To study the prevalence of glucose 6 phosphate dehydrogenase(G6PD) deficiency in neonates with neonatal hyperbilirubinemia and to compare the course of the neonatal jaundice in deficient versus non deficient neonates

Sinha, Rahul Janak; Badal, Sachendra; Syed, V Sabid; Nair, Lakshmi; John, BM

doi:10.4103/jcn.jcn_59_16

Cited by 10 publications

(11 citation statements)

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“…Neonates with G6PD deficiency showed higher levels of bilirubin, and this result is in parallel to that of Bahraini and Nigerian studies conducted by Isa et al 16 and Badejoko et al ,17 respectively. Male gender is associated with a higher risk for G6PD deficiency, which is similar to the findings reported in Egypt by Abo El Fotoh and Rizk,9 Elella et al ,10 and El-Menshay et al ,12 in India by Sinha et al ,18 and in Iran by Eghbalian and Monsef 19. Family history of G6PD deficiency and consanguinity are risk factors for G6PD deficiency, which coincide with an Egyptian study conducted by Abo El Fotoh and Rizk10 and Garg and Joag 20.…”

Section: Discussionsupporting

confidence: 83%

“…The neonates were subjected to phototherapy according to phototherapy guidelines for hospitalised infants from ≥35 weeks of gestation 25. In G6PD deficiency, hyperbilirubinaemia is thought to be secondary to reduced hepatic conjugation and excretion of bilirubin, rather than increased bilirubin production resulting from haemolysis 18. Total bilirubin was obviously higher among G6PD-deficient cases than those with Rh or ABO incompatibility, and this finding agrees with that concluded by Das and Singh26 in India and Hussain et al 27 in Pakistan, but also in contrast to the findings obtained by Shah and Yeo28 in Singapore and Aletayeb et al 29 in Iran.…”

Section: Discussionmentioning

confidence: 99%

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Prevalence of and mothers’ knowledge, attitude and practice towards glucose-6-phosphate dehydrogenase deficiency among neonates with jaundice: a cross-sectional study

et al. 2020

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BackgroundNeonatal jaundice (NNJ) is a frequent complication of glucose-6-phosphate dehydrogenase (G6PD) deficiency.ObjectivesTo estimate the prevalence of G6PD deficiency among neonates with jaundice and to assess mothers’ perception towards G6PD and NNJ.MethodsA cross-sectional study was carried out on 487 ethnic Egyptian neonates with indirect hyperbilirubinaemia from June 2018 to July 2019. The collected data included maternal and neonatal characteristics. Laboratory investigations included serum bilirubin, reticulocyte count, ABO grouping, Rh typing and neonatal serum G6PD test. Mothers were interviewed individually using a structured, researcher-administered questionnaire to assess their perceptions of G6PD deficiency and NNJ.ResultsThe prevalence of G6PD deficiency was 10.10%. Neonates with G6PD deficiency showed higher levels of serum bilirubin (p<0.001). Male gender, family history of G6PD deficiency and consanguinity were risk factors for G6PD deficiency (OR=4.27, 95% CI 1.66 - 10.99; OR=9.54, 95% CI 4.80- 18.95; OR=10.219, 95% CI 5.39 - 19.33, respectively). Mothers’ perceptions of NNJ and G6PD were low, with only 30% having good knowledge on NNJ and 17.10% on G6PD deficiency, 46.8% with positive attitude towards NNJ and 45.0% towards G6PD deficiency, and 29.9% with good practice towards NNJ and 19.9% towards G6PD deficiency.ConclusionG6PD deficiency seems to be an important cause of NNJ. Mothers’ perceptions of both NNJ and G6PD deficiency were low. A mass health education programme on both of these diseases is needed to ensure better and early detection, good timing of treatment, and better prevention of the triggering factors to ensure better health for children.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Prevalence of and mothers’ knowledge, attitude and practice towards glucose-6-phosphate dehydrogenase deficiency among neonates with jaundice: a cross-sectional study

et al. 2020

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“…Glucose-6-phosphate-dehydrogenase ( G6PD ) is a “housekeeping” gene encoding the G6PD enzyme which catalyzes glucose-6-phoshpate conversion to 6-phosphogluconolactone in the pentose monophosphate pathways in all cells [1, 2]. This enzyme is also important for maintaining red blood cells (RBCs) and protecting them from damages or premature destruction caused by oxidative stress through the maintenance of Nicotinamide Adenine Dinucleotide (NADP) and Nicotinamide Adenine Dinucleotide Phosphate Hydrogen (NADPH) levels [1, 2]. Although G6PD deficiency affects all cells in the body, the most affected cells are RBCs because these cells have no alternative pathways to produce NADPH [1].…”

Section: Introductionmentioning

confidence: 99%

“…This enzyme is also important for maintaining red blood cells (RBCs) and protecting them from damages or premature destruction caused by oxidative stress through the maintenance of Nicotinamide Adenine Dinucleotide (NADP) and Nicotinamide Adenine Dinucleotide Phosphate Hydrogen (NADPH) levels [1, 2]. Although G6PD deficiency affects all cells in the body, the most affected cells are RBCs because these cells have no alternative pathways to produce NADPH [1]. The G6PD gene, 18 k base (kb) long and is located on chromosome Xq28, consists of 13 exons and 12 introns.…”

Section: Introductionmentioning

confidence: 99%

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G6PD genetic variations in neonatal Hyperbilirubinemia in Indonesian Deutromalay population

et al. 2019

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BackgroundNeonatal jaundice is a common finding in newborns in Asia, including Indonesia. In some cases, the serum total bilirubin levels exceeds the 95th percentile for hours of life (neonatal hyperbilirubinemia). Severe neonatal hyperbilirubinemia (NH) could lead to kernicterus and neonatal death. Glucose-6-Phosphage Dehydrogenase (G6PD) genetic variations and deficiency have been reported in several studies to be associated with NH. This study aimed to analyze the G6PD genetic variations and its activity in neonates with and without hyperbilirubinemia in the Deutromalay Indonesian population.MethodsDeoxyribose Nucleic Acid (DNA) was isolated from peripheral blood of 116 and 115 healthy term neonates with and without hyperbilirubinemia. All infants underwent the following laboratory examinations: routine hematologic evaluation, Coombs test, G6PD activity measurement using the Randox kit method, and serum total bilirubin level. All exons of the G6PD gene were targeted for deep sequencing using MiSeq (Illumina). An association study of G6PD polymorphisms with NH was performed using PLINK.ResultsThe prevalence of G6PD deficiency in neonates with and without hyperbilirubinemia in Indonesian Deutromalay population were 1.72% (95% Confidence Interval (CI): 0.6–4.1%) and 1.74% (95% CI: 0.7–4.1%), respectively. The most common G6PD polymorphisms, i.e. rs1050757/c.* + 357A > G, rs2230037/c.1311C > T, and rs2071429/c.1365-13 T/IVS11, were identified. However, none of those polymorphisms and their haplotype were associated with NH (p > 0.05, Odds Ratio (OR) ~1.00). The prevalence of G6PD mutations in neonates with and without hyperbilirubinemia were 6.8% (95% CI: 2.3–11.5%) and 6.9% (95% CI: 2.3–11.6%), respectively. The most frequently identified G6PD mutation was the Viangchan variant (p.V291 M), which was followed by the Canton (p.R459L) and Vanua Lava (p.L128P) variants. Two novel mutations were identified both in case (p.V369A, p.I167F) and control (p.L474=, p.I36T) groups.ConclusionThe prevalence of G6PD deficiency is low in neonates with or without hyperbilirubinemia in Deutromalay Indonesian population. The majority of G6PD mutations identified among Indonesian Deutromalay population in this study are Viangchan, Canton and Vanua Lava variants.

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Hexose monophosphate shunt, the role of its metabolites and associated disorders: A review

Akram

Shah

Munir

et al. 2019

Journal Cellular Physiology

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The hexose monophosphate (HMP) shunt acts as an essential component of cellular metabolism in maintaining carbon homeostasis. The HMP shunt comprises two phases viz. oxidative and nonoxidative, which provide different intermediates for the synthesis of biomolecules like nucleotides, DNA, RNA, amino acids, and so forth; reducing molecules for anabolism and detoxifying the reactive oxygen species during oxidative stress. The HMP shunt is significantly important in the liver, adipose tissue, erythrocytes, adrenal glands, lactating mammary glands and testes. We have researched the articles related to the HMP pathway, its metabolites and disorders related to its metabolic abnormalities. The literature for this paper was taken typically from a personal database, the Cochrane database of systemic reviews, PubMed publications, biochemistry textbooks, and electronic journals uptil date on the hexose monophosphate shunt. The HMP shunt is a tightly controlled metabolic pathway, which is also interconnected with other metabolic pathways in the body like glycolysis, gluconeogenesis, and glucuronic acid depending upon the metabolic needs of the body and depending upon the biochemical demand. The HMP shunt plays a significant role in NADPH2 formation and in pentose sugars that are biosynthetic precursors of nucleic acids and amino acids. Cells can be protected from highly reactive oxygen species by NADPH 2. Deficiency in the hexose monophosphate pathway is linked to numerous disorders. Furthermore, it was also reported that this metabolic pathway could act as a therapeutic target to treat different types of cancers, so treatments at the molecular level could be planned by limiting the synthesis of biomolecules required for proliferating cells provided by the HMP shunt, hence, more experiments still could be carried out to find additional discoveries.

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To study the prevalence of glucose 6 phosphate dehydrogenase(G6PD) deficiency in neonates with neonatal hyperbilirubinemia and to compare the course of the neonatal jaundice in deficient versus non deficient neonates

Cited by 10 publications

References 0 publications

Prevalence of and mothers’ knowledge, attitude and practice towards glucose-6-phosphate dehydrogenase deficiency among neonates with jaundice: a cross-sectional study

Prevalence of and mothers’ knowledge, attitude and practice towards glucose-6-phosphate dehydrogenase deficiency among neonates with jaundice: a cross-sectional study

G6PD genetic variations in neonatal Hyperbilirubinemia in Indonesian Deutromalay population

Hexose monophosphate shunt, the role of its metabolites and associated disorders: A review

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