The incidence and outcome of Bilirubin Encephalopathy in Nigeria: a Bi-centre study

Ogunlesi, TA; Dedeke, I O F; Adekanmbi, AF; Fetuga, MB; Ogunfowora, OB

doi:10.4314/njm.v16i4.37337

Cited by 44 publications

(55 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Fourth, the present article focused on SNHL; other bilirubin-related neurologic morbidities were not evaluated. In addition, although kernicterus is rare in the United States, it is more common in developing countries, perhaps due to increased sepsis, 27,28 Rh isoimmunization, 27 and G6PD deficiency. 28 Our results may thus be less generalizable to subjects in resource-poor settings.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, although kernicterus is rare in the United States, it is more common in developing countries, perhaps due to increased sepsis, 27,28 Rh isoimmunization, 27 and G6PD deficiency. 28 Our results may thus be less generalizable to subjects in resource-poor settings. Advantages of our study include the large size of the cohort (.500 000 subjects) from which our double cohort was derived, the larger number of cases of SNHL compared with previous population-based studies, and the ability to stratify risk according to higher bilirubin levels than those studied in the past.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Risk of Sensorineural Hearing Loss and Bilirubin Exchange Transfusion Thresholds

et al. 2015

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Risk of Sensorineural Hearing Loss and Bilirubin Exchange Transfusion Thresholds

et al. 2015

View full text Add to dashboard Cite

show abstract

“…[1][2][3][4] A previous study in Nigeria identified G6PD deficiency in up to 62% of infants admitted from home with severe neonatal jaundice and kernicterus. 4 In the current study, the …”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4] In 1 study, G6PD deficiency was identified in up to 62% of infants with kernicterus. 4 Most of those neonates who had G6PD deficiency and kernicterus were admitted from home with a history of inadvertent previous exposure to known icterogenic agents.…”

mentioning

confidence: 99%

Early Neonatal Bilirubin, Hematocrit, and Glucose-6-Phosphate Dehydrogenase Status

Badejoko¹,

Owa

Oseni

et al. 2014

Pediatrics

View full text Add to dashboard Cite

OBJECTIVE: To document the patterns of bilirubin and hematocrit values among glucose-6-phosphate dehydrogenase (G6PD)-deficient and G6PD-normal Nigerian neonates in the first week of life, in the absence of exposure to known icterogenic agents. METHODS: The G6PD status of consecutive term and near-term neonates was determined, and their bilirubin levels and hematocrits were monitored during the first week of life. Infants were stratified into G6PD deficient, intermediate, and normal on the basis of the modified Beutler’s fluorescent spot test. Means of total serum bilirubin (TSB) and hematocrits of the 3 groups of infants were compared. RESULTS: The 644 neonates studied comprised 353 (54.8%) boys and 291 (45.2%) girls and 540 (83.9%) term and 104 (16.1%) near-term infants. They consisted of 129 (20.0%) G6PD-deficient, 69 (10.7%) G6PD-intermediate, and 446 (69.3%) G6PD-normal neonates. The G6PD-deficient and G6PD-intermediate infants had higher mean TSB than their G6PD-normal counterparts at birth and throughout the first week of life (P < .001). Mean peak TSB levels were 14.1 (9.48), 10.2 (3.8), and 6.9 (3.3) mg/dL for G6PD-deficient, G6PD-intermediate, and G6PD-normal neonates, respectively. Peak TSB was attained on approximately day 4 in all 3 groups, and trends in TSB were similar. Mean hematocrits at birth were similar in the 3 G6PD groups. However, G6PD-deficient and -intermediate infants had higher declines in hematocrit, bilirubin levels, and need for phototherapy than G6PD-normal infants (P < .001). CONCLUSIONS: The G6PD-deficient and G6PD-intermediate neonates had a higher risk of neonatal hyperbilirubinemia and would therefore need greater monitoring in the first week of life, even without exposure to known icterogenic agents.

show abstract

“…[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. 1,2,5,6,9,10 Thus, despite neonatal hyperbilirubinemia being 1 of the most frequent hospital-treated conditions in the developed world with 2% to 7% of a population receiving phototherapy in the first days of life, much is still not understood about its development.…”

mentioning

confidence: 99%

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

Petersen

Henriksen²,

Hollegaard

et al. 2014

Pediatrics

View full text Add to dashboard Cite

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.

show abstract

The incidence and outcome of Bilirubin Encephalopathy in Nigeria: a Bi-centre study

Cited by 44 publications

References 0 publications

Risk of Sensorineural Hearing Loss and Bilirubin Exchange Transfusion Thresholds

Risk of Sensorineural Hearing Loss and Bilirubin Exchange Transfusion Thresholds

Early Neonatal Bilirubin, Hematocrit, and Glucose-6-Phosphate Dehydrogenase Status

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

Contact Info

Product

Resources

About