THE AFRICAN CHILD AND G6PD DEFECT

THE AFRICAN CHILD AND G6PD DEFECT 

  By  Rita Gavor

Kofi,(not real name) a six-year-old boy was not well and was taken to the hospital. After he was diagnosed, he was put on an antibiotic. After a week’s treatment, he had rashes on his tongue and developed high temperature. The normal reaction of the family was to get back to the hospital for malaria drugs and vitamin C, which was an attempt to correct the situation by the health official. He refused to eat and his urine turned brownish the next day. The boy was sent back  to the hospital again and after series of medical examinations, was diagnosed as having a full version of the Glucose-6-Phosphate Dehydrogenase (G6PD) defect.

The family’s first reaction was what is the meaning of this condition? How did he get that?  Fortunately, Kofi’s grandfather who is a health expert, said, he has a partial version of the condition. The boy likely inherited it from him through the mother. The summary of the diagnosis was that, he was not supposed to take some medications, which he took, thus his condition.

 Research from the Internet indicates that the G6PD condition is hereditary. The red blood cell breaks down when the body is exposed to certain foods, drugs or infections in the body. The condition occurs when a person does not have enough of an enzyme called G6PD, which helps red blood cells work properly. This process is called haemolysis. When this process is actively occurring, it is called a haemolytic episode. This was what the six-year-old boy was going through. Either the infections or one of the drugs he took, which contained some of the chemicals that G6PD deficient people were to avoid, triggered his blood cell destruction. This could be an Anti-malarial drug, Aspirin, Nitrofurantoin, Nonsteroidal anti-inflammatory drugs (NSAIDs), Quinidine, Quinine or Sulfa drugs.

People with this condition do not show any signs until their red blood cells are exposed to certain chemicals in food or medicine. They then display symptoms such as dark urine, enlarged spleen, fatigue, paleness, shortness of breath and yellow skin color (jaundice). This was the condition of Kofi, before he got to the hospital. You can just image what would have happened if the condition was not detected early.

A lot of people especially, Africa children die without detecting the cause of death. How many African children (even adult) know about these condition and have the prepare information to manage it? An African male child with a family history of the deficiency such as that of Kofi has the highest possibility of developing the condition. The process if not managed can affect the liver and kidney thus the discolouration of the urine. Fortunately, for Kofi, he spent some weeks in the hospital to correct the condition and is aware of his condition even at the age of six.

 My question is, how many African families know about this condition and will avoid buying malaria drugs and  antibiotics from the next available chemical shop for children and adults when they have headache? How can Kofi’s parent ensure that he does not get into contact with any of the chemicals and food he is to avoid?  I am sure a number of people both adult and children die because they have such a condition they do not know about and are given medicines that destroys their red blood cells. Even if they are aware, how do they communicate with medical official in emergencies/accident case?

 I wish there was some data on the number of people who have the condition and those who die annual with complication of G6PD.Can health officials run mandatory test for newborn babies at birth for an early detection to save the life of African children.  Is there something people with the condition can have on their bodies for emergencies cases to communicate to medical officials?  African Health expects, researchers and advocates need to collect and share information on G6PD to help save the life of the poor and marginalised in Africa especially children. Furthermore, as with other health conditions, is there a drug to correct the defect?  Over to the health expects