 gm), we assessed tracheobronchial aspirate fluid for chemotactic activity and concentrations of mediators of inflammation. In a prospective study, 21 infants still undergoing mechanical ventilation at day 10 of postnatal age who required a fraction of inspired oxygen > or = 0.3, a peak inspiratory pressure > or = 16 cm H2O, or both were randomly assigned to treatment with dexamethasone at day 10 (early treatment group, n = 10) or day 16 (late treatment group, n = 11). The groups were compared with respect to all measurements on day 15; the late treatment group served as a control group. Additionally, the effects of dexamethasone within both groups were evaluated. In the early treatment group, the chemotactic response of peripheral blood neutrophils exposed to tracheobronchial aspirate fluid was significantly reduced 5 days after initiation of dexamethasone treatment compared with pretreatment values of the late treatment group (median (25th to 75th percentile): migratory distance before dexamethasone, 149 microns (140 to 173 microns); after dexamethasone, 81 microns (68 to 114 microns); p < 0.01). In addition, the following values were decreased after dexamethasone therapy in the early treatment group: number of neutrophils in tracheobronchial aspirate fluid (p < 0.05), and concentrations of leukotriene B4 (p < 0.01), interleukin-1 (p < 0.01), elastase-alpha 1-proteinase inhibitor (p < 0.01), and albumin (p < 0.01). Free elastase activity was found in only two infants; detectable activity of protective alpha 1-proteinase inhibitor was present in the others. Analysis of dexamethasone effects within the groups showed that all measurements were significantly decreased after both the early and the late treatment regimens, with the exception of leukotriene B4 and interleukin-1, which declined only after early dexamethasone treatment. Our results indicate that the pulmonary inflammatory response and microvascular permeability are decreased by dexamethasone, which affects the release of inflammatory mediators and neutrophil influx into the airways of preterm infants who require mechanical ventilation.
为评估地塞米松对慢性肺病高危早产儿（出生体重<1200克）肺部炎症和通透性的影响，我们检测了气管支气管吸出液的趋化活性和炎症介质浓度。在一项前瞻性研究中，21例出生后第10天仍在接受机械通气、吸入氧分数≥0.3、吸气峰压≥16厘米水柱或二者皆有的婴儿，被随机分为在第10天接受地塞米松治疗的早期治疗组（n = 10）或第16天接受治疗的晚期治疗组（n = 11）。在第15天对两组进行所有测量指标的比较；晚期治疗组作为对照组。此外，还评估了两组内地塞米松的作用。在早期治疗组中，与晚期治疗组治疗前的值相比，地塞米松治疗开始5天后，暴露于气管支气管吸出液的外周血中性粒细胞的趋化反应显著降低（中位数（第25至75百分位数）：地塞米松治疗前的迁移距离，149微米（140至173微米）；地塞米松治疗后，81微米（68至114微米）；p<0.01）。此外，早期治疗组在地塞米松治疗后，以下指标降低：气管支气管吸出液中的中性粒细胞数量（p<0.05）、白三烯B4浓度（p<0.01）、白细胞介素-1浓度（p<0.01）、弹性蛋白酶-α1-蛋白酶抑制剂浓度（p<0.01）和白蛋白浓度（p<0.01）。仅在两名婴儿中发现游离弹性蛋白酶活性；其他婴儿中存在可检测到的保护性α1-蛋白酶抑制剂活性。组内地塞米松作用分析显示，除白三烯B4和白细胞介素-1仅在早期地塞米松治疗后下降外，早期和晚期治疗方案后所有测量指标均显著降低。我们的结果表明，地塞米松可降低肺部炎症反应和微血管通透性，这影响了炎症介质的释放以及中性粒细胞流入需要机械通气的早产儿气道。
