Surveillance of extreme hyperbilirubinaemia in Denmark. A method to identify the newborn infants

Bjerre, Jesper Vandborg; Petersen, J; Ebbesen, Finn

doi:10.1111/j.1651-2227.2008.00879.x

Cited by 66 publications

(67 citation statements)

References 20 publications

(50 reference statements)

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“…2 In Denmark, extreme hyperbilirubinemia and chronic bilirubin encephalopathy (kernicterus) occur in 1 in 2000 live births and 1 in 95 000 live births, respectively. [3][4][5][6] These rates correspond well with reports from other parts of the privileged world, 7 but in the developing world, bilirubin encephalopathy persists as a frequent cause of neonatal morbidity. 8 Severalriskfactorsforhyperbilirubinemia are known, among these are blood type iso-immunization, congenital hemolytic diseases, gender, prematurity, race, starvation, and early discharge from hospital, but in a large number of patients, a causal factor is never established.…”

supporting

confidence: 73%

“…4 At birth, all Danish citizens are assigned a unique 10-digit civil registration number, which gives data on date of birth and gender and allows unambiguous individual-level identification and data linkage across nationwide public health registers. 21 We used the civil registration number to identify cases in the Danish Neonatal Screening Biobank.…”

Section: Methodsmentioning

confidence: 99%

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Extreme Neonatal Hyperbilirubinemia and a Specific Genotype: A Population-Based Case-Control Study

Petersen

Henriksen²,

Hollegaard

et al. 2014

Pediatrics

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WHAT'S KNOWN ON THIS SUBJECT: For newborn infants, extreme hyperbilirubinemia ($24.5 mg/dL) is associated with risk for severe bilirubin encephalopathy. The causal factor of extreme hyperbilirubinemia is often not established. The genotype of Gilbert syndrome, the UGT1A1*28 allele, is considered a potential risk factor. WHAT THIS STUDY ADDS:The UGT1A1*28 allele was not associated with risk for developing extreme hyperbilirubinemia. abstract OBJECTIVES: Extreme hyperbilirubinemia (plasma bilirubin $24.5 mg/dL) is an important risk factor for severe bilirubin encephalopathy. Several risk factors for hyperbilirubinemia are known, but in a large number of patients, a causal factor is never established. UGT1A1 is the rate-limiting enzyme in bilirubin' s metabolism. The genotype of Gilbert syndrome, the UGT1A1*28 allele, causes markedly reduced activity of this enzyme, but its association with neonatal hyperbilirubinemia is uncertain and its relationship with extreme hyperbilirubinemia has not been studied. We examined whether the UGT1A1*28 allele is associated with extreme hyperbilirubinemia. METHODS:The UGT1A1*28 allele was assessed in a case-control study of 231 white infants who had extreme hyperbilirubinemia in Denmark from 2000 to 2007 and 432 white controls. Cases were identified in the Danish Extreme Hyperbilirubinemia Database that covers the entire population. Genotypes were obtained through the Danish Neonatal Screening Biobank. Subgroup analysis was done for AB0 incompatible cases. RESULTS:No association was found between the UGT1A1*28 allele and extreme hyperbilirubinemia. With the common genotype as reference, the odds ratio of extreme hyperbilirubinemia was 0.87 (range, 0.68-1.13) for UGT1A1*28 heterozygotes and 0.77 (range, 0.46-1.27) for homozygotes. Also, no association was found for AB0 incompatible cases.

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confidence: 73%

Section: Methodsmentioning

confidence: 99%

Extreme Neonatal Hyperbilirubinemia and a Specific Genotype: A Population-Based Case-Control Study

Petersen

Henriksen²,

Hollegaard

et al. 2014

Pediatrics

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“…Between 2002 and 2005, with a more vigilant approach to newborn jaundice management, the overall incidence reduced to 1.1/100 000 live births between 1994 and 2005. 44, 45 We have estimated that risk of kernicterus in infants with TSB >25 mg per 100 ml ranged from 1 in 14 to 16 to a risk range of 1 in 4 to 7 in infants with TSB >30 mg per 100 ml. None of the retrospective data provide any insight into signs of acute kernicterus in infants with TSB <25 mg per 100 ml.…”

Section: Discussionmentioning

confidence: 99%

Universal bilirubin screening for severe neonatal hyperbilirubinemia

2010

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To reduce the incidence of severe neonatal hyperbilirubinemia affecting newborns with jaundice in the United States and to prevent kernicterus, there is a need to implement proven prevention strategies for severe neonatal hyperbilirubinemia as recommended in the 2004 American Academy of Pediatrics Guidelines for newborns >35 weeks gestational age. The purpose of universal predischarge bilirubin screening is to identify infants with bilirubin levels >75th percentile for age in hours and track those with rapid rates of bilirubin rise (>0.2 mg per 100 ml per h). Early identification has been reported to predict severe hyperbilirubinemia and allow for evidence-based targeted interventions. A systems approach is likely to reduce the preventable causes of acute bilirubin encephalopathy. To do so, highest priority should be given to (i) designating extreme hyperbilirubinemia (total serum bilirubin >427 mmol l À1 or >25 mg per 100 ml) as a reportable condition by laboratories and health-care providers through public health mandates; (ii) implementation of Joint Commission's Sentinel Report for kernicterus; (iii) nursing outreach to communities for education of prospective parents; (iv) development of clinical pathways to monitor, evaluate and track infants with extreme hyperbilirubinemia; and (v) societal awareness. These efforts should be monitored by a state and national surveillance system in order to critically improve the timeliness and completeness of notifications and to allow evaluation and interventions at the policy and individual family level.

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“…[1][2][3][4] Although there is no single threshold at which bilirubin becomes neurotoxic, 5 a 2003 Eunice Kennedy Shriver National Institute of Child Health and Human Development sponsored conference proposed that TSB levels $30 mg/dL be defined as "hazardous" hyperbilirubinemia because of the perceived higher risk of neurologic injury. 6 The incidence of hazardous hyperbilirubinemia in populations in Western Europe [7][8][9][10][11][12] and the United States [13][14][15][16][17] ranges from 2 to 12/100 000, with the lowest rates in Switzerland (where the mean postpartum stay after a vaginal delivery was 5.6 days) 11 and in US hospital systems after implementation of universal bilirubin screening. 14,15,17 The distribution of causes of hazardous hyperbilirubinemia varies in different populations, with isoimmunization more common in Europe 9,10,12 and glucose-6-phosphate dehydrogenase (G6PD) deficiency predominating in the United States and Canada.…”

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confidence: 99%

Incidence, Etiology, and Outcomes of Hazardous Hyperbilirubinemia in Newborns

et al. 2014

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WHAT'S KNOWN ON THIS SUBJECT: Total serum bilirubin levels $30 mg/dL have been labeled as "hazardous." Levels this high are rare, occurring in 3 to 10 per 100 000 births. Few studies have examined etiologies and long-term outcomes in these infants.WHAT THIS STUDY ADDS: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a major identifiable cause, but is underassessed. Chronic, bilirubin-induced neurotoxicity is rare and only occurred in the setting of additional risk factors (prematurity, G6PD deficiency, sepsis) and at levels far above recommended exchange transfusion thresholds. abstract BACKGROUND AND OBJECTIVES: Total serum bilirubin (TSB) levels $30 mg/dL are rare but potentially hazardous. A better understanding of their incidence, causes, and outcomes could help inform preventive efforts. METHODS:We identified infants born $35 weeks' gestational age from 1995-2011 in Kaiser Permanente Northern California (n = 525 409) and examined the medical records of infants with a TSB $30 mg/dL to determine etiology and the occurrence of acute bilirubin encephalopathy. We reviewed inpatient and outpatient encounters through 2013 for evidence of sensorineural hearing loss (SNHL) or cerebral palsy (CP). RESULTS:We identified 47 infants with TSB $30 mg/dL (8.6 per 100 000 births). In 44 infants (94%), the hyperbilirubinemia occurred after the initial birth hospitalization. The etiology was not identified in 33 (70%). Glucose-6-phosphate dehydrogenase (G6PD) activity was measured in only 25 (53%) of whom 10 (40%) were deficient. Four children had acute bilirubin encephalopathy of whom 2 developed both CP and SNHL, and 1 developed isolated SNHL. These 3 infants all had G6PD deficiency and TSB .40 mg/dL. One additional 35-week infant with TSB 38.2 mg/dL had SNHL.CONCLUSIONS: Hazardous ($30 mg/dL) hyperbilirubinemia is a rare event. No etiology could be identified from the clinical record in most cases. G6PD deficiency was the leading cause of hazardous hyperbilirubinemia when an etiology was identified, but many were not tested. Chronic, bilirubin-induced neurotoxicity was uncommon and occurred only in the setting of additional risk factors and TSB values well over (.15 mg/dL)

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Surveillance of extreme hyperbilirubinaemia in Denmark. A method to identify the newborn infants

Abstract: A method to obtain the national epidemiological data is presented. The observed incidence of extreme hyperbilirubinaemia is higher than previously reported in Denmark. This is mainly due to a very sensitive method of identifying the study group.

Cited by 66 publications

References 20 publications

Extreme Neonatal Hyperbilirubinemia and a Specific Genotype: A Population-Based Case-Control Study

Extreme Neonatal Hyperbilirubinemia and a Specific Genotype: A Population-Based Case-Control Study

Universal bilirubin screening for severe neonatal hyperbilirubinemia

Incidence, Etiology, and Outcomes of Hazardous Hyperbilirubinemia in Newborns

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