Na Wang

Background: Neonatal hyperbilirubinaemia (NHB) affects approximately 60% of term infants and is a recognised cause of bilirubin-induced neurologic dysfunction (BIND); however, its subclinical neurodevelopmental sequelae have not been well characterised at the level of specific developmental domains. Objectives: We aimed to use the Griffiths Developmental Scales–Chinese Edition (GDS-C) to characterise the domain-specific neurodevelopmental profile of term infants with NHB and to identify clinical risk factors for adverse outcomes. Methods: We conducted a single-centre, retrospective cohort study of 123 term newborns delivered between September 2019 and August 2023 at a tertiary hospital in Shanghai, China; 77 had NHB and 46 were healthy controls. Neurodevelopmental outcomes were assessed using the GDS-C at a median age of 46.9 months (interquartile range [IQR], 36.4–59.7) by a single certified examiner who was blinded to bilirubin status. A developmental quotient (DQ) below 85 (>1 SD below the standardised mean of 100) or at or below the 10th percentile was classified as below cutoff; otherwise, performance was classified as within the normal range. To account for testing across six domains, a Bonferroni-adjusted significance threshold of p < 0.0083 was applied. Results: Compared to the control group, the jaundice group had higher proportions of below-cutoff performance in the Locomotor (26.0% vs. 10.9%; p = 0.045), Personal–Social (28.6% vs. 10.9%; p = 0.022), Eye and Hand Coordination (29.9% vs. 10.9%; p = 0.015) and Performance (35.1% vs. 15.2%; p = 0.018) domains. Among infants with severe hyperbilirubinaemia (total serum bilirubin (TSB) ≥ 342 μmol/L; n = 19), the proportions of below-cutoff performance in the Locomotor (47.4% vs. 19.0%; p = 0.032), Personal–Social (57.9% vs. 19.0%; p = 0.003) and Performance (57.9% vs. 27.6%; p = 0.034) domains exceeded those in the non-severe subgroup. Jaundice lasting ≥ 14 days was associated with poorer personal–social outcomes (p = 0.007). In multivariable logistic regression, both a peak TSB ≥ 342 μmol/L (adjusted odds ratio [aOR], 5.59; 95% confidence interval [CI], 1.64–19.02; p = 0.006) and a jaundice duration ≥ 14 days (aOR, 5.68; 95% CI, 1.61–20.04; p = 0.007) were independently associated with below-cutoff personal–social performance. Conclusions: Among term infants, NHB was associated with an increased risk of below-cutoff performance across several GDS-C domains, particularly those reflecting gross motor, personal–social and visual-spatial functions. Severe hyperbilirubinaemia and prolonged jaundice were independent risk factors. The GDS-C may serve as a sensitive, domain-specific instrument for the early identification of infants at risk of adverse neurodevelopmental outcomes.

This study aimed to investigate the relationship between serum lactate levels at admission to the intensive care unit (ICU) and the clinical outcomes of children with sepsis. We used the Pediatric Intensive Care (PIC) database to identify 288 pediatric patients with sepsis. We analyzed the relationship between lactate levels and hospital and ICU mortality in sepsis by establishing a segmented multivariable Cox regression model. We also conducted subgroup analysis as well as analyzed the restricted cubic spline curves. After adjusting for all potential confounding factors, an increase of 1 mmol/L in lactate levels was found to be associated with an 17% rise in the 28-day hospital mortality risk among sepsis patients (HR: 1.17, 95% CI: 1.08–1.27, P = 0.0002). When considering lactate as a categorical variable, the mortality risk of patients with lactate levels ≥ 2.2 mmol/L was significantly increased (HR: 3.61, 95% CI: 1.24–10.54, P = 0.0189). The restricted cubic spline curve analysis revealed a nonlinear correlation between lactate and 28-day mortality, with an inflection point at 2.2 mmol/L. Similar findings were also observed in the assessment of secondary outcomes. Our study demonstrates a non-linear correlation between lactate levels and 28-day mortality in pediatric sepsis, with a critical threshold of 2.2mmol/l for lactate levels in septic patients. Early assessment of lactate levels is recommended for children with sepsis to facilitate prompt intervention and mitigate the risk of fatality.

To investigate the methylation, expression and clinical significance of miR-203 in pediatric acute leukemia. The methylation status of miR-203 promoter CpG islands was detected with methylation-specific polymerase chain reaction. The expression of miR-203 was detected by Taqman real- time quantitative polymerase chain reaction. And the clinical significance of miR-203 in pediatric acute leukemia (ALL) was also analyzed. The promoter of miR-203 was unmethylated in all of 31 pediatric acute lymphoblastic leukemia, all of 15 pediatric acute myeloid leukemia (AML) and all of 23 controls. The relative expression levels of miR-203 in controls, pediatric acute leukemia, ALL and AML were 16.93±6.31, 48.97±10.38, 55.88±12.91, 24.28±9.10 respectively. The results indicated that miR-203 was significantly up- regulated in pediatric acute leukemia (P=0.011) and ALL (P=0.009), not in pediatric AML (P=0.514) compared with control. The expression of miR-203 was significantly related with the gender, immunophenotype, chromosome, fusion gene, BCR-ABL, SIL-TAL1 and prednisone experiment in pediatric ALL and the gender, chromosome, fusion gene, SIL-TAL1 in pediatric acute leukemia (P<0.05). And in risk stratification pairwise comparisons, the expression of miR-203 in the medium-risk and high-risk groups appeared significantly different (P=0.022). miR-203 may not be regulated with methylation mechanism in pediatric acute leukemia. miR- 203 may be a protooncogene involved in the formation of pediatric acute leukemia and ALL. Further analyses indicated that high expression of miR-203 may be associated with poor prognosis of pediatric ALL and acute leukemia.