Reduced Albumin Binding of MADDS–a Measure for Bilirubin Binding–in Sick Children

Ebbesen, Finn; Foged, N; Brodersen, Rolf

doi:10.1111/j.1651-2227.1986.tb10248.x

Cited by 9 publications

(5 citation statements)

References 12 publications

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“…This means that neonates strongly suspected of having sepsis are at slightly increased risk of bilirubin encephalopathy when compared to healthy newborns. This is in accordance with our previous findings of lower reserve albumin concentrations in a group of children older than one year of age with a severe bacterial infection (20).…”

Section: Discussionsupporting

confidence: 94%

The risk of bilirubin encephalopathy, as estimated by plasma parameters, in neonates strongly suspected of having sepsis

Ebbesen

Knudsen

1993

Acta Paediatrica

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The study comprises 18 mature newborns, strongly suspected of having sepsis, and a control group of 18 mature, healthy newborns with the same postnatal age. The object of the investigation was to compare the risk of development of bilirubin encephalopathy between the two groups, as estimated by plasma parameters. The sepsis group had significantly lower reserve albumin concentration for binding of MADDS (p < 0.01) and significantly lower total albumin concentration (p < 0.01). No significant differences were observed in unconjugated bilirubin concentration and plasma pH. It is suggested that mature newborns with sepsis have a slightly increased risk of developing bilirubin encephalopathy.

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Section: Discussionsupporting

confidence: 94%

The risk of bilirubin encephalopathy, as estimated by plasma parameters, in neonates strongly suspected of having sepsis

Ebbesen

Knudsen

1993

Acta Paediatrica

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“…Because unbound bilirubin (UB) is generally considered to be the form of bilirubin that can cross the blood brain barrier and neuronal membranes to cause neurotoxicity (13,14), it has been suggested that this bilirubin variable would have a better association with neurodevelopmental outcomes in high risk newborns (15). Furthermore, clinical conditions such as respiratory distress, acidosis, hypoxemia, and sepsis may impair bilirubin binding (6,16–19), and many pharmacologic agents administered to sick ELBW infants may also interfere with bilirubin: albumin binding resulting in higher UB levels (20–25). For these reasons, it is important to assess the relationships between intravascular bilirubin variables and adverse outcomes in these vulnerable infants with reference to their clinical status.…”

Section: Introductionmentioning

confidence: 99%

Influence of clinical status on the association between plasma total and unbound bilirubin and death or adverse neurodevelopmental outcomes in extremely low birth weight infants

Oh¹,

Dk²,

Tyson³

et al. 2010

Acta Paediatrica

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Objectives To assess the influence of clinical status on the association between total plasma bilirubin and unbound bilirubin on death or adverse neurodevelopmental outcomes at 18–22 months corrected age in extremely low birth weight infants. Method Total plasma biirubin and unbound biirubin were measured in 1,101 extremely low birth weight infants at 5±1 day of age. Clinical criteria were used to classify infants as clinically stable or unstable. Survivors were examined at 18–22 months corrected age by certified examiners. Outcome variables were death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss, and death prior to follow-up. For all outcomes, the interaction between bilirubin variables and clinical status was assessed in logistic regression analyses adjusted for multiple risk factors. Results Regardless of clinical status, an increasing level of unbound bilirubin was associated with higher rates of death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss and death before follow-up. Total plasma bilirubin values were directly associated with death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss, and death before follow-up in unstable infants, but not in stable infants. An inverse association between total plasma bilirubin and death or cerebral palsy was found in stable infants. Conclusions In extremely low birth weight infants, clinical status at 5 days of age affects the association between total plasma and unbound bilirubin and death or adverse neurodevelopmental outcomes at 18–22 months of corrected age. An increasing level of UB is associated a higher risk of death or adverse neurodevelopmental outcomes regardless of clinical status. Increasing levels of total plasma bilirubin are directly associated with increasing risk of death or adverse neurodevelopmental outcomes in unstable, but not in stable infants.

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“…However, when the BBC is exceeded, UB concentrations can increase significantly (118,337). Although BBC increases with postnatal age, in sick newborns and those having endogenous or exogenous bilirubin displacers, it becomes reduced (67,80,100,191). In addition to albumin, bilirubin can also bind to other proteins (e.g.…”

Section: Bilirubin Binding and Transport In Bloodmentioning

confidence: 99%

Molecular Physiology and Pathophysiology of Bilirubin Handling by the Blood, Liver, Intestine, and Brain in the Newborn

Hansen

Wong

Stevenson

2020

Physiological Reviews

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Bilirubin is the end product of heme catabolism formed during a process that involves oxidation-reduction reactions and conserves iron body stores. Unconjugated hyperbilirubinemia is common in newborn infants, but rare later in life. The basic physiology of bilirubin metabolism, such as production, transport, and excretion, has been well described. However, in the neonate, numerous variables related to nutrition, ethnicity, and genetic variants at several metabolic steps may be superimposed on the normal physiological hyperbilirubinemia that occurs in the first week of life and results in bilirubin levels that may be toxic to the brain. Bilirubin exists in several isomeric forms that differ in their polarities and is considered a physiologically important antioxidant. Here we review the chemistry of the bilirubin molecule and its metabolism in the body with a particular focus on the processes that impact the newborn infant, and how differences relative to older children and adults contribute to the risk of developing both acute and long-term neurological sequelae in the newborn infant. The final section deals with the interplay between the brain and bilirubin and its entry, clearance, and accumulation. We conclude with a discussion of the current state of knowledge regarding the mechanism(s) of bilirubin neurotoxicity.

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Reduced Albumin Binding of MADDS–a Measure for Bilirubin Binding–in Sick Children

Cited by 9 publications

References 12 publications

The risk of bilirubin encephalopathy, as estimated by plasma parameters, in neonates strongly suspected of having sepsis

The risk of bilirubin encephalopathy, as estimated by plasma parameters, in neonates strongly suspected of having sepsis

Influence of clinical status on the association between plasma total and unbound bilirubin and death or adverse neurodevelopmental outcomes in extremely low birth weight infants

Molecular Physiology and Pathophysiology of Bilirubin Handling by the Blood, Liver, Intestine, and Brain in the Newborn

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