Bovine surfactant in the treatment of pneumonia-induced-neonatal acute respiratory distress syndrome (NARDS) in neonates beyond 34 weeks of gestation: a multicentre, randomized, assessor-blinded, placebo-controlled trial.

Neonatal acute respiratory distress syndrome (NARDS) reflects pulmonary surfactant dysfunction, and the usage of bovine surfactant (Calsurf) supplement may therefore be beneficial. To determine whether bovine surfactant given in NARDS can improve oxygenation and survival rate, we conducted a multicenter, randomized trial between January 2018 and June 2019, and we compared Calsurf treatment to controls in neonates with pneumonia accompanied by NARDS. Neonates who met the Montreux criteria definition of NARDS were included, and those with congenital heart and lung malformations were excluded. Primary outcomes were oxygenation index (OI) after Calsurf administration, and secondary outcomes were mortality, and duration of ventilator and oxygen between the two groups, and also other morbidities. Cumulatively, 328 neonates were recruited and analyzed, 162 in the control group, and 166 in the Calsurf group. The results shows that OI in the Calsurf group were significantly lower than that in the control group at 4 h (7.2 ± 2.7 and 11.4 ± 9.1, P = 0.001); similarly, OI in the Calsurf group were significantly lower than in the control group at 12 h ( 7.5 ± 3.1 and 11.2 ± 9.2, P = 0.001). Mortality and duration of ventilator support or oxygen use between the two groups were not significantly different.Conclusion: Calsurf acutely improved OI immediately after administration in pneumonia-induced NARDS; although, we observed no significant decrease in mortality, duration of ventilator or oxygen, or major morbidity. What is known: • The definition proposed as the Monteux criteria for neonatal acute respiratory distress syndrome (NARDS). • Surfactant acutely improved oxygenation and significantly decreased mortality in children and adolescents with acute lung injury. What is new: • This is the first large randomized controlled trail to study on surfactant treatment of neonates with acute respiratory distress syndromes. • Surfactant acutely improved oxygenation immediately after administration in pneumonia-induced NARDS at a gestational age beyond 34 weeks.

Interleukin 17 is an important pathogenicity gene in pediatric sepsis.

OBJECTIVE: Sepsis represents a complex disease with the dysregulated inflammatory response. The purpose of this study is to explore the role of interleukin 17 (IL-17, also known as IL-17A) in the occurrence and development of pediatric sepsis. METHODS: We established the sepsis neonatal rat model with the method of intraperitoneal injection of Escherichia coli (E coli). At each target time point, we got the blood from heart after anesthetizing animals, and the lung and liver tissues were fixed in formalin. Immunohistochemistry and enzyme-linked immunosorbent assay assay was used to analyze the expression of IL-17A in the lung/liver and plasma respectively. A public data set of neonatal sepsis gene microarray was used to verify our result, and explore main functions of IL-17A in sepsis. RESULTS: The expression levels of IL-17A in the plasma, lung and liver gradually increased with the extension of the experimental time in sepsis group, and were significantly higher than control group at 4 hours after injection of E coli (P < 0.01). In our study, we found the levels of IL-17A mRNA in pediatric sepsis group were significantly higher than control group, which is consistent with the neonatal rat septicemia model. In addition, through the functional (GO) enrichment analysis, we found the genes associated with IL-17A in pediatric sepsis are mainly enriched in the functions of immune response and cell membrane formation. CONCLUSION: IL-17A might be a potential therapeutic target for pediatric sepsis.

[Detection of CPS1 gene mutation in a neonate with carbamoyl phosphate synthetase I deficiency].

OBJECTIVE: To explore the genetic basis for a neonate featuring hyperammonemia. METHODS: The patient was examined and tested by tandem mass spectrometry and next generation sequencing (NGS). Suspected mutations were confirmed by Sanger sequencing of the proband and her parents. Potential impact of the mutation was predicted with SIFT, PolyPhen-2 and MutationTaste software. RESULTS: Plasma ammonia and alanine were significantly increased in the proband, while serum citrulline was decreased. The neonate was found to harbor compound heterozygous mutations of the CPS1 gene [c.1631C>T(p.T544M) and c.1981G>T(p.G661C)], which were respectively inherited from her father and mother. CONCLUSION: The carbamoyl phosphate synthetase I deficiency of the proband can probably be attributed to the mutations of the CPS1 gene. Above finding has expanded the spectrum of CPS1 mutations in association with carbamoyl phosphate synthetase I deficiency.