Search Results (3)

Background: Neonatal jaundice is a common condition with potentially severe complications such as bilirubin-induced neurological dysfunction and kernicterus. While serum bilirubin (SBR) remains the standard laboratory measurement, point-of-care methods, such as transcutaneous bilirubinometry (TcB) and blood gas analysers (BGAs), offer rapid, less invasive alternatives. Direct comparisons of their diagnostic accuracy remain limited. Objective: The aim of this study was to assess and compare diagnostic accuracy and clinical utility of TcB and BGA against SBR in neonatal hyperbilirubinaemia screening. Methods: This retrospective study included neonates (n = 221) with concurrent SBR, BGA, and TcB measurements (n = 333). Assessment was via Passing–Bablok regression, Bland–Altman analysis, and Spearman correlation. Diagnostic performance was evaluated against jaundice thresholds in phototherapy charts (≥95th percentile threshold). Subgroup analyses considered phototherapy status, haemoglobin concentration, and Fitzpatrick skin type. Results: BGA showed stronger agreement with SBR (R² = 0.88) than TcB (R² = 0.43). BGA remained accurate regardless of phototherapy or haemoglobin levels. TcB accuracy declined post-phototherapy with reduced predictive value in darker-skinned neonates (Fitzpatrick III–VI) and increased false discovery rates. Both methods demonstrated low sensitivity (45.8%) but high specificity (>95%) and negative predictive value (~91%) for clinically significant hyperbilirubinaemia. BGA had a higher diagnostic odds ratio (47.5) than TcB (19.3). When individual patient sequential SBR and BGA measurements were compared for jaundice tracking (n = 175), there was high correlation, (r = 0.971) with no statistical differences, and 50% of measurements achieving agreement within 10 μmol/L. Conclusions: BGA is a more reliable alternative to SBR than TcB, particularly in time-critical or resource-limited settings. While TcB remains a non-invasive screening tool, limited accuracy post-phototherapy and with darker skinned neonates indicate confirmatory SBR testing. These findings support the selective and context-aware use of BGA and TcB to optimise neonatal hyperbilirubinaemia management and reduce interventions. Full article

Kernicterus is a serious complication of hyperbilirubinemia, caused by neuronal injury due to excessive unconjugated bilirubin (UCB) in specific brain areas. This injury induced by this accumulation in the globus pallidus can induce severe motor dysfunction. Repetitive transcranial magnetic stimulation (rTMS) has shown neuroprotective effects in various neurological diseases. This study aimed to investigate the effects of rTMS on pallidal nerve damage and motor dysfunction in a rat model of kernicterus. Rats were divided into a sham group (n = 16), a model group (bilirubin with sham rTMS; n = 16) and an rTMS group (bilirubin with rTMS; n = 16). High-frequency rTMS (10 Hz) was applied starting from 24 h postmodeling for 7 days. The rotarod test, western blotting and immunohistochemical staining were performed to measure motor function and protein expression levels. The rTMS mitigated the negative effects of UCB on the general health of kernicterus-model rats and improved their growth and development. Furthermore, the rTMS alleviated UCB-induced motor dysfunction and increased the expression of GABAergic neuronal marker GAD67 in the globus pallidus. Notably, it also inhibited apoptosis-related protein caspase-3 activation. In conclusion, rTMS could alleviate motor dysfunction by inhibiting apoptosis and increasing globus pallidus GAD67 in kernicterus rat models, indicating that it may be a promising treatment for kernicterus. Full article

Increased levels of unconjugated bilirubin are neurotoxic, but the mechanism leading to neurological damage has not been completely elucidated. Innovative strategies of investigation are needed to more precisely define this pathological process. By longitudinal in vivo bioluminescence imaging, we noninvasively visualized the brain response to hyperbilirubinemia in the MITO-Luc mouse, in which light emission is restricted to the regions of active cell proliferation. We assessed that acute hyperbilirubinemia promotes bioluminescence in the brain region, indicating an increment in the cell proliferation rate. Immunohistochemical detection in brain sections of cells positive for both luciferase and the microglial marker allograft inflammatory factor 1 suggests proliferation of microglial cells. In addition, we demonstrated that brain induction of bioluminescence was altered by pharmacological displacement of bilirubin from its albumin binding sites and by modulation of the blood–brain barrier permeability, all pivotal factors in the development of bilirubin-induced neurologic dysfunction. We also determined that treatment with minocycline, an antibiotic with anti-inflammatory and neuroprotective properties, or administration of bevacizumab, an anti-vascular endothelial growth factor antibody, blunts bilirubin-induced bioluminescence. Overall the study supports the use of the MITO-Luc mouse as a valuable tool for the rapid response monitoring of drugs aiming at preventing acute bilirubin-induced neurological dysfunction. Full article