Neurodevelopmental Outcome of Acute Bilirubin Encephalopathy

Mukhopadhyay, Kanya; Chowdhary, Gurdev; Singh, Paramjeet; Prabhash, Kumar; Narang, Anil

doi:10.1093/tropej/fmp142

Cited by 25 publications

(22 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Kernicterus, a preventable neurodisability resulting from severe jaundice, is common in developing countries and also occurs infrequently in developed countries. [3][4][5][6]10,13,14 The consensus-based AAP guidelines for the management of severe jaundice in late preterm and term neonates are based on TSB, which has failed to discriminate neonates at risk for kernicterus. 1,8 Identification of a better biochemical measure will not only improve management of severe jaundice, but may also help reduce the morbidity and mortality associated with severe jaundice and related therapeutic interventions.…”

Section: Discussionmentioning

confidence: 99%

“…Severe jaundice may be associated with kernicterus, and therefore necessitates urgent readmission to the hospital for appropriate evaluations and therapeutic interventions to prevent and/or reduce bilirubin‐induced neurotoxicity (BINT) . Despite preventive and therapeutic interventions, severe jaundice remains one of the leading causes of neurodevelopmental disabilities, specifically in developing countries with significant impact on societal cost . Total serum bilirubin (TSB), the primary biochemical measure used for the management of jaundice, is a poor predictor of BINT, resulting in unwarranted costly interventions to prevent neurotoxicity .…”

mentioning

confidence: 99%

“…1 Despite preventive and therapeutic interventions, severe jaundice remains one of the leading causes of neurodevelopmental disabilities, specifically in developing countries with significant impact on societal cost. [2][3][4][5][6][7] Total serum bilirubin (TSB), the primary biochemical measure used for the management of jaundice, is a poor predictor of BINT, resulting in unwarranted costly interventions to prevent neurotoxicity. 1,2,8 This underscores the importance of identifying a better predictor than TSB for BINT.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Auditory toxicity in late preterm and term neonates with severe jaundice

Amin

Saluja

Saili

et al. 2016

Develop Med Child Neuro

View full text Add to dashboard Cite

AIM Jaundice may cause auditory toxicity (auditory neuropathy and hearing loss). However, total serum bilirubin (TSB) does not discriminate neonates at risk for auditory toxicity. We compared TSB, bilirubin:albumin molar ratio (BAMR), and unbound bilirubin for their association with auditory toxicity in neonates with severe jaundice (TSB ≥342μmol/L, or that met exchange transfusion). METHOD Neonates greater or equal to 34 weeks’ gestational age with severe jaundice during the first two postnatal weeks were eligible for prospective cohort study, unless they had craniofacial malformations, chromosomal disorders, toxoplasmosis, other infections, rubella, cytomegalovirus, and herpes simplex infections, surgery, or family history of congenital deafness. RESULTS Twenty-eight out of 100 neonates (mean gestational age 37.4wks; 59 males, 41 females) had auditory toxicity. Peak unbound bilirubin, but not peak TSB and BAMR, was associated with auditory toxicity (p<0.05) in neonates with severe (TSB <427.5μmol/L) and extreme hyperbilirubinemia (TSB ≥427.5μmol/L). Area under the receiver operating characteristic curve for unbound bilirubin (0.78) was significantly greater (p=0.03) than TSB (0.54) among neonates with severe but not extreme hyperbilirubinemia. INTERPRETATION Unbound bilirubin is more strongly associated with auditory toxicity than TSB and/or BAMR in greater or equal to 34 weeks’ gestational age neonates with severe jaundice. Unbound bilirubin is a better predictor than TSB in neonates with severe hyperbilirubinemia.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Auditory toxicity in late preterm and term neonates with severe jaundice

Amin

Saluja

Saili

et al. 2016

Develop Med Child Neuro

View full text Add to dashboard Cite

show abstract

“…Administration of albumin 1 h prior to ET was shown to significantly reduce the tissue-bound UCB and to increase ET efficacy (Shahian and Moslehi, 2010; Mitra et al, 2011). However, ET is not always successful in preventing acute bilirubin encephalopathy and adverse outcome (Mukhopadhyay et al 2010), and complications such as thrombocytopenia and seizure were indicated to be present in 21.5% of jaundiced neonates performing such intervention (Davutoglu et al, 2010). Since kernicterus continues to occur whereas it ought to be avoidable (Hansen, 2011), recognition of new therapeutic modulation capacities as adjunctive therapies may contribute to a more consistent regimen for treatment and prevention of kernicterus.…”

Section: Bind: In Search Of Potential Neurotherapeuticsmentioning

confidence: 99%

The Evolving Landscape of Neurotoxicity by Unconjugated Bilirubin: Role of Glial Cells and Inflammation

Brites¹

2012

Front. Pharmacol.

112

103

View full text Add to dashboard Cite

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 (BIND) may be produced. There is a tremendous variability in babies’ vulnerability toward UCB for reasons not yet explained, but preterm birth, sepsis, hypoxia, and hemolytic disease are comprised as risk factors. Therefore, UCB levels and neurological abnormalities are not strictly correlated. Even nowadays, the mechanisms of UCB neurotoxicity are still unclear, as are specific biomarkers, and little is known about lasting sequelae attributable to hyperbilirubinemia. On autopsy, UCB was shown to be within neurons, neuronal processes, and microglia, and to produce loss of neurons, demyelination, and gliosis. In isolated cell cultures, UCB was shown to impair neuronal arborization and to induce the release of pro-inflammatory cytokines from microglia and astrocytes. However, cell dependent sensitivity to UCB toxicity and the role of each nerve cell type remains not fully understood. This review provides a comprehensive insight into cell susceptibilities and molecular targets of UCB in neurons, astrocytes, and oligodendrocytes, and on phenotypic and functional responses of microglia to UCB. Interplay among glia elements and cross-talk with neurons, with a special emphasis in the UCB-induced immunostimulation, and the role of sepsis in BIND pathogenesis are highlighted. New and interesting data on the anti-inflammatory and antioxidant activities of different pharmacological agents are also presented, as novel and promising additional therapeutic approaches to BIND.

show abstract

“…This is based on the evidence from studies demonstrating timely ET/RET to be effective in reversing the neurologic signs of ABE and/or arresting its progression to chronic bilirubin encephalopathy (kernicterus) (24,34). However, although the early phase of ABE is generally considered reversible (24), studies investigating the reversibility of neurologic abnormalities in infants with intermediateto-advanced ABE after ET have shown mixed results (35,36). Notwithstanding, prevention of ABE remains a crucial goal in any effort to reduce RET.…”

Section: Discussionmentioning

confidence: 99%