A study of glucose-6-phosphate dehydrogenase deficiency in neonatal hyperbilirubinemia

Abstract

The G6PD deficiency increases hemoglobin vulnerability to oxidative damage, leading to hemoglobin instability and precipitation of Heinz bodies. [1] G6PD deficiency is the most common red cell enzyme abnormality associated with hemolysis. It is also known to be associated with neonatal jaundice, kernicterus, and even death. The marked elevation of bilirubin levels that sometimes occurs in the neonatal period raises the risk of kernicterus. Neonatal hyperbilirubinemia often arises in association with Gilbert's syndrome. [2,3] It affects over 400 million people worldwide. [4] G6PD deficiency occurs with increased frequency throughout Africa, Asia, the Mediterranean, and the Middle East. In the United States, black males are most commonly affected, with a prevalence of approximately 10%. [5] The global distribution and health burden of G6PD deficiency has Background: Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme essential for basic cellular functions, including protection of red cell proteins from oxidative damage. G6PD deficiency is the most common red cell enzyme abnormality associated with hemolysis as well as with neonatal jaundice, kernicterus, and even death. It plays a protective role against malaria. It is a genetically inherited sex-linked abnormality. Objectives: To determine the age, sex, and different community-wise incidence of G6PD deficiency in neonatal subjects having neonatal hyperbilirubinemia.

A comparative study between glucose 6-phosphate dehydrogenase deficient and normal term neonates with indirect hyperbilirubinemia in a rural tertiary care hospital of Eastern India

“…17 In our study, we found that about two-third of the G6PD deficient neonates with indirect hyperbilirubinemia were presented early within 24-48 h, whereas G6PD normal neonates presented late with jaundice. This is in accordance with other studies which states that though the presentation of jaundice common in 2 nd or 3 rd day but it may present as early as in first 24 h. 18 This is probably due to the ongoing hemolysis in the fetus due to perinatal stress factors in G6PD deficient babies.…”

G6PD Deficiency Prevalence as a Cause of Neonatal Jaundice in a Neonatal Ward in Dohuk, Iraq

“…14 Male considered to be independent risk factor for NHB as the current study revealed a male:female ratio of 2.13:1, and these data are comparable to those reported from southern part of the country as shown by a study from Najaf, 15 and also to studies from other parts of the world including the China, India, and from Canada. [16][17][18] Male predominance had been contributed to their higher metabolic rate and their association with the dysfunction of the placenta. 15 Despite using expensive and sophisticated investigations, the underlying cause cannot be identified in a group of patients.…”

Prevalence and Genetic Characterization of Glucose-6-Phosphate Dehydrogenase Deficiency in Anemic Subjects from Uttar Pradesh, India

“…It could have been hypothesized that alterations in this part of the gene could lead to similar biochemical properties and affecting the surrounding G6P binding site. 18,19 Glucose-6-phosphate dehydrogenase -deficient persons are predisposed to the development of sepsis, complications related to sepsis after a severe injury, hepatitis, malaria, and drug intake. These are the main factors causing hemolytic crisis in G6PD-deficient children.…”