2012
DOI: 10.3389/fphar.2012.00088
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Abstract: Unconjugated hyperbilirubinemia is a common condition in the first week of postnatal life. Although generally harmless, some neonates may develop very high levels of unconjugated bilirubin (UCB), which may surpass the protective mechanisms of the brain in preventing UCB accumulation. In this case, both short-term and long-term neurodevelopmental disabilities, such as acute and chronic UCB encephalopathy, known as kernicterus, or more subtle alterations defined as bilirubin-induced neurological dysfunction (BIN… Show more

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Cited by 108 publications
(92 citation statements)
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References 281 publications
(389 reference statements)
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“…High systemic concentrations of UCB in certain disease states are potentially injurious to the basal ganglia and neurons (1). However, physiological concentrations of this metabolite have immunomodulatory effects on antigen-presenting cells (2,3) and effector cells (2,4), ultimately favoring the expansion of FOXP3 + Tregs (5,6).…”
Section: Introductionmentioning
confidence: 99%
“…High systemic concentrations of UCB in certain disease states are potentially injurious to the basal ganglia and neurons (1). However, physiological concentrations of this metabolite have immunomodulatory effects on antigen-presenting cells (2,3) and effector cells (2,4), ultimately favoring the expansion of FOXP3 + Tregs (5,6).…”
Section: Introductionmentioning
confidence: 99%
“…In this situation bilirubin leads to cellular neuroinflammation with activation of astrocytes and microglia, as well as gliosis. (Shapiro, 2005;Yueh et al, 2014;Johnson and Bhutani, 2011;Brites, 2012). The benchmark of extreme bilirubin neurotoxicity or kernicterus is an irreversible posticteric sequelae, presented as icteric or yellow staining of brain tissue resulting from the accumulation of UCB in selective regions of the brain (Johnson and Bhutani, 2011).…”
Section: Introductionmentioning
confidence: 99%
“…En cultivos de células, la bilirrubina, impide la arborización neuronal, e induce la liberación de citoquinas pro inflamatorias por parte de la microglía y los astrocitos. Hay evidencias preclínicas que el pigmento puede concentrarse en la corteza cerebral, hipocampo, cerebro medio, hipotálamo, cerebelo y medula (8) espinal .…”
Section: Fisiopatología Del Daño Al Snc Inducida Por La Bilirrubinaunclassified
“…Estos conocimientos abren nuevos campos en la utilización de agentes anti inflamatorios y anti oxidantes en el tratamiento y prevención de la (8,9,10) hiperbilirrubinemia severa en el futuro .…”
Section: Fisiopatología Del Daño Al Snc Inducida Por La Bilirrubinaunclassified