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[PMID]:28762235
[Au] Autor:Lai NM; Ahmad Kamar A; Choo YM; Kong JY; Ngim CF
[Ad] Endereço:School of Medicine, Taylor's University, Subang Jaya, Malaysia.
[Ti] Título:Fluid supplementation for neonatal unconjugated hyperbilirubinaemia.
[So] Source:Cochrane Database Syst Rev;8:CD011891, 2017 08 01.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Neonatal hyperbilirubinaemia is a common problem which carries a risk of neurotoxicity. Certain infants who have hyperbilirubinaemia develop bilirubin encephalopathy and kernicterus which may lead to long-term disability. Phototherapy is currently the mainstay of treatment for neonatal hyperbilirubinaemia. Among the adjunctive measures to compliment the effects of phototherapy, fluid supplementation has been proposed to reduce serum bilirubin levels. The mechanism of action proposed includes direct dilutional effects of intravenous (IV) fluids, or enhancement of peristalsis to reduce enterohepatic circulation by oral fluid supplementation. OBJECTIVES: To assess the risks and benefits of fluid supplementation compared to standard fluid management in term and preterm newborn infants with unconjugated hyperbilirubinaemia who require phototherapy. SEARCH METHODS: We used the standard search strategy of Cochrane Neonatal to search the Cochrane Central Register of Controlled Trials (CENTRAL; 2017, Issue 5), MEDLINE via PubMed (1966 to 7 June 2017), Embase (1980 to 7 June 2017), and CINAHL (1982 to 7 June 2017). We also searched clinical trials databases, conference proceedings, and the reference lists of retrieved articles for randomised controlled trials and quasi-randomised trials. SELECTION CRITERIA: We included randomised controlled trials that compared fluid supplementation against no fluid supplementation, or one form of fluid supplementation against another. DATA COLLECTION AND ANALYSIS: We extracted data using the standard methods of the Cochrane Neonatal Review Group using the Covidence platform. Two review authors independently assessed the eligibility and risk of bias of the retrieved records. We expressed our results using mean difference (MD), risk difference (RD), and risk ratio (RR) with 95% confidence intervals (CIs). MAIN RESULTS: Out of 1449 articles screened, seven studies were included. Three articles were awaiting classification, among them, two completed trials identified from the trial registry appeared to be unpublished so far.There were two major comparisons: IV fluid supplementation versus no fluid supplementation (six studies) and IV fluid supplementation versus oral fluid supplementation (one study). A total of 494 term, healthy newborn infants with unconjugated hyperbilirubinaemia were evaluated. All studies were at high risk of bias for blinding of care personnel, five studies had unclear risk of bias for blinding of outcome assessors, and most studies had unclear risk of bias in allocation concealment. There was low- to moderate-quality evidence for all major outcomes.In the comparison between IV fluid supplementation and no supplementation, no infant in either group developed bilirubin encephalopathy in the one study that reported this outcome. Serum bilirubin was lower at four hours postintervention for infants who received IV fluid supplementation (MD -34.00 µmol/L (-1.99 mg/dL), 95% CI -52.29 (3.06) to -15.71 (0.92); participants = 67, study = 1) (low quality of evidence, downgraded one level for indirectness and one level for suspected publication bias). Beyond eight hours postintervention, serum bilirubin was similar between the two groups. Duration of phototherapy was significantly shorter for fluid-supplemented infants, but the estimate was affected by heterogeneity which was not clearly explained (MD -10.70 hours, 95% CI -15.55 to -5.85; participants = 218; studies = 3; I² = 67%). Fluid-supplemented infants were less likely to require exchange transfusion (RR 0.39, 95% CI 0.21 to 0.71; RD -0.01, 95% CI -0.04 to 0.02; participants = 462; studies = 6; I² = 72%) (low quality of evidence, downgraded one level due to inconsistency, and another level due to suspected publication bias), and the estimate was similarly affected by unexplained heterogeneity. The frequencies of breastfeeding were similar between the fluid-supplemented and non-supplemented infants in days one to three based on one study (estimate on day three: MD 0.90 feeds, 95% CI -0.40 to 2.20; participants = 60) (moderate quality of evidence, downgraded one level for imprecision).One study contributed to all outcome data in the comparison of IV versus oral fluid supplementation. In this comparison, no infant in either group developed abnormal neurological signs. Serum bilirubin, as well as the rate of change of serum bilirubin, were similar between the two groups at four hours after phototherapy (serum bilirubin: MD 11.00 µmol/L (0.64 mg/dL), 95% CI -21.58 (-1.26) to 43.58 (2.55); rate of change of serum bilirubin: MD 0.80 µmol/L/hour (0.05 mg/dL/hour), 95% CI -2.55 (-0.15) to 4.15 (0.24); participants = 54 in both outcomes) (moderate quality of evidence for both outcomes, downgraded one level for indirectness). The number of infants who required exchange transfusion was similar between the two groups (RR 1.60, 95% CI 0.60 to 4.27; RD 0.11, 95% CI -0.12 to 0.34; participants = 54). No infant in either group developed adverse effects including vomiting or abdominal distension. AUTHORS' CONCLUSIONS: There is no evidence that IV fluid supplementation affects important clinical outcomes such as bilirubin encephalopathy, kernicterus, or cerebral palsy in healthy, term newborn infants with unconjugated hyperbilirubinaemia requiring phototherapy. In this review, no infant developed these bilirubin-associated clinical complications. Low- to moderate-quality evidence shows that there are differences in total serum bilirubin levels between fluid-supplemented and control groups at some time points but not at others, the clinical significance of which is uncertain. There is no evidence of a difference between the effectiveness of IV and oral fluid supplementations in reducing serum bilirubin. Similarly, no infant developed adverse events or complications from fluid supplementation such as vomiting or abdominal distension. This suggests a need for future research to focus on different population groups with possibly higher baseline risks of bilirubin-related neurological complications, such as preterm or low birthweight infants, infants with haemolytic hyperbilirubinaemia, as well as infants with dehydration for comparison of different fluid supplementation regimen.
[Mh] Termos MeSH primário: Hidratação/efeitos adversos
Hiperbilirrubinemia Neonatal/terapia
Kernicterus/prevenção & controle
Fototerapia
[Mh] Termos MeSH secundário: Administração Intravenosa
Administração Oral
Bilirrubina/sangue
Aleitamento Materno/estatística & dados numéricos
Paralisia Cerebral/prevenção & controle
Transfusão Total/estatística & dados numéricos
Hidratação/métodos
Seres Humanos
Hiperbilirrubinemia Neonatal/sangue
Recém-Nascido
Peristaltismo
Fototerapia/métodos
Fototerapia/estatística & dados numéricos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD011891.pub2


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[PMID]:28503958
[Au] Autor:Ree IMC; Smits-Wintjens VEHJ; van der Bom JG; van Klink JMM; Oepkes D; Lopriore E
[Ad] Endereço:a Department of Pediatrics , Leiden University Medical Center , Leiden , The Netherlands.
[Ti] Título:Neonatal management and outcome in alloimmune hemolytic disease.
[So] Source:Expert Rev Hematol;10(7):607-616, 2017 Jul.
[Is] ISSN:1747-4094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Hemolytic disease of the fetus and newborn (HDFN) occurs when fetal and neonatal erythroid cells are destroyed by maternal erythrocyte alloantibodies, it leads to anemia and hydrops in the fetus, and hyperbilirubinemia and kernicterus in the newborn. Postnatal care consists of intensive phototherapy and exchange transfusions to treat severe hyperbilirubinemia and top-up transfusions to treat early and late anemia. Other postnatal complications have been reported such as thrombocytopenia, iron overload and cholestasis requiring specific management. Areas covered: This review focusses on the current neonatal management and outcome of hemolytic disease and discusses postnatal treatment options as well as literature on long-term neurodevelopmental outcome. Expert commentary: Despite major advances in neonatal management, multiple issues have to be addressed to optimize postnatal management and completely eradicate kernicterus. Except for strict adherence to guidelines, improvement could be achieved by clarifying the epidemiology and pathophysiology of HDFN. Several pharmacotherapeutic agents should be further researched as alternative treatment options in hyperbilirubinemia, including immunoglobulins, albumin, phenobarbital, metalloporphyrins, zinc, clofibrate and prebiotics. Larger trials are warranted to evaluate EPO, folate and vitamin E in neonates. Long-term follow-up studies are needed in HDFN, especially on thrombocytopenia, iron overload and cholestasis.
[Mh] Termos MeSH primário: Anemia Hemolítica/imunologia
Anemia Hemolítica/terapia
Anemia Neonatal/imunologia
Anemia Neonatal/terapia
Isoanticorpos/imunologia
[Mh] Termos MeSH secundário: Anemia Hemolítica/complicações
Anemia Hemolítica/diagnóstico
Anemia Neonatal/complicações
Anemia Neonatal/diagnóstico
Terapia Combinada
Gerenciamento Clínico
Transfusão Total
Hidratação/métodos
Seres Humanos
Hiperbilirrubinemia/diagnóstico
Hiperbilirrubinemia/etiologia
Hiperbilirrubinemia/terapia
Imunoglobulinas Intravenosas
Recém-Nascido
Kernicterus/diagnóstico
Kernicterus/etiologia
Kernicterus/terapia
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunoglobulins, Intravenous); 0 (Isoantibodies)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE
[do] DOI:10.1080/17474086.2017.1331124


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[PMID]:28131490
[Au] Autor:El Houchi SZ; Iskander I; Gamaleldin R; El Shenawy A; Seoud I; Abou-Youssef H; Wennberg RP
[Ad] Endereço:Department of Pediatrics, Cairo University, Cairo, Egypt. Electronic address: salmelhouchi@yahoo.com.
[Ti] Título:Prediction of 3- to 5-Month Outcomes from Signs of Acute Bilirubin Toxicity in Newborn Infants.
[So] Source:J Pediatr;183:51-55.e1, 2017 Apr.
[Is] ISSN:1097-6833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate the ability of the bilirubin-induced neurologic dysfunction (BIND) score to predict residual neurologic and auditory disability and to document the relationship of BIND score to total serum bilirubin (TSB) concentration. STUDY DESIGN: The BIND score (assessing mental status, muscle tone, and cry patterns) was obtained serially at 6- to 8-hour intervals in 220 near-term and full-term infants with severe hyperbilirubinemia. Neurologic and/or auditory outcomes at 3-5 months of age were correlated with the highest calculated BIND score. The BIND score was also correlated with TSB. RESULTS: Follow-up neurologic and auditory examinations were performed for 145/202 (72%) surviving infants. All infants with severe acute bilirubin encephalopathy (BIND scores 7-9) either died or suffered residual neurologic and auditory impairment. Of 24 cases with moderate encephalopathy (BIND 4-6), 15 (62.5%) resolved following aggressive intervention and were normal at follow-up. Three of 73 infants with mild encephalopathy (BIND scores 1-3) but severe jaundice (TSB ranging 33.5-38 mg/dL; 573-650 µmol/L) had residual neurologic and/or auditory impairment. A BIND score ≥4 had a specificity of 87.3% and a sensitivity of 97.4% for predicting poor neurologic outcomes (receiver operating characteristic analysis). BIND scores trended higher with severe hyperbilirubinemia (r = 0.54, P < .005), but 5/39 (13%) infants with TSB ≥36.5 mg/dL (624 µmol/L) had BIND scores ≤3, and normal outcomes at 3-5 months. CONCLUSIONS: The BIND score can be used to evaluate the severity of acute bilirubin encephalopathy and predict residual neurologic and hearing dysfunction.
[Mh] Termos MeSH primário: Bilirrubina/sangue
Deficiências do Desenvolvimento/fisiopatologia
Icterícia Neonatal/diagnóstico
Kernicterus/diagnóstico
[Mh] Termos MeSH secundário: Doença Aguda
Estudos de Coortes
Deficiências do Desenvolvimento/epidemiologia
Feminino
Seguimentos
Idade Gestacional
Seres Humanos
Incidência
Lactente
Recém-Nascido
Recém-Nascido Prematuro
Icterícia Neonatal/epidemiologia
Kernicterus/epidemiologia
Masculino
Exame Neurológico
Valor Preditivo dos Testes
Curva ROC
Estudos Retrospectivos
Medição de Risco
Sensibilidade e Especificidade
Índice de Gravidade de Doença
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170615
[Lr] Data última revisão:
170615
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE


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[PMID]:27746217
[Au] Autor:Amini N; Vousooghi N; Soleimani M; Samadikuchaksaraei A; Akbari M; Safakheil H; Atafimanesh P; Shahbazi A; Brouki Milan P; Ramezani S; Mozafari M; Joghataei MT
[Ad] Endereço:Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran; Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Título:A new rat model of neonatal bilirubin encephalopathy (kernicterus).
[So] Source:J Pharmacol Toxicol Methods;84:44-50, 2017 Mar - Apr.
[Is] ISSN:1873-488X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Hemolytic kernicterus, an indirect bilirubin-induced brain dysfunction, is associated with hyper-bilirubinemia in mammalian neonates. In this study, a new model of kernicterus has been developed using intra-peritoneal injections of phenyl hydrazine and subcutaneous injections of sulfisoxazole. These drugs can potentially induce kernicterus in neonatal through changes in hemolysis and hypo-albumin. METHODS: For this purpose, 7-day-old male Wistar rats (n=72; mean weight 11±1g) were used. The animals have been divided into six different groups which received the drugs alone and their combination, and the drugs' solvents and their combination. Biochemical parameters, brain iron and bilirubin, behavioural performance, auditory function and apoptosis were measured using auto-analyser instruments; atomic absorption spectroscopy, Sawasaki, footprint, auditory brainstem response (ABR) and TUNEL test, respectively. RESULT: The drug-injected groups showed a significant reduction in serum haematocrit and an increase in the concentration of brain bilirubin, total and indirect bilirubin as well as TUNEL positive cells in basal ganglia. In addition, the obtained results showed that there was a significant increase in behavioural disturbance and auditory dysfunction in the group injected with the combination of two drugs. CONCLUSION: This kernicterus-induced rat model could perfectly mimic the common conditions of the hyperbilirubinemia in human neonates. This study offers an easy technique to develop more stable models for follow-up studies.
[Mh] Termos MeSH primário: Bilirrubina/metabolismo
Modelos Animais de Doenças
Kernicterus/induzido quimicamente
Kernicterus/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos
Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia
Kernicterus/patologia
Masculino
Fenil-Hidrazinas/toxicidade
Distribuição Aleatória
Ratos
Ratos Wistar
Sulfisoxazol/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phenylhydrazines); 064F424C9K (phenylhydrazine); 740T4C525W (Sulfisoxazole); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE


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[PMID]:27609825
[Au] Autor:Ahlfors CE
[Ad] Endereço:Consulting Professor, Stanford University School of Medicine, Stanford, California ligand@centurytel.net.
[Ti] Título:The Bilirubin Binding Panel: A Henderson-Hasselbalch Approach to Neonatal Hyperbilirubinemia.
[So] Source:Pediatrics;138(4), 2016 Oct.
[Is] ISSN:1098-4275
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Poor plasma bilirubin binding increases the risk of bilirubin neurotoxicity in newborns with hyperbilirubinemia. New laboratory tests may soon make it possible to obtain a complete bilirubin binding panel when evaluating these babies. The 3 measured components of the panel are the plasma total bilirubin concentration (B ), which is currently used to guide clinical care; the bilirubin binding capacity (BBC); and the concentration of non-albumin bound or free bilirubin (B ). The fourth component is the bilirubin-albumin equilibrium dissociation constant, K , which is calculated from B , BBC, and B The bilirubin binding panel is comparable to the panel of components used in the Henderson-Hasselbalch approach to acid-base assessment. Bilirubin binding population parameters (not prospective studies to determine whether the new bilirubin binding panel components are better predictors of bilirubin neurotoxicity than B ) are needed to expedite the clinical use of bilirubin binding. At any B , the B and the relative risk of bilirubin neurotoxicity increase as the K /BBC ratio increases (ie, bilirubin binding worsens). Comparing the K /BBC ratio of newborns with B of concern with that typical for the population helps determine whether the risk of bilirubin neurotoxicity varies significantly from the inherent risk at that B Furthermore, the bilirubin binding panel individualizes care because it helps to determine how aggressive intervention should be at any B , irrespective of whether it is above or below established B guidelines. The bilirubin binding panel may reduce anxiety, costs, unnecessary treatment, and the likelihood of undetected bilirubin neurotoxicity.
[Mh] Termos MeSH primário: Bilirrubina/sangue
Hiperbilirrubinemia Neonatal/sangue
Kernicterus/sangue
[Mh] Termos MeSH secundário: Seres Humanos
Hiperbilirrubinemia Neonatal/complicações
Hiperbilirrubinemia Neonatal/diagnóstico
Recém-Nascido
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160910
[St] Status:MEDLINE


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[PMID]:27235216
[Au] Autor:Stevenson DK; Bhutani VK
[Ad] Endereço:Stanford University School of Medicine, Department of Pediatrics, Division of Neonatal and Developmental Medicine, 1265 Welch Road, X157, Stanford, CA 94305, USA. Electronic address: dstevenson@stanford.edu.
[Ti] Título:Preterm Neonates: Beyond the Guidelines for Neonatal Hyperbilirubinemia.
[So] Source:Clin Perinatol;43(2):xvii-xviii, 2016 Jun.
[Is] ISSN:1557-9840
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Hiperbilirrubinemia Neonatal/terapia
Kernicterus/prevenção & controle
[Mh] Termos MeSH secundário: Surdez/etiologia
Deficiência de Glucosefosfato Desidrogenase/metabolismo
Hemólise
Seres Humanos
Hiperbilirrubinemia Neonatal/complicações
Hiperbilirrubinemia Neonatal/metabolismo
Recém-Nascido
Recém-Nascido Prematuro
Kernicterus/etiologia
Kernicterus/metabolismo
Fototerapia
Guias de Prática Clínica como Assunto
Ligação Proteica
[Pt] Tipo de publicação:EDITORIAL; INTRODUCTORY JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160529
[St] Status:MEDLINE


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[PMID]:27235215
[Au] Autor:Jain L
[Ad] Endereço:Emory University School of Medicine, Department of Pediatrics, Children's Healthcare of Atlanta, 2015 Uppergate Drive, Atlanta, GA 30322, USA. Electronic address: ljain@emory.edu.
[Ti] Título:Why the Premature Brain Is More Prone to Bilirubin-induced Injury.
[So] Source:Clin Perinatol;43(2):xv-xvi, 2016 Jun.
[Is] ISSN:1557-9840
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Encéfalo/fisiopatologia
Hiperbilirrubinemia Neonatal/fisiopatologia
Kernicterus/fisiopatologia
[Mh] Termos MeSH secundário: Bilirrubina/metabolismo
Encéfalo/metabolismo
Comorbidade
Seres Humanos
Hiperbilirrubinemia Neonatal/complicações
Hiperbilirrubinemia Neonatal/metabolismo
Recém-Nascido
Recém-Nascido Prematuro
Kernicterus/etiologia
Kernicterus/metabolismo
[Pt] Tipo de publicação:EDITORIAL; INTRODUCTORY JOURNAL ARTICLE
[Nm] Nome de substância:
RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160529
[St] Status:MEDLINE


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[PMID]:27235212
[Au] Autor:Cunningham AD; Hwang S; Mochly-Rosen D
[Ad] Endereço:Department of Chemical and Systems Biology, Stanford University, 269 Campus Drive, Stanford, CA 94305, USA.
[Ti] Título:Glucose-6-Phosphate Dehydrogenase Deficiency and the Need for a Novel Treatment to Prevent Kernicterus.
[So] Source:Clin Perinatol;43(2):341-54, 2016 Jun.
[Is] ISSN:1557-9840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hyperbilirubinemia occurs frequently in newborns, and in severe cases can progress to kernicterus and permanent developmental disorders. Glucose-6-phosphate dehydrogenase (G6PD) deficiency, one of the most common human enzymopathies, is a major risk factor for hyperbilirubinemia and greatly increases the risk of kernicterus even in the developed world. Therefore, a novel treatment for kernicterus is needed, especially for G6PD-deficient newborns. Oxidative stress is a hallmark of bilirubin toxicity in the brain. We propose that the activation of G6PD via a small molecule chaperone is a potential strategy to increase endogenous defense against bilirubin-induced oxidative stress and prevent kernicterus.
[Mh] Termos MeSH primário: Antioxidantes/uso terapêutico
Deficiência de Glucosefosfato Desidrogenase/metabolismo
Hiperbilirrubinemia Neonatal/terapia
Kernicterus/prevenção & controle
Chaperonas Moleculares/uso terapêutico
Fototerapia
[Mh] Termos MeSH secundário: Deficiência de Glucosefosfato Desidrogenase/complicações
Seres Humanos
Hiperbilirrubinemia Neonatal/complicações
Hiperbilirrubinemia Neonatal/metabolismo
Recém-Nascido
Kernicterus/etiologia
Kernicterus/metabolismo
Kernicterus/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antioxidants); 0 (Molecular Chaperones)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160529
[St] Status:MEDLINE


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[PMID]:27235210
[Au] Autor:Olds C; Oghalai JS
[Ad] Endereço:Department of Otolaryngology - Head and Neck Surgery, Stanford University, 801 Welch Road, CA 94305, USA.
[Ti] Título:Bilirubin-Induced Audiologic Injury in Preterm Infants.
[So] Source:Clin Perinatol;43(2):313-23, 2016 06.
[Is] ISSN:1557-9840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although hyperbilirubinemia is extremely common among neonates and is usually mild and transient, it sometimes leads to bilirubin-induced neurologic damage (BIND). The auditory pathway is highly sensitive to the effects of elevated total serum/plasma bilirubin (TB) levels, with damage manifesting clinically as auditory neuropathy spectrum disorder. Compared to full-term neonates, preterm neonates are more susceptible to BIND and suffer adverse effects at lower TB levels with worse long-term outcomes. Furthermore, although standardized guidelines for management of hyperbilirubinemia exist for term and late preterm neonates, similar guidelines for neonates less than 35 weeks gestational age are limited.
[Mh] Termos MeSH primário: Nervo Coclear/fisiopatologia
Núcleo Coclear/fisiopatologia
Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia
Perda Auditiva Central/fisiopatologia
Hiperbilirrubinemia Neonatal/fisiopatologia
Kernicterus/fisiopatologia
[Mh] Termos MeSH secundário: Perda Auditiva Central/etiologia
Seres Humanos
Hiperbilirrubinemia Neonatal/complicações
Hiperbilirrubinemia Neonatal/terapia
Recém-Nascido
Recém-Nascido Prematuro
Kernicterus/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160529
[St] Status:MEDLINE


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[PMID]:27235211
[Au] Autor:Kaplan M; Hammerman C; Bhutani VK
[Ad] Endereço:Faculty of Medicine, The Hebrew University of Jerusalem, Ein Kerem, P.O. Box 12271, Jerusalem, 9112102 Israel; Department of Neonatology, Shaare Zedek Medical Center, PO Box 3235, Jerusalem 91031, Israel. Electronic address: mkaplan@mail.huji.ac.il.
[Ti] Título:The Preterm Infant: A High-Risk Situation for Neonatal Hyperbilirubinemia Due to Glucose-6-Phosphate Dehydrogenase Deficiency.
[So] Source:Clin Perinatol;43(2):325-40, 2016 Jun.
[Is] ISSN:1557-9840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prematurity and glucose-6-phosphate dehydrogenase (G6PD) deficiency are risk factors for neonatal hyperbilirubinemia. The 2 conditions may interact additively or synergistically, contributing to extreme hyperbilirubinemia, with the potential for bilirubin neurotoxicity. This hyperbilirubinemia is the result of sudden, unpredictable, and acute episodes of hemolysis in combination with immaturity of bilirubin elimination, primarily of conjugation. Avoidance of contact with known triggers of hemolysis in G6PD-deficient individuals will prevent some, but not all, episodes of hemolysis. All preterm infants with G6PD deficiency should be vigilantly observed for the development of jaundice both in hospital and after discharge home.
[Mh] Termos MeSH primário: Deficiência de Glucosefosfato Desidrogenase/epidemiologia
Hiperbilirrubinemia Neonatal/epidemiologia
Kernicterus/epidemiologia
[Mh] Termos MeSH secundário: Deficiência de Glucosefosfato Desidrogenase/diagnóstico
Hemólise
Seres Humanos
Hiperbilirrubinemia Neonatal/complicações
Recém-Nascido
Recém-Nascido Prematuro
Kernicterus/etiologia
Programas de Rastreamento
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160529
[St] Status:MEDLINE



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