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The Prevalence of Glucose-6-Phosphate Dehydrogenase Deficiency Among Apparently Healthy Children In Ebonyi Central Senatorial Zone, Ebonyi State, Nigeria


1.0                                                   INTRODUCTION

1.1  Background of the Study

The red blood cells have occupied a unique position in the study of human biology, physiology and biochemistry. Red blood cells are the most common type of blood cell and the principal means of delivering oxygen (O2) to the body tissue via the blood flow through the circulatory system. Red blood cells are also known as red blood Corpuscles, RBCS, haematids, red cells, erythrocytes or erythroid cells. The cells develop in the bone marrow and circulate for about 100-120 days in the body before their components are recycled by macrophages. 2.4 million new erythrocytes are produced per seconds (Erich, 1995). Each circulation takes about 20 seconds. About quarter of the cells in the human body are red blood cells (Pierige et al., 2008). In humans, mature red blood cells are oval and flexible biconcave discoid in shape, it is smaller than most other human cells. They are non-nucleated cells in their mature form. These cells have nuclei during early phases of erythropoiesis but extrude them when development is going on as they mature in order to provide more space for hemoglobin. It also loses all other cellular organelles such as their mitochondria, endoplasmic reticulum and Golgi apparatus. Red cells have a unique metabolism, since they lack nuclei and mitochondria; they rely almost entirely on the glycolysis of glucose and pentose phosphate pathway for their energy needs (ATP).

Deficiencies in the enzymes controlling erythrocytes metabolism may be conveniently divided into two groups: firstly, defect in embden-meyerhof pathway caused by deficiencies in hexokinase, triose isomerase and pyruvate kinase (which is the most common enzyme defect involving this pathway etc). Secondly, defect in Hexose monophosphate shunt owing to deficiencies in glucose-6-phosphate dehydrogenase, glutathione reductase, peroxidase and synthetase.

Fifty years ago, three enzymes deficiencies that produce disease in humans had been identified, all in human erythrocyte. These enzymes were catalase, galactose-1-phosphate uridyltransferase and glucose-6-phosphate dehydrogenase (G6PD). Although all of these deficiencies were discovered in red blood cells, only G6PD deficiency produces a hematologic disorder namely anaemia and it was as a result of investigation of haemolytic anaemia that brought this common enzymatic defect to light. In 1973, it was estimated that 3 million people worldwide were G6PD deficient (Luzatto, 1973). In order words, we will restrict our study to G6PD since it is the most common clinically manifested red cell enzymopathy.

GIucose-6-phosphate dehydrogenase (G-6-PD) deficiency is the most common enzymopathy in humans (Mehta et al., 2000). G6PD deficiency was discovered for the first time when hemolytic anaemia occurred in some persons who consumed anti-malarial drug named primaquine (Beutler, 1994). It is an X-linked disorder and is a highly polymorphic enzyme. Most deficient people do not show any symptoms until following exposure to oxidative drugs, some infections and ingestion of fava bean (Mehta, 2000).

G6PD deficiency is most prevalent among people of Africa because of the highest incidence occurring in the darkly pigmented racial and ethnic groups especially G6PD A variant. The prevalence of G6PD deficiency ranges from 4-26% in Nigeria (Luzatto, 2001 and Ademowo, 2002) due to its malarial endemicity. This prevalence rate varies from one locality to another.

Mediterranean mutation is the most common variant of enzyme deficiency and often associated with favism (Beutler, 1994). Avoiding of the oxidative agents that induce hemolytic anaemia is the most important treatment in the enzyme deficiency. Neonatal screening and health education can reduce the incidence rate of G6PD deficiency.


G6PD is the key enzyme in the pentose phosphate pathway that converts glucose-6-phosphate to 6-phosphoglucono-8-lactone, and during this conversion, the important reluctant metabolite named Nicotinamide Adenine Dinucleotide photsphate (NADPH) is provided. The pathway is the only source for producing NADPH in red blood cell (Beutler, 1994), because they lack mitochondria, nucleus, and ribosome’s and other pathways that produce NADPH (Prchal et al., 2005). NADPH is necessary for generating GSH from its oxidized form, GSSG, and subsequent maintenance of intracellular GSH pools. GSH maintains normal structure; elasticity and integrity of red blood cells, and sustain hemoglobin in ferrous state that is essential for carrying oxygen.

Catalase is another anti-oxidant enzyme that is abundant in red blood cells and help in the removal of peroxides from red blood cells through activation of NADPH (Beutler, 1994). Unless peroxides are neutralized, they will cause oxidative injuries. Hemoglobin and red blood cell membrane molecules that contain sulfhyhryl (SH) groups are destroyed (Mehta, 2000).

1.3 Importance of G6PD enzyme

The importance of G6PD cannot be underestimated hence, Superoxide, hydrogen peroxide, hydroxyl radical is called ROS (Reactive Oxygen Species). These cause oxidative stress and damage cell’s membrane (Shihabi, 2002).

Increased production of ROS or decreased anti-oxidant defense enzyme plays a major role in oxidation injuries in different organs, tissues, and cells including brain, heart, vascular (Leopold et al, 2005) and cause brain diseases like Alzheimer and Parkinson diseases and also considered to contribute to the aging process (Tsun-yee et la., 1997).

Enzymes like superoxide dimutases, catalase, glutathione peroxidases, gitttatm’one reductase and glueose-6-phosphate dehydrogenase are modulator enzyme that has a very important role in all cells especially in red blood cells. G6PD is a key enzyme for maintenance of redox potential in cells. G6PD produced NADPH in pentose monophosphate pathway. NADPH is important as a central reductant and regulates redox potential (Tian et al., 1999).


The current economic hardship confronting individuals in Ebonyi Central Senatorial Zone as a developing or sub-urban area in the South-eastern region of Nigeria on Sub-Saharan Africa, has posed threat in the investigation of G6PD deficiency. It is suspected that we may also be harbouring some G6PD deficiency variants owing to the fact that it’s malaria endemic area. Having observed that the people are prone to this, therefore we wish to verify the prevalence of G6PD deficiency among apparently healthy children in Ebonyi Central Senatorial zone.

1.5       AIM:   To evaluate the prevalence of G6PD deficiency in apparently healthy Children in Ebonyi Central Senatorial Zone.


This study is intended to do the following;

  • To assess the proportion of children within the population that has the enzyme defect.
  • To make an inference if the prevalence is high, this may be transferred to next generation.
  • To provide information to the scientific community.


The area under study comprises of rural dwellers with low standard of living…….

—This article is incomplete———–This article is incomplete———— It was extracted from a well articulated quality Project, Research Work/Material

 Topic: Prevalence of Glucose-6-Phosphate Dehydrogenase Deficiency Among Apparently Healthy Children In Ebonyi Central Senatorial Zone, Ebonyi State Nigeria.

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