Clinical and genetic risk factors for moderate hyperbilirubinemia in Brazilian newborn infants

Abstract

Objective: To identify clinical and genetic risk factors for moderate hyperbilirubinemia during the first week of life.Study Design: Using univariate and multivariate multiple regression analyses, the RR for clinical factors, the African variant of glucose-6-phosphate dehydrogenase (G6PD) deficiency (G202A/A376G), and (TA) n UGT1A1 polymorphisms were established in a cohort of 608 Brazilian newborn infants. Hyperbilirubinemia was monitored until 134.5±49.8 h of life (IQR, 111.0 to 156.7). The dependent variable was total bilirubinemia (TB)X12.9 mg per 100 ml estimated by transcutaneous or plasma bilirubin measurements.Result: The African variant of G6PD deficiency and (TA) 7 /(TA) 7 and (TA) 7 /(TA) 8 polymorphisms present in 6.1 and 12.0% of newborns, respectively, were not risk factors for moderate hyperbilirubinemia. Coexpression of G6DP deficiency and UGT1A1 polymorphisms occurred in 0.49% of the subjects. Independent clinical predictors for TBX12.9 mg per 100 ml were gestational age <38 weeks and reference curve percentiles >P40th. Conclusion:In this study, G6PD deficiency and UGT1A1 gene promoter polymorphisms were not risk factors for moderate hyperbilirubinemia. Genetic factors may vary considerably in importance among different populations.

UGT1A1, SLCO1B1, and SLCO1B3 polymorphisms vs. neonatal hyperbilirubinemia: is there an association?

“…In the multivariate analysis, only the ABO incompatibility and gestational age remained in the model, showing the large impact of these two variables in hyperbilirubinemia. Although the mean gestational ages of the control and case groups of term neonates were 38.1 and 39.5 wk, respectively, the control group showed a remarkably higher frequency of premature newborns; this result is consistent with the data published by Mezzacappa et al (11). In addition, neonates born before 39 wk require neonatal intensive care and have increased rates of neonatal and infant morbidity and mortality (12).…”

“…The statistical difference diminishes when the genotypic frequencies are compared; however, genotypes carrying the TA 5 allele were more frequent among the control subjects. The frequencies for UGT1A1 polymorphism observed in our study (23) are consistent with those described in Brazil by Mezzacappa et al (11).…”

“…Several studies have failed to demonstrate the relationship between jaundice and the rs8175347 polymorphism of UGT1A1 (3,11,20). Our study presented a higher frequency of the TA 5 allele among the control subjects, and this allele is associated with an increase in UGT1A1 expression (22).…”

Systematic follow-up of hyperbilirubinemia in neonates with a gestational age of 35 to 37 weeks

“…Reconhecidamente, os RNs entre 35-37 semanas de idade gestacional têm maior risco de hiperbilirrubinemia que RNs com 38 semanas ou mais 2,[11][12][13][14] . Existem poucas informações sobre o acompanhamento na primeira semana de vida e a Tabela 2 -Análise de regressão logística univariada e multivariada para reinternação para fototerapia (n = 392) IC95% = intervalo de confiança de 95%; NA = nascimento e alta; NR = nascimento e retorno; RR = risco relativo.…”

Neonatal hyperbilirubinemia, acute bilirubin encephalopathy and Kernicterus: The conti-nuum is still valid in the 21st century

“…No obstante, el tratamiento de la hiperbilirrubinemia severa basado solo en el nivel de bilirrubina tiene un valor limitado para prevenir daño neurológico, porque existen otros factores biológicos, que estarían (32) implicados en la patogenia . Existen complicaciones clínicas que pueden incrementar la vulnerabilidad a la neurotoxicidad, como la sepsis neonatal, la deshidratación y la enfermedad hemolíticas, la hipoalbuminemia acidosis metabólica, la asfixia (33) perinatal y algunas enfermedades genéticas con trastornos del metabolismo de la bilirrubina como el Crigler Najer Tipo I y II (UGT1 y UGTII deficiencias de la uridil amino trasglutaminasa), la deficiencia de (34,35) la G6PD (Glucosa 6 fosfato deshidrogenasa) .…”