Altered glucose metabolic pattern in basal ganglia: 18F-FDG PET/CT semi-quantitative analysis of metabolic signatures in neonatal bilirubin encephalopathy

Neonatal bilirubin encephalopathy arises from unconjugated bilirubin deposition in the brain. Conventional tests are limited: serum bilirubin does not reflect intracerebral load, and MRI T1 changes are late and confounded by myelination. We evaluated whether 18 F-FDG PET detects early metabolic abnormalities and monitor progression. Twelve Sprague–Dawley rat were randomly assigned to bilirubin-exposed or control groups. The bilirubin-exposed group received intraperitoneal bilirubin from postnatal day 3. 18 F-FDG PET/CT was performed on days 7 and 21, and regional standardized uptake values and cerebellum-normalized SUV ratios were quantified. Serum bilirubin, histology, immunohistochemistry and qRT-PCR were assessed in parallel. The model showed elevated serum bilirubin ( p  < 0.001) and neuronal injury. On day 7, PET revealed regional hypermetabolism in hippocampus and thalamus ( p  < 0.01), coinciding with increased IL-6 (cortex, thalamus) and TNF-α (thalamus). By day 21, widespread hypometabolism involved cortex, basal ganglia, hippocampus, thalamus, and brainstem ( p  < 0.001), with only residual thalamic IL-6. GFAP indicated persistent astrocytic activation, whereas MAP2 and NeuN were largely preserved. The SUV ratio analysis showed a pattern consistent with the SUV-based findings. 18 F-FDG PET detected age-dependent metabolic alterations in bilirubin encephalopathy and may be useful for early detection and longitudinal monitoring.