Glucose-6-Phosphate-Dehydrogenase Deficiency and Neonatal Jaundice in Chinese Male Infants in Hong Kong

Yue, PaulC.K.; Strickland, Maureen

doi:10.1016/s0140-6736(65)91780-0

Cited by 33 publications

(7 citation statements)

References 6 publications

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“…The increased incidence of neonatal jaundice in babies with G6PD deficiency has been well documented and the results of this survey of Hong Kong neonates is in keeping with these reports (Yue and Strickland, 1965). There is much less information about the relation of PK deficiency to neonatal jaundice.…”

Section: Discussionsupporting

confidence: 75%

Screening of pyruvate kinase deficiency and G6PD deficiency in Chinese newborn in Hong Kong.

Fung¹,

Keung²,

Chung³

1969

Archives of Disease in Childhood

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Section: Discussionsupporting

confidence: 75%

Screening of pyruvate kinase deficiency and G6PD deficiency in Chinese newborn in Hong Kong.

Fung¹,

Keung²,

Chung³

1969

Archives of Disease in Childhood

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“…23,24 The reported favism, kernicterus, and neonatal jaundice are consequences of G6PD deficiency. [25][26][27] An outbreak of hemolytic anemia claiming several lives occurred in Hsin-Chu, and was linked to ingestion of fava beans. 28 G6PD deficiency is a common genetic disorder in the south-east of China and Taiwan.…”

Section: G6pd Deficiency In Taiwan and Southern Chinamentioning

confidence: 99%

Glucose-6-phosphate dehydrogenase – from oxidative stress to cellular functions and degenerative diseases

2007

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Glucose-6-phosphate dehydrogenase (G6PD), the first and rate-limiting enzyme of the pentose phosphate pathway, is indispensable to maintenance of the cytosolic pool of NADPH and thus the cellular redox balance. The role of G6PD as an antioxidant enzyme has been recognized in erythrocytes for a long time, as its deficiency is associated with neonatal jaundice, drug- or infection-mediated hemolytic crisis, favism and, less commonly, chronic non-spherocytic hemolytic anemia. To a large extent, advances in the field were made on the pathophysiology of G6PD-deficient erythrocytes, and the molecular characterization of different G6PD variants. Not until recently did numerous studies cast light on the importance of G6PD in other aspects of the physiology of both cells and organisms. Deficiency in G6PD activity, and hence a disturbance in redox homeostasis, can lead to dysregulation of cell growth and signaling, anomalous embryonic development, altered susceptibility to viral infection as well as increased susceptibility to degenerative diseases. The present review covers recent developments in this field. Additionally, molecular characterization of G6PD variants, especially those frequently found in Taiwan and Southern China, is also addressed.

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“…Yue (1965) found that in 73 percent of his cases jaundice appeared on the 3rd or 4th day. This is also what we found in our series.…”

Section: Onset Of Jaundicementioning

confidence: 89%

Glucose-6-Phosphate Dehydrogenase Deficiency in the Dr. Cipto Mangunkusumo General Hospital

Suradi

Monitja

Munthe

et al. 2017

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Glucose-6-Phosphate-Dehydrogenase Deficiency and Neonatal Jaundice in Chinese Male Infants in Hong Kong

Cited by 33 publications

References 6 publications

Screening of pyruvate kinase deficiency and G6PD deficiency in Chinese newborn in Hong Kong.

Screening of pyruvate kinase deficiency and G6PD deficiency in Chinese newborn in Hong Kong.

Glucose-6-phosphate dehydrogenase – from oxidative stress to cellular functions and degenerative diseases

Glucose-6-Phosphate Dehydrogenase Deficiency in the Dr. Cipto Mangunkusumo General Hospital

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