PEDEGO Research Unit and MRC Oulu, University of Oulu, Oulu, Finland; Department of Children and Adolescents, Oulu University Hospital, Oulu, Finland.
PEDEGO Research Unit and MRC Oulu, University of Oulu, Oulu, Finland; Department of Children and Adolescents, Oulu University Hospital, Oulu, Finland.
Early Hum Dev. 2021 Oct;161:105464. doi: 10.1016/j.earlhumdev.2021.105464. Epub 2021 Sep 7.
Paracetamol promotes early closure of patent ductus arteriosus (PDA), and it may affect inflammation after preterm birth.
The aim of this study was to evaluate the association between paracetamol treatment and serum inflammatory biomarkers in very preterm infants with respiratory distress.
The infants were randomly assigned to intravenous paracetamol or placebo during the first 4 days of life, and others received a lower dose of paracetamol unblinded. Serum samples were used for the analysis of 10 cytokines, C-reactive protein (CRP) and malondialdehyde (MDA). The impact of paracetamol on the biomarkers was evaluated, based on the levels during the early (<60 h) and the later (60-120 h) postnatal age.
Altogether, 296 serum samples from 31 paracetamol and 25 placebo group infants were analysed. Paracetamol had no effect on cytokine levels during the first 60 h when most induced PDA contractions took place. Later paracetamol treatment was associated with lower serum levels of several cytokines, including interleukin (IL-) 10, interferon gamma-induced protein (IP-) 10, and monocyte chemoattractant protein-1. CRP levels were lower in the paracetamol group during the early treatment. Amongst the infants who had severe morbidities, MDA was higher (p = .045), regardless of paracetamol treatment.
No significant differences in the cytokine levels were evident between the treatment and placebo groups. However, during early treatment, CRP levels were lower in the paracetamol group. To clarify whether this was due to a decrease in cardiopulmonary distress, or a distinct anti-inflammatory effect, requires further studies.
对乙酰氨基酚可促进动脉导管提前关闭(PDA),并可能影响早产儿出生后的炎症反应。
本研究旨在评估对患有呼吸窘迫的极早产儿使用对乙酰氨基酚治疗与血清炎症生物标志物之间的相关性。
婴儿在出生后的前 4 天内随机接受静脉用对乙酰氨基酚或安慰剂治疗,其余婴儿接受较低剂量的对乙酰氨基酚治疗但不设盲。使用血清样本分析 10 种细胞因子、C 反应蛋白(CRP)和丙二醛(MDA)。根据出生后早期(<60 小时)和晚期(60-120 小时)的水平,评估对乙酰氨基酚对生物标志物的影响。
共分析了 31 名接受对乙酰氨基酚治疗和 25 名接受安慰剂治疗的婴儿的 296 份血清样本。在大多数诱导的 PDA 收缩发生期间,对乙酰氨基酚在最初 60 小时内对细胞因子水平没有影响。后期对乙酰氨基酚治疗与几种细胞因子(包括白细胞介素(IL)-10、干扰素诱导蛋白(IP)-10 和单核细胞趋化蛋白-1)的血清水平较低相关。在早期治疗期间,对乙酰氨基酚组的 CRP 水平较低。在患有严重合并症的婴儿中,MDA 更高(p=0.045),无论是否接受对乙酰氨基酚治疗。
治疗组和安慰剂组之间的细胞因子水平没有明显差异。然而,在早期治疗中,对乙酰氨基酚组的 CRP 水平较低。为了明确这是由于心肺窘迫减轻,还是由于其具有明显的抗炎作用,需要进一步研究。