Erythrocyte glucose-6-phosphate dehydrogenase deficiency in male newborn babies and its relationship with neonatal jaundice

Iglessias, Marli Auxiliadora C.; Santos, Rosa Maria Vaz dos; Amorim, Maria do Socorro T.; Silva, Rosângela T.; Moreira, Susiane S.; Barretto, Orlando César de Oliveira; Medeiros, Tereza Maria Dantas de

doi:10.1590/s1516-84842010005000086

Cited by 5 publications

(5 citation statements)

References 16 publications

(16 reference statements)

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“…On the other hand, G6PDd was detected in 3.4% of male new-borns with NNJ in the absence of foetal-maternal incompatibility in Costa Rica [ 59 ] and in 69.6% of a group of neonates who had unexplained moderate to severe jaundice [ 60 ]. Four studies reported no severe complications in G6PD-deficient new-borns with NNJ [ 53 , 54 , 56 , 59 ], while three works described the need for exchange transfusions [ 50 , 51 , 55 ], three described the occurrence of kernicterus [ 51 , 60 , 61 ], and two described fatal outcomes [ 29 , 60 ].…”

Section: Resultsmentioning

confidence: 99%

Clinical complications of G6PD deficiency in Latin American and Caribbean populations: systematic review and implications for malaria elimination programmes

Monteiro

Franca

Queiroz

et al. 2014

Malar J

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BackgroundAlthough G6PDd individuals are generally asymptomatic throughout their life, the clinical burden of this genetic condition includes a range of haematological conditions, including acute haemolytic anaemia (AHA), neonatal jaundice (NNJ) and chronic non-sphaerocytic anaemia (CNSA). In Latin America (LA), the huge knowledge gap regarding G6PDd is related to the scarce understanding of the burden of clinical manifestation underlying G6PDd carriage. The aim of this work was to study the clinical significance of G6PDd in LA and the Caribbean region through a systematic review.MethodsA systematic search of the published literature was undertaken in August 2013. Bibliographies of manuscripts were also searched and additional references were identified. Only original research was included. All study designs were included, as long as any clinical information was present. Studies were eligible for inclusion if they reported clinical information from populations living in LA or Caribbean countries or about migrants from these countries living in countries outside this continent.ResultsThe Medline search generated 487 papers, and the LILACS search identified 140 papers. After applying the inclusion criteria, 100 original papers with any clinical information on G6PDd in LA were retrieved. Additionally, 16 articles were included after reading the references from these papers. These 116 articles reported data from 18 LA and Caribbean countries. The major clinical manifestations reported from LA countries were those related to AHA, namely drug-induced haemolysis. Most of the published works regarding drug-induced haemolysis in LA referred to haemolytic crises in P. vivax malaria patients during the course of the treatment with primaquine (PQ). Favism, infection-induced haemolysis, NNJ and CNSA appear to play only a minor public health role in this continent.ConclusionHaemolysis in patients using PQ seems to be the major clinical manifestation of G6PDd in LA and contributes to the morbidity of P. vivax infection in this continent, although the low number of reported cases, which could be linked to under-reporting of complications. These results support the need for better strategies to diagnose and manage G6PDd in malaria field conditions. Additionally, Malaria Control Programmes in LA should not overlook this condition in their national guidelines.

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Section: Resultsmentioning

confidence: 99%

Clinical complications of G6PD deficiency in Latin American and Caribbean populations: systematic review and implications for malaria elimination programmes

Monteiro

Franca

Queiroz

et al. 2014

Malar J

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“…A serious life‐threatening manifestations of G6PD deficiency can be seen in the neonatal period including early and late onset hyperbilirubinemia (neonatal jaundice), risk of kernicterus, death, and spastic cerebral palsy . Several studies have shown that the risk of neonatal jaundice is much greater in G6PD‐deficient neonates than in non‐deficient neonates . The American Academy of Pediatrics considers G6PD deficiency as a key etiologic risk factor for the development of severe hyperbilirubinemia and kernicterus, and the enzyme deficiency was found to increase the severity of prognosis of kernicterus among infants.…”

Section: G6pd Deficiencymentioning

confidence: 99%

National G6PD neonatal screening program in Gaza Strip of Palestine: rationale, challenges and recommendations

Sirdah

Al-Kahlout²,

Reading

2016

Clin Genet

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Congenital genetic disorders affecting neonates or young children can have serious clinical consequences if undiagnosed and left untreated. Early detection and an accurate diagnosis are, therefore, of major importance for preventing negative patient outcomes. Even though the occurrence of each specific metabolic disorder may be rare, their collective impact of preventable complications may be of considerable importance to the public health. Our previous studies showed that glucose-6-phosphate dehydrogenase (G6PD) deficiency is a problem of public health importance that has been shown to be a predominant cause of acute hemolytic anemia requiring hospitalization in Palestinian young children in Gaza Strip. Intriguingly, the majority of these children had one of the three variants, Mediterranean(c.) (563T) , African G6PD A-(c.) (202A) (/c.) (376G) and heretofore unrecognized as a common G6PD-deficient variant G6PD Cairo(c.) (404C) . The high prevalence of G6PD deficiency, as well as dietary factors in the region that precipitate anemia, argues for a need to protect the Palestinian children from a treatable and manageable genetic and metabolic disorder. This work reviews and discusses rationales and challenges of G6PD screening program in Gaza Strip. We advocate adopting a national neonatal G6PD screening program in Gaza Strip to identify children at risk and promote wellness and health for Palestine.

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“…A Glucose 6-fosfato desidrogenase (G6PD) é uma enzima encontrada em todas as células do corpo. Catalisadora da primeira etapa na via da pentose fosfato, com a função de proteger as células contra danos oxidativos, a G6PD converte a coenzima Nicotinamida Adenina Dinucleotídeo Fosfato (NADP) em sua forma reduzida Nicotinamida Adenina Dinucleotídeo reduzida (NADPH), sendo, praticamente, toda fonte geradora de NADPH, que tem como função combater os efeitos prejudiciais das espécies reativas de oxigênio (IGLESSIAS MAC, et al, 2010).…”

Section: Introductionunclassified

“…Universidade do Vale do Sapucaí (UNIVAS), Pouso Alegre -MG 6. Faculdade de Minas (FAMINAS), Belo Horizonte -MG 7. Universidade Federal do Amapá (UNIFAP), Macapá -AP.…”

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Implicações do diagnóstico precoce da deficiência de glicose-6-fosfato desidrogenase (G6PD) no prognóstico neurológico de neonatos

Pinto

Gonçalves²,

Sabbi³

et al. 2020

Acervo Saúde

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Objetivo: Compreender a importância de realizar diagnósticos ágeis de deficiência de Glicose-6-Fosfato Desidrogenase (G6PD) a fim de evitar sequelas neurológicas graves em lactentes. Revisão bibliográfica: Foram selecionados estudos que abordassem população de 0 a 23 meses de idade e complicações neurológicas decorrente de hiperbilirrubinemia patológica. Constatou-se que essa doença hemolítica possui incidência universal, embora não seja rastreada difusamente. Por ser assintomática e nem sempre estar disponível a triagem neonatal, há brechas para evoluir para sua mais grave complicação, kernicterus. Dessa forma, é preconizado a instituição de tratamento enquanto a encefalopatia aguda é reversível, o qual consiste principalmente em fototerapia e transfusão sanguínea. Especialmente em lugares onde não se realiza a busca ativa de casos, o tratamento deve estar aliado à conscientização dos pais, que devem estar vigilantes quanto à icterícia e realizar busca rápida de assistência médica, uma vez que o momento de maior vulnerabilidade é após a alta hospitalar do recém-nascido. Considerações finais: A deficiência de G6PD é relevante e pode colaborar para evoluções graves do quadro de hiperbilirrubinemia. Há limitações na abordagem dos neonatos acometidos, com escassez de estudos na área e reflexos da falta de investimentos no prognóstico destes.

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Erythrocyte glucose-6-phosphate dehydrogenase deficiency in male newborn babies and its relationship with neonatal jaundice

Abstract: Deficiência de glicose-6-fosfato desidrogenase eritrocitária em recém-nascidos do sexo masculino e sua relação com a icterícia neonatal

Cited by 5 publications

References 16 publications

Clinical complications of G6PD deficiency in Latin American and Caribbean populations: systematic review and implications for malaria elimination programmes

Clinical complications of G6PD deficiency in Latin American and Caribbean populations: systematic review and implications for malaria elimination programmes

National G6PD neonatal screening program in Gaza Strip of Palestine: rationale, challenges and recommendations

Implicações do diagnóstico precoce da deficiência de glicose-6-fosfato desidrogenase (G6PD) no prognóstico neurológico de neonatos

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