Related Experiment Video

Updated: Jan 3, 2026

Quantification of Colonic Stem Cell Mutations
07:53

Quantification of Colonic Stem Cell Mutations

Published on: September 25, 2015

7.0K

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

Adil Abozaid Eissa1, Bijar Ali Haji2, Adnan Anwar Al-Doski1

  • 1Department of Pathology, College of Medicine, University of Duhok, Duhok, Iraq.

American Journal of Perinatology
|November 19, 2019
PubMed

Insights

Glucose-6-phosphate dehydrogenase (G6PD) deficiency significantly increases the risk and severity of neonatal hyperbilirubinemia (NHB). G6PD deficiency in newborns leads to higher bilirubin levels, requiring longer phototherapy and hospitalization.

Area of Science:

  • Neonatal Medicine
  • Hematology
  • Genetics

Background:

  • Neonatal hyperbilirubinemia (NHB) is a common condition in newborns.
  • Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an inherited condition that can affect red blood cells.

Purpose of the Study:

  • To investigate the impact of G6PD deficiency on the development and severity of NHB.
  • To compare bilirubin levels, treatment duration, and hospitalization in G6PD-deficient and non-deficient neonates with NHB.

Main Methods:

  • A case-control study involving 100 newborns with moderate to severe NHB and 50 controls.
  • Comprehensive laboratory tests including blood grouping, bilirubin levels, complete blood count, and G6PD enzyme assay were performed.

Main Results:

  • 16% of neonates with NHB were G6PD deficient, compared to 6% in the control group (p<0.05).
  • G6PD-deficient neonates had significantly higher indirect serum bilirubin levels, leading to longer phototherapy and hospitalization.
  • No significant differences were observed in presentation onset, reticulocyte count, or age between the groups.

Conclusions:

  • G6PD deficiency plays a significant role in the etiology and severity of NHB in the studied region.
  • While G6PD deficiency is linked to NHB, the exact mechanism beyond hemolysis requires further investigation due to similar reticulocyte and hemoglobin levels.
Abstract

More Related Videos

Biochemical Measurement of Neonatal Hypoxia13:13

Biochemical Measurement of Neonatal Hypoxia

Published on: August 24, 2011

14.3K
Isolation of Neonatal Extrahepatic Cholangiocytes07:54

Isolation of Neonatal Extrahepatic Cholangiocytes

Published on: June 5, 2014

10.7K

Related Concept Videos

Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
663
Pharmacokinetics in Pediatric Patients: Overview and Drug Absorption01:23

Pharmacokinetics in Pediatric Patients: Overview and Drug Absorption

Understanding the physiological differences in the pediatric population is crucial for effective pharmacotherapy. Neonates, infants, and children exhibit significant variations in gastric pH, gastric emptying time, intestinal transit time, and biliary function. These variations profoundly affect oral drug absorption, necessitating a nuanced approach to pediatric dosing.Neonates present with a unique physiological profile, having a gastric pH greater than 4 and faster and more irregular gastric...
206
Pharmacokinetics in Pediatric Patients: Drug Metabolism01:24

Pharmacokinetics in Pediatric Patients: Drug Metabolism

In pediatric care, understanding the nuances of hepatic drug metabolism is crucial, as it significantly differs from that of adults. This divergence is primarily due to the developmental stage of drug-metabolizing enzymes, which affects how medications are processed in the body. In neonates, for instance, the activity of Phase I enzymes—critical for the initial breakdown of drugs—is markedly reduced, functioning at just 20–40% of the levels seen in adults. This reduction poses...
156
Drug Dosing: Infants and Children01:29

Drug Dosing: Infants and Children

Pediatric patient dosages diverge from adults due to disparities in body surface area, total body water, and extracellular fluid per kilogram of body weight. The dosing regimen considers the variations in pharmacokinetics and pharmacology across distinct age groups, encompassing preterm newborns, infants, young children, older children, and adolescents. Calculation of pediatric patient doses is predicated on determining body surface area, which exhibits a superior correlation with the child's...
218
Pharmacokinetics in Pediatric Patients: Drug Distribution01:17

Pharmacokinetics in Pediatric Patients: Drug Distribution

Drug distribution in the pediatric population exhibits unique challenges and considerations due to the physiological differences between children, particularly neonates and infants, and adults. A crucial aspect of pediatric pharmacology is understanding how these differences impact the pharmacokinetics of various drugs, necessitating age-specific dosing strategies to ensure efficacy and safety.Neonates and infants have a higher total body water content, ~75%–90% of their body weight,...
215
Glucose Transporters01:27

Glucose Transporters

Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
27.0K