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首页> 外文期刊>Pediatrics: Official Publication of the American Academy of Pediatrics >Chorioamnionitis and early lung inflammation in infants in whom bronchopulmonary dysplasia develops.
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Chorioamnionitis and early lung inflammation in infants in whom bronchopulmonary dysplasia develops.

机译：发生支气管肺发育不良的婴儿的绒毛膜羊膜炎和早期肺部炎症。

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OBJECTIVE: The development of bronchopulmonary dysplasia (BPD) often has been attributed to injury from mechanical ventilation and supplemental oxygen. Early lung inflammation in infants with BPD has been thought to be secondary to these factors. The purpose of this study was to evaluate whether preexisting (prenatal) inflammation may be a primary causative factor in the development of BPD. METHODS: Intubated newborns of less than 2,000 g birth weight were prospectively enrolled. The presence or absence of chorioamnionitis was documented. Lung inflammation was evaluated on days 1, 2, and 4 of intubation by assaying concentrations of interleukin 1 beta (IL-1 beta), thromboxane B2, leukotriene B4, and prostaglandin E2 in tracheal lavages. Infants in whom BPD developed were compared with those in whom it did not using these measures. RESULTS: Fifty-three infants were enrolled; 41 survived. Thirty-eight had respiratory distress syndrome; 15 were intubated for other diagnoses. Infants prenatally exposed to chorioamnionitis were less likely to present with respiratory distress syndrome; however, chorioamnionitis was significantly associated with both the presence of IL-1 beta from the first day of intubation and the development of BPD. Tracheal lavage concentrations of IL-1 beta were higher in infants in whom BPD developed. Thromboxane B2 concentrations were similar on day 1 but were higher on days 2 and 4 in infants in whom BPD developed. CONCLUSIONS: In this study, intubated infants weighing less than 2,000 g at birth in whom BPD developed had increased exposure to inflammation prenatally (chorioamnionitis) and evidence of increased lung inflammation from the first postnatal day. We speculate that chorioamnionitis may accelerate lung maturation but that it also causes lung inflammation and subsequent lung injury in intubated infants, fostering the development of BPD.
机译：目的：支气管肺发育不良（BPD）的发展通常归因于机械通气和补充氧气所致的伤害。 BPD婴儿的早期肺部炎症被认为是这些因素的继发性疾病。这项研究的目的是评估先前存在的（产前）炎症是否可能是BPD发生的主要致病因素。方法：前瞻性研究了出生体重小于2,000 g的插管新生儿。有无绒毛膜羊膜炎的记录。在插管的第1、2和4天，通过分析气管灌洗液中白介素1 beta（IL-1 beta），血栓素B2，白三烯B4和前列腺素E2的浓度来评估肺部炎症。将BPD发生的婴儿与未使用这些方法的婴儿进行比较。结果：53例婴儿入选。 41名幸存者。 38名患有呼吸窘迫综合征;进行了15例其他诊断。产前暴露于绒毛膜羊膜炎的婴儿较少出现呼吸窘迫综合征。然而，绒毛膜羊膜炎与插管第一天的IL-1β的存在和BPD的发展密切相关。 BPD患儿的气管灌洗液中IL-1β的浓度较高。 BPD患儿的血栓烷B2浓度在第1天相似，但在第2天和第4天更高。结论：在这项研究中，BPD患儿出生时体重小于2,000 g的插管婴儿增加了产前炎症（绒毛膜羊膜炎）的暴露，并从出生后第一天开始就出现了肺部炎症的证据。我们推测绒毛膜羊膜炎可能会加速肺成熟，但也会在插管婴儿中引起肺部炎症和随后的肺损伤，从而促进BPD的发展。

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