Glucose-6-phosphate dehydrogenase deficiency

No. A person cannot acquire G6PD deficiency from a blood transfusion from a donor with G6PD. G6PD is a genetic disorder and is inherited in an X-linked recessive manner.

Due to many unanswered questions, there is controversy about whether G6PD-deficient people should become blood donors and about the quality of their blood during processing and storage. Risk factors associated with the use of G6PD-deficient blood in transfusion have not been well established. There is little evidence that G6PD-deficient people should be excluded from donating red blood cells. But, most studies on newborns and children have recommended routine screening for G6PD deficiency because their immature hepatic (liver) function potentially lessens their ability to handle any excess bilirubin. Transfusions of G6PD-deficient blood also may potentially have negative effects on premature newborns, or people who need repeated transfusions. For these recipients, screening for G6PD deficiency may be appropriate. The potential effects may differ depending on the region, the specifics of the recipient, the quantity transfused, and the type of G6PD deficiency.^[1]

The World Health Organization (WHO) guidelines recommend that blood be accepted from “individuals with G6PD deficiency or other inherited red cell membrane defects, without a history of hemolysis; however, their blood is not suitable for intrauterine transfusion, neonatal exchange transfusion or for patients with G6PD deficiency."^[1] According to the G6PD Deficiency Association, the Red Cross does not accept G6PD deficient blood.^[2]

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is caused by mutations in the G6PD gene. This gene gives the body instructions to make an enzyme called G6PD, which is involved in processing carbohydrates. This enzyme also protects red blood cells from potentially harmful molecules called reactive oxygen species. Chemical reactions involving G6PD produce compounds that prevent reactive oxygen species from building up to toxic levels within red blood cells.^[3]

Mutations in the G6PD gene lower the amount of G6PD or alter its structure, lessening its ability to play its protective role. As a result, reactive oxygen species can accumulate and damage red blood cells. Factors such as infections, certain drugs, or eating fava beans can increase the levels of reactive oxygen species, causing red blood cells to be destroyed faster than the body can replace them. This reduction of red blood cells causes the signs and symptoms of hemolytic anemia in people with G6PD deficiency.^[3]

G6PD deficiency is inherited in an X-linked recessive manner.^[3] X-linked recessive conditions are much more common in males, who have only one X chromosome (and one Y chromosome). Females have two X chromosomes, so if they have a mutation on one of them, they still have one X chromosome without the mutation. Females with one X chromosome mutation are known as carriers and are usually unaffected. However, females can be affected if they have a mutation in both copies of the G6PD gene, or in some cases, if they have only one mutation. Females with one mutation may have lower G6PD activity than would normally be expected due to a phenomenon called skewed lyonization.^[4]

If a mother is a carrier of an X-linked recessive condition and the father is not, the risk to each child depends on whether the child is male or female.

• Each son has a 50% chance to be unaffected, and a 50% chance to be affected
• Each daughter has a 50% chance to be unaffected, and a 50% chance to be a carrier

If a father has the condition and the mother is not a carrier, all sons will be unaffected, and all daughters will be carriers.

There is nothing either parent can do, before or during a pregnancy, to cause a child to have this condition.