RESUMO
BACKGROUND: Preterm infants often present with hyperkalemia during the first days after birth without showing oliguria. This is known as nonoliguric hyperkalemia (NOHK). As its clinical features have not been completely understood to date, we aimed to elucidate the characteristics of NOHK, including its risk factors, in preterm infants. METHODS: For this case-control study, we reviewed the files of all infants born before 32 weeks of gestational age in our neonatal intensive care unit between 2011 and 2018. We distinguished the NOHK and non-NOHK groups and compared their characteristics and blood potassium levels. Nonoliguric hyperkalemia was defined as peak blood potassium concentration of ≥6.0 mmol/L during the first 72 h of life with a urine output of ≥1 mL/kg/h. RESULTS: Of the 99 infants enrolled, 21 (21%) demonstrated NOHK. Infants with NOHK were more likely to have been exposed to antenatal magnesium sulfate (MgSO4 ) (P = 0.019) than those in the non-NOHK group. Acute morbidities and mortality were not statistically different. Multivariate analysis indicated that administration of maternal MgSO4 for longer than 24 h at any point before delivery was a risk factor for NOHK. Its adjusted odds ratio and 95% confidence interval were 4.0 and 1.4-12.3, respectively (P = 0.012). CONCLUSIONS: In this study, maternal MgSO4 administration for longer than 24 h proved to be a risk factor for NOHK in infants born before 32 weeks of gestational age. Infants born to mothers who have received MgSO4 should be regularly monitored for their electrolytes.
Assuntos
Hiperpotassemia/epidemiologia , Doenças do Prematuro/epidemiologia , Adulto , Estudos de Casos e Controles , Feminino , Idade Gestacional , Humanos , Hiperpotassemia/sangue , Recém-Nascido , Recém-Nascido Prematuro , Doenças do Prematuro/sangue , Sulfato de Magnésio/efeitos adversos , Sulfato de Magnésio/uso terapêutico , Masculino , Mães , Análise Multivariada , Razão de Chances , Oligúria/epidemiologia , Potássio/sangue , Gravidez , Fatores de RiscoRESUMO
Neonates have physiologically increased bilirubin production and immature bilirubin metabolism, and present hyperbilirubinemia in association with genetic and or epigenetic factors. We previously reported that maximal body weight loss (inadequate feeding) is an independent risk factor for the development of hyperbilirubinemia in breast-fed Japanese neonates, and the UGT1A1 211G>A genotype becomes a risk factor under conditions of inadequate feeding. We extended the study to the association of other genetic factors, the UGT1A1 (TA)7 and solute-carrier organic anion transporters (SLCOs) polymorphisms with neonatal hyperbilirubinemia. We enrolled 401 full-term Japanese infants who were exclusively breastfeeding and classified them into two groups based on the degree of maximal body weight loss. We analyzed the clinical characteristics and UGT1A1 and SLCOs genotypes. Statistical analysis revealed that maximal body weight loss is the only independent risk factor for the development of neonatal hyperbilirubinemia. UGT1A1, SLCO1B1 and SLCO1B3 polymorphisms become risk factors in neonates showing 10% or greater body weight loss during the neonatal period. Inadequate feeding may increase the bilirubin burden and cause apparent hyperbilirubinemia in neonates, who have a polymorphic change in the genes involved in the transport and/or metabolism of bilirubin.
Assuntos
Aleitamento Materno/efeitos adversos , Glucuronosiltransferase/genética , Hiperbilirrubinemia Neonatal/genética , Transportadores de Ânions Orgânicos Sódio-Independentes/genética , Transportadores de Ânions Orgânicos/genética , Polimorfismo Genético , Bilirrubina/genética , Bilirrubina/metabolismo , Epigênese Genética , Feminino , Estudos de Associação Genética , Humanos , Hiperbilirrubinemia Neonatal/etiologia , Recém-Nascido , Japão , Transportador 1 de Ânion Orgânico Específico do Fígado , Masculino , Fatores de Risco , Membro 1B3 da Família de Transportadores de Ânion Orgânico Carreador de Soluto , Redução de Peso/genéticaRESUMO
Breastfeeding jaundice is a well-known phenomenon, but its pathogenesis is still unclear. Increased production of bilirubin, impaired hepatic uptake and metabolism of bilirubin, and increased enterohepatic circulation of bilirubin account for most cases of pathological neonatal hyperbilirubinemia. We previously reported that 211G>A (G71R) mutation of the UGT1A1 gene is prevalent in East Asians and is associated with the development of neonatal hyperbilirubinemia. Recently, significant association of G71R mutation with hyperbilirubinemia in breast-fed neonates was reported. We enrolled 401 full-term Japanese infants, who were exclusively breast-fed without supplementation of formula before developing hyperbilirubinemia, and classified them into two groups based on the degree of maximal body weight loss during the neonatal period. We analyzed the sex, gestational age, delivery mode, body weight at birth, maximal body weight loss and genotypes of G71R and (TA)(7) polymorphic mutations of UGT1A1. Statistical analysis revealed that maximal body weight loss during the neonatal period is the only independent risk factor for the development of neonatal hyperbilirubinemia. The effect of G71R mutation on neonatal hyperbilirubinemia is significant in neonates with 5% or greater maximal body weight loss and its influence increases in parallel with the degree of maximal body weight loss. Our study indicates that G71R mutation is a risk factor for neonatal hyperbilirubinemia only in infants with inadequate breastfeeding and suggests that adequate breastfeeding may overcome the genetic predisposing factor, G71R mutation, for the development of neonatal hyperbilirubinemia.
