Gonzalez A, Sosenko I R, Chandar J, Hummler H, Claure N, Bancalari E
Department of Pediatrics, Division of Neonatology, University of Miami School of Medicine, Florida, USA.
J Pediatr. 1996 Apr;128(4):470-8. doi: 10.1016/s0022-3476(96)70356-6.
To test the hypotheses that (1) infection increases ductal dilatory prostaglandins and inflammatory mediators that may influence the closure of a patent ductus arteriosus (PDA), increasing the incidence of late episodes of PDA (after 7 days) and the rate of closure failures, and (2) the concurrence of PDA and infection increases the risk of chronic lung disease (CLD).
One hundred fourteen premature infants (birth weight, 500 to 1000 gm) were prospectively assessed for PDA and infection. Serum levels of 6-ketoprostaglandin F1 alpha and tumor necrosis factor alpha were measured routinely in all infants and when PDA or infection was present. Multivariate assessment of risk factors for PDA closure failure and for CLD was done by logistic regression, and expressed as an odds ratio and as 95% confidence intervals.
Late PDA episodes were more frequent in infants with infection than in those without infection. A temporally related infection (<5 days between both diagnoses) was associated with an increased risk of PDA closure failure (odds ratio, 19.1 (confidence interval, 4 to 90)). In addition to birth weight and the severity of initial respiratory failure, PDA and infection increased the risk of CLD (odds ratio, 11.7 (confidence interval, 1.7 to 81) for PDA; odds ration, 3.1 (confidence interval, 1 to 11) for infection). Furthermore, when both factors were temporally related, they further increased the risk of CLD (odds ratio, 29.6 (confidence interval, 4.5 to >100)). Infants with infection and those with PDA had higher levels of 6-ketoprostaglandin F1 alpha than did control subjects. Levels of tumor necrosis factor alpha were also elevated in infants with infection and in those with late PDA.
Infection adversely influences PDA outcome by increasing the risk of late ductal reopening and PDA closure failures. Increased levels of prostaglandins and tumor necrosis factor alpha in infants with infection may explain the poor PDA outcome. The concurrence of PDA and infection potentiates their negative effects on the risk of CLD.
验证以下假设：（1）感染会增加导管扩张性前列腺素和炎症介质，这些物质可能影响动脉导管未闭（PDA）的闭合，从而增加PDA晚期发作（7天后）的发生率和闭合失败率；（2）PDA与感染同时存在会增加慢性肺病（CLD）的风险。
对114例早产儿（出生体重500至1000克）进行前瞻性PDA和感染评估。所有婴儿在常规情况下以及出现PDA或感染时，均检测血清6-酮前列腺素F1α和肿瘤坏死因子α水平。通过逻辑回归对PDA闭合失败和CLD的危险因素进行多变量评估，并以比值比和95%置信区间表示。
感染婴儿的PDA晚期发作比未感染婴儿更频繁。时间上相关的感染（两次诊断间隔<5天）与PDA闭合失败风险增加相关（比值比，19.1（置信区间，4至90））。除出生体重和初始呼吸衰竭的严重程度外，PDA和感染会增加CLD的风险（PDA的比值比，11.7（置信区间，1.7至81）；感染的比值比，3.1（置信区间，1至11））。此外，当这两个因素在时间上相关时，它们会进一步增加CLD的风险（比值比，29.6（置信区间，4.5至>100））。感染婴儿和PDA婴儿的6-酮前列腺素F1α水平高于对照组。感染婴儿和晚期PDA婴儿的肿瘤坏死因子α水平也升高。
感染通过增加导管晚期重新开放和PDA闭合失败的风险，对PDA的转归产生不利影响。感染婴儿中前列腺素和肿瘤坏死因子α水平升高可能解释了PDA转归不良的原因。PDA与感染同时存在会增强它们对CLD风险的负面影响。
