G6PD Deficiency

ByMina ZabihiNarges Abedi

G6PD Deficiency G6PD Deficiency is also called Glucose-6-

phosphate Dehydrogenate. It is a common enzyme deficiency. There

are about 400 million people do have G6PD Deficiency.

In Africa, there’s one G6PD Deficient person per four people.

Percent of people who have G6PD Deficiency

G6PD Deficiency G6PD enzyme is located on sex chromosome X at

q28 locus. Thus, G6PD enzyme is X-linked gene.

Males are more likely to have defective gene than females do because G6PD deficiency will only manifest itself in females when there are two defective copies of the gene in the genome. As long as there is one good copy of the G6PD gene in a female, a normal enzyme will be produced and this normal enzyme can then take over the function that the defective enzyme lacks.

The q28 locus of the X-chromosome

Hemolytic Anemia G6PD deficiency cause red blood cells no longer

transport oxygen effectively throughout the body. This condition is called Hemolytic Anemia Arises.

There are other conditions that also caused by G6PD deficiency- neonatal jaundice, abdominal back pain, dizziness, headache, irregular breathing, and palpitations.

Hemolytic Anemia An anemic response can occur when G6PD

deficient individual takes oxidative drugs or fava beans.

Some G6PD deficient individuals are allergic to fava beans and the smell of the fava pollen. This condition is called Favism.

The fava beans

Diagnosis If a doctor suspects a G6PD deficiency on a

new-born child, a Complete Blood Count or Screening Test is used to test and measure G6PD enzyme’s activity.

Treatment Scientists can genetic engineer fava bean, so

that it will no longer react to G6PD individual’s red blood cells.

The best treatment now to prevent favism and hemolytic anemia is to have drug control. G6PD deficient people should not eat fava beans or take drugs that contain oxidizing agent.

The End