scholarly journals FREQUENCY OF GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY IN NEONATAL JAUNDICE IN DISTRICT SWAT, PAKISTAN

1969 ◽  
Vol 3 (1) ◽  
pp. 242-247
Author(s):  
AMREEK LAL ◽  
S.M.NAEEM ◽  
SHAHJEHAN ◽  
ASHFAQ AHMAD ◽  
ISRARUL HAQ
Keyword(s):  
G6pd Deficiency ◽  
Neonatal Jaundice ◽  
Dehydrogenase Deficiency ◽  
Reduction Method ◽  
Serum Bilirubin ◽  
Newborn Infants ◽  
Dye Reduction ◽  
Complete Blood Counts ◽  
Deficiency Screening ◽  
Glucose 6 Phosphate Dehydrogenase

Background: Hyperbilirubinemia is the most common cause of neonatal jaundice. Severe neonatalhyperbilirubinemia and kemicterus continue to be reported worldwide in otherwise healthy term infants.We conducted this study to estimate the incidence of severe neonatal hyperbilirubinemia and to determineunderlying causes, improved knowledge of which would be valuable to help identify strategies for riskreduction.Methods: 100 infants of both sexes, of the age between 1-28 days, with no infection and Rh incompatibilitywere included in the study. The activity of G6PD was determined by a dye-reduction method screening testdevised by Sigma Diagnostics USA. Complete blood counts (CBC) with reticulocyte count, serum bilirubin(total and indirect) were performed and the results were recorded for further analyses.Results: Out of the total 100 subjects, classified in two groups on the basis of presence of jaundice, 14 (14%)were G6PD deficient. The frequency of G6PD deficiency was markedly prominent, in neonates withjaundice.Discussion: G6PD deficiency is one of the major causes of jaundice in neonates. The study area also have aconsiderable number of G6PD deficient individuals. This indicates a need for a more thorough assessmentof newborn infants and consideration of strategies to identify at-risk newborns, such as pre-dischargemeasurement of serum bilirubin levels and G6PD deficiency screening.

FREQUENCY OF SURGICAL SITE INFECTION IN MESH REPAIR FOR INGUINAL HERNIA

1969 ◽  
Vol 3 (2) ◽  
pp. 308-313
Author(s):  
MUHAMMAD KHAN ◽  
MUNIR AHMAD ◽  
MUHAMMAD HUSSAIN ◽  
MUHMMAD UZAIR
Keyword(s):  
Inguinal Hernia ◽  
G6pd Deficiency ◽  
Mesh Repair ◽  
Neonatal Jaundice ◽  
Serum Bilirubin ◽  
Newborn Infants ◽  
Site Infection ◽  
Common Cause ◽  
Complete Blood Counts ◽  
Deficiency Screening

BACKGROUND: Hyperbilirubinemia is the mo$t common cause of neonatal jaundice. Severe neonatalhyperbilirubinemia and kernicterus continue to be reported worldwide in otherwise healthy term infants.We conducted this study to estimate the incidence of severe neonatal hyperbilirubinemia and to determineunderlying causes, improved knowledge of which would be valuable to help identify strategies for riskreduction.METHODS: 100 infants of both sexes, of the age between 1-28 days, with no infection and Rhincompatibility were included in the study. The activity of G6PD was determined by a dye-reductionmethod screening test devised by Sigma Diagnostics USA. Complete blood counts (CBC) with reticulocytecount, serum bilirubin (total and indirect) were performed and the results were recorded for further analyses.RESULTS: Out of the total 100 subjects, classified in two groups on the basis of presence of jaundice, 14(14%) were G6PD deficient. The frequency of G6PD deficiency was markedly prominent, in neonates withjaundice.DISCUSSION: G6PD deficiency is one of the major causes of jaundice in neonates. The study area alsohave a considerable number of G6PD deficient individuals. This indicates a need for a more thoroughassessment of newborn infants and consideration of strategies to identify at-risk newborns, such as predischarge measurement of serum bilirubin levels and G6PD deficiency screening.

scholarly journals Glucose-6-phosphate Dehydrogenase Deficiency: A Case Report

2017 ◽  
Vol 12 (1) ◽  
pp. 47-49
Author(s):  
Md Kamrul Hassan ◽  
Aloke Kumar Saha ◽  
Lakshman Chandra Kundu ◽  
Poly Begum ◽  
Abu Yousuf
Keyword(s):  
G6pd Deficiency ◽  
Neonatal Jaundice ◽  
Dehydrogenase Deficiency ◽  
Cultural Factors ◽  
Enzyme Defect ◽  
Asian Populations ◽  
Hemolytic Crisis ◽  
Life Threatening ◽  
Fava Beans ◽  
Glucose 6 Phosphate Dehydrogenase

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common hereditary enzyme disorder and more than 200 million people have a deficiency in this enzyme. G6PD deficiency is an X-linked enzyme defect, and one of its main signs is the presence of hemolytic anemia. It is a worldwide important cause of neonatal jaundice and causes life threatening hemolytic crisis in childhood. At later ages, certain drugs such as anti-malarial drugs and fava beans cause hemolysis among G6PD deficiency patients. The frequency and severity is influenced by genetic and cultural factors. It is common in Mediterranean, African and some East Asian populations but rare in Bangladeshi peoples. Genetic counseling may be of benefit for patients and their families. Other treatment is symptomatic and supportive.Faridpur Med. Coll. J. Jan 2017;12(1): 47-49

scholarly journals Neonatal jaundice and glucose-6-phosphate dehydrogenase deficiency

2016 ◽  
Vol 11 (4) ◽  
Author(s):  
Sohail Rasheed ◽  
Abdul Hayee ◽  
Yasmeen Lodhi ◽  
Rafi Ahmed
Keyword(s):  
Bilirubin Level ◽  
G6pd Deficiency ◽  
Neonatal Jaundice ◽  
Dehydrogenase Deficiency ◽  
Total Bilirubin ◽  
Total Bilirubin Level ◽  
Normal Subjects ◽  
Group I ◽  
Level Of Significance ◽  
Glucose 6 Phosphate Dehydrogenase

One hundred new born males babies aged 7 days and above were included in this study. These were divided into two groups — Group I included G6PD normal subjects and Group II included G6PD deficient subjects. Total bilirubin and G6PD enzyme levels were done by commercially available kits. Results were analysed by using students `t` test and level of significance was done. A significant increase in total bilirubin level was observed in infants of G6PD deficiency, Erythrocyte G6PD level is significantly decreased in 06% of infants born with neonatal jaundice.

scholarly journals From Prejudice to Evidence: The Case of Rhizoma Coptidis in Singapore

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Chin Ee Ho ◽  
You Li Goh ◽  
Chang Zhang
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
G6pd Deficiency ◽  
Neonatal Jaundice ◽  
Therapeutic Effects ◽  
Evidence Based ◽  
Rhizoma Coptidis ◽  
History Of ◽  
Hepatoprotective Effects ◽  
Glucose 6 Phosphate Dehydrogenase

Rhizoma Coptidis (RC), commonly known ashuanglian, is a herb frequently used in Traditional Chinese Medicine (TCM) prescriptions. Known to have “clearing damp-heat, quenching fire and counteracting poison” properties, it was widely used in the Chinese community in Singapore. Berberine, an alkaloid isolated from RC, is known to have a wide array of therapeutic effects including antimicrobial, antineoplastic, and hepatoprotective effects. In 1978, RC was implicated in causing neonatal jaundice (NNJ) and kernicterus in neonates suffering from glucose-6-phosphate dehydrogenase (G6PD) deficiency, leading to the banning of RC and berberine in Singapore. More than three decades later, accumulating evidence-based studies pointing to the safety of RC for general public and better understanding of G6PD deficiency, the Health Sciences Authority (HSA) in Singapore reviewed and lifted the prohibition on RC and berberine, turning a brand new chapter in the history of TCM in Singapore. This paper aims to review the safety of RC and berberine, using the prohibition of use and subsequent lifting of ban on RC and berberine in Singapore as an illustration to highlight the importance of evidence-based studies in Traditional Chinese Medicine (TCM).

scholarly journals A Rare Case of Coexistence of Homozygous β-Thalassaemia and Glucose 6 Phosphate Dehydrogenase Deficiency

2020 ◽  
Author(s):  
Jitendar Mohan Khunger ◽  
Monika Gupta ◽  
Ankur Jain ◽  
Monica Khunger Malhotra
Keyword(s):  
Oxidative Stress ◽  
Blood Cells ◽  
G6pd Deficiency ◽  
Rare Case ◽  
Dehydrogenase Deficiency ◽  
Globin Gene ◽  
Genetic Abnormality ◽  
Wide Range ◽  
Symptomatic Anaemia ◽  
Glucose 6 Phosphate Dehydrogenase

β-thalassaemia is one of the most prevalent autosomal disorders worldwide. Mutations/deletions in globin gene underlie deficiencies in Haemoglobin (Hb) production, which can interfere with oxygen delivery by Hb, resulting in thalassaemias causing anaemias with a wide range of disease severity. Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is a genetic abnormality resulting in inadequate amount of G6PD in the Red Blood Cells (RBCs). In patients with G6PD deficiency, the reduced or absent activity of the enzyme in RBCs causes premature haemolysis and symptomatic anaemia. The marked oxidative stress caused by homozygous β-thalassaemia is apparently incompatible with G6PD deficiency. Here, a rare case of six-month-old male child is described who presented with severe pallor hepato-splenomegaly and these two conditions co-existed in this patient.

scholarly journals Case report: Acute Hepatitis E Infection with Co-Existent Glucose-6-Phosphate Dehydrogenase Deficiency

2003 ◽  
Vol 14 (4) ◽  
pp. 230-231 ◽  
Author(s):  
Amitabh Monga ◽  
Ravinder PS Makkar ◽  
Anju Arora ◽  
Surabhi Mukhopadhyay ◽  
Ajay K Gupta
Keyword(s):  
Viral Hepatitis ◽  
G6pd Deficiency ◽  
Hepatitis E Virus ◽  
Dehydrogenase Deficiency ◽  
Acute Viral Hepatitis ◽  
Hepatitis E ◽  
Severe Anemia ◽  
Northern India ◽  
Acute Hepatitis E ◽  
Glucose 6 Phosphate Dehydrogenase

Hepatitis E virus is one of the leading causes of acute viral hepatitis in India but usually manifests as a mild self-limiting illness. Viral hepatitis in the presence of glucose-6-phosphate dehydrogenase (G6PD) deficiency may be associated with complications such as severe anemia, hemolysis, renal failure, hepatic encephalopathy and even death. The incidence of G6PD deficiency in the general population of northern India is reported to be between 2.2% and 14%. Despite both hepatitis E infection and G6PD deficiency being common, their impact on patient illness has only recently been reported. The present study reports a case of severe hemolysis in a patient with G6PD deficiency and hepatitis E infection.

Phototherapy for Neonatal Jaundice in Erythrocyte Glucose-6-Phosphate Dehydrogenase-Deficient Infants

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 1023-1026
Author(s):  
K. L. Tan
Keyword(s):  
G6pd Deficiency ◽  
Neonatal Jaundice ◽  
Significant Rise ◽  
Neonatal Hyperbilirubinemia ◽  
Control Group ◽  
Rapid Rise ◽  
Glucose 6 Phosphate Dehydrogenase

The effectiveness of phototherapy in the management of neonatal hyperbilirubinemia in glucose-6-phosphate dehydrogenase (G6PD)-deficient infants was studied. "Prophylactic" phototherapy for six continuous days commencing from the first day of life was effective in preventing a significant rise in bilirubin levels in 12 G6PD-deficient infants in the first three days, during which period a rapid rise was observed in a control group of G6PD-deficient infants. The hemoglobin levels on the first and eighth postnatal days were comparable in both groups. "Therapeutic" phototherapy proved equally effective in reducing bilirubin levels in 24 infants with nonhemolytic hyperbilirubinemia and an equal number of infants with hyperbilirubinemia associated with G6PD deficiency. Phototherapy was efficacious in the prevention or treatment of neonatal hyperbilirubinemia associated with G6PD deficiency; even if its use is prolonged it does not cause hemolysis in such infants.

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

2019 ◽  
Vol 08 (02) ◽  
pp. 047-053 ◽  
Author(s):  
Poonam Tripathi ◽  
Sarita Agarwal ◽  
Srinivasan Muthuswamy
Keyword(s):  
G6pd Deficiency ◽  
Dehydrogenase Deficiency ◽  
Genetic Characterization ◽  
Gene Mutations ◽  
Uttar Pradesh ◽  
Chromosome X ◽  
G6pd Gene ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Fluorescent Spot

AbstractGlucose-6-phosphate dehydrogenase (G6PD) deficiency is caused by one or more mutations in the G6PD gene on chromosome X. It affects approximately 400 million people worldwide. The purpose of this study was to detect the prevalence of G6PD deficiency and G6PD gene mutations in the hospital-based settings in patients referred for suspected G6PD deficiency. A qualitative fluorescent spot test and dichlorophenol-indolphenol (DCIP) test were performed. G6PD-deficient, positive samples were further processed for mutation analysis by Sanger sequencing. Out of 1,069 cases, 95 (8.8%) were detected as G6PD deficient (by DCIP test) and were sent for molecular analysis. The G6PD Mediterranean mutation (563C > T) is the most common variant among G6PD-deficient individuals followed by the Coimbra (592C→T) and Orissa (131C→G) variants. We concluded that all symptomatic patients (anemic or jaundiced) should be investigated for G6PD deficiency. Our findings will inform our population screening approach and help provide better management for G6PD-deficient patients.

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