Bilirubin Binding and Acid‐Base Equilibrium in Newborn Infants with Low Birthweight

Meisel, Peter; Jährig, D; Beyersdorff, E; Jährig, K

doi:10.1111/j.1651-2227.1988.tb10690.x

Cited by 9 publications

(5 citation statements)

References 16 publications

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“…9 It was established early that being a sick (pre)term newborn reduces bilirubinbinding capacity for at least 1 week after birth. 35 This reduction is independent of serum albumin level. Postmortem cohort studies introduced controversy about the role of acidosis.…”

Section: Discussionmentioning

confidence: 81%

Changes in Globus Pallidus With (Pre)Term Kernicterus

et al. 2003

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ABSTRACT. Objective. We report serial magnetic resonance (MR) and sonographic behavior of globus pallidus in 5 preterm and 3 term infants with kernicterus and describe the clinical context in very low birth weight preterm infants. On the basis of this information, we suggest means of diagnosis and prevention.Methods. Charts and MR and ultrasound images of 5 preterm infants and 3 term infants with suspected bilirubin-associated brain damage were reviewed. Included were preterm infants with severe hearing loss, quadriplegic hypertonia, and abnormal hypersignal of globus pallidus on T2-weighted MR imaging (MRI). In 1 infant who died on day 150, the diagnosis was confirmed during the neonatal period. The others were picked up as outpatients and scanned at 12 or 22 months' corrected age. Three instances of term kernicterus were included for comparison of serial MRI in the neonatal period and early infancy: they were caused by glucose-6-phosphate dehydrogenase deficiency, urosepsis, and dehydration plus fructose 1-6 biphosphatase deficiency.Results. Five preterm infants of 25 to 29 weeks' gestational age presented with total serum bilirubin (TSB) levels below exchange transfusion thresholds commonly advised. Mixed acidosis was present in 3 infants around the TSB peak. The bilirubin/albumin molar ratio was >0.5 in all, in the absence of displacing drugs. All failed to pass bedside hearing screen tests and had severe hearing loss on auditory brain response testing. Symmetrical homogeneous hyperechogenicity of globus pallidus was the alerting feature in 1 infant. Globus pallidus was hyperintense on T1-weighted MR images in this child. The other infants presented with severe developmental delay as a result of dyskinetic quadriplegia and hearing loss. Globus pallidus was normal on T1-but hyperintense on T2-weighted MR images at 12 or 22 months' corrected age. Subthalamic involvement was documented in coronal fluid attenuated inversion recovery MRI in 2 infants. The term infants with classical clinical presentation in the neonatal period had MR behavior similar to the preterms, but pallidal injury was not recognized with targeted sonographic examination. Their

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Section: Discussionmentioning

confidence: 81%

Changes in Globus Pallidus With (Pre)Term Kernicterus

et al. 2003

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“…Although UCB entrance into the brain is prevented by the brain microvascular endothelial cells tightly jointed by the elaborated junctional complexes that form the blood–brain barrier (BBB; Cardoso et al, 2010; Figure 1A), Bf diffuses into the brain (Ostrow et al, 2003b), and its accumulation in the CNS will depend on the total amount of Bf in the systemic circulation, on the efficacy of BBB transporters, and on the presence of acidosis, which increases binding of Bf to the brain parenchyma and the risk of kernicterus (Cashore et al, 1983; Meisel et al, 1988), due to its decreased solubility in acidic aqueous solutions (less than 1 nM at pH = 7 and about 0.1 μM at pH = 8; Ostrow and Celic, 1984). …”

Section: Determinants Of Brain Bilirubin Entrance and Loadmentioning

confidence: 99%

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

Brites¹

2012

Front. Pharmacol.

116

103

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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.

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“…[4] In an earlier study involving 76 infants, reserve albumin concentration determined by dialysis with 14 C-monoacetyl diamino diphenyl sulfone was decreased and the bilirubin toxicity index was increased in the presence of clinical risk factors (hypoxia, acidosis, or sepsis), suggesting an increased risk of bilirubin-induced neurotoxicity in the presence of these risk factors. [50] Maisels, et al [51] evaluated the influence of acid–base status on bilirubin-albumin binding in 254 low birthweight (LBW) infants at the ages of 3, 4, 5, and 8 days and reported a weak, but significant, correlation between metabolic acidosis and the bilirubin:reserve albumin ratio as well as the bilirubin toxicity index. A decrease in bilirubin-albumin binding and a doubling of the toxic potential of bilirubin occurred with shifts to a metabolically acidic state with a base deficit of 10.…”

Section: Introductionmentioning

confidence: 99%

“…A decrease in bilirubin-albumin binding and a doubling of the toxic potential of bilirubin occurred with shifts to a metabolically acidic state with a base deficit of 10. [51] In another study, involving 11 late preterm infants, the correction of a metabolic acidosis (pH 7.12 to 7.34) during the first postnatal day resulted in an improvement of apparent bilirubin-albumin binding affinity and a decrease in UB levels. [52] Although the exact mechanism is unclear, neonatal sepsis by decreasing albumin production and increasing free fatty acid (FFA) concentration, a known bilirubin displacer, may adversely influence bilirubin-albumin binding.…”

Section: Introductionmentioning

confidence: 99%

Bilirubin Binding Capacity in the Preterm Neonate

Amin

2016

Clinics in Perinatology

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SYNOPSIS Total serum/plasma bilirubin (TB), the biochemical measure currently used to evaluate and manage hyperbilirubinemia, is not a useful predictor of bilirubin-induced neurotoxicity in premature infants. Altered bilirubin-albumin binding in premature infants limits the usefulness of TB in premature infants. In this article, bilirubin-albumin binding, a modifying factor for bilirubin-induced neurotoxicity, in premature infants is reviewed.

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Bilirubin Binding and Acid‐Base Equilibrium in Newborn Infants with Low Birthweight

Cited by 9 publications

References 16 publications

Changes in Globus Pallidus With (Pre)Term Kernicterus

Changes in Globus Pallidus With (Pre)Term Kernicterus

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

Bilirubin Binding Capacity in the Preterm Neonate

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