G6PD Deficiency Mnemonic

Lack of NADPH and glutathione caused by G6PD deficiency causes red blood cells to be susceptible to oxidative damage causing hemolysis.

Inflammatory states can increase production of reactive oxygen species, causing hemolytic anemia in patients with G6PD deficiency in times of infection.

Fava beans contain alkaloids that can induce a state of oxidative stress, causing hemolytic anemia in patients with G6PD deficiency.

Sulfonamides are a group of antibiotic drugs that contain the sulfonamide group. Because the sulfonamide group can act as an oxidant, sulfonamides can induce states of oxidative stress, causing hemolytic anemia in patients with G6PD deficiency.

Primaquine is a drug used in the treatment of malaria that can generate reactive oxygen species within red blood cells, causing hemolytic anemia in patients with G6PD deficiency.

Para aminosalicyclic acid is an anti-tuberculosis drug that can induce a state of oxidative stress, causing hemolytic anemia in patients with G6PD deficiency.

Heinz bodies are small round inclusions seen in red blood cells formed by denatured hemoglobin, usually through oxidant damage. Heinz bodies can also be seen in chronic liver disease.

Heinz bodies are cleared by macrophages in the spleen via removal of the inclusion and the damaged membrane, leading to characteristic bite cells. Bite cells are defined as abnormally shaped red blood cells with semicircular portions removed from the cell margin, as if someone took a bite out of the cell.

This disease is more prevalent in African Americans because an advantage of this disease is that it confers protection against malaria, particularly Plasmodium falciparum. It is thought that cells infected with the parasite are cleared more rapidly by the spleen giving individuals with the G6PD deficiency gene an evolutionary advantage in malarial endemic environments. Other susceptible populations include Kurdish Jews, Sardinians, Nigerians, and Thai people.