They also discuss the pathobiology of bilirubin-induced neurotoxicity, the clinical diagnosis and outcome of kernicterus, the contributions of hemolytic disease and glucose-6-phosphate dehydrogenase deficiency to hyperbilirubinemia, and risk assessment and treatment with phototherapy and other inherited disorder characterized by red cells partially or completely deficient in G6PD, an enzyme critical in aerobic glycolysis.

Glucose-6-phosphate dehydrogenase (G6PD) is a red blood cell (RBC) enzyme.

It is involved in the hexose monophosphate shunt, and its function is to protect hemoglobin from oxidation.

G6PD deficiency is an inherited X-linked abnormality; approximately 20% of female carriers are heterozygous.

This deficiency results in hemolysis of varying degrees and acuity depending on the severity of the abnormality.

The anemia that results is a nonspherocytic hemolytic anemia.

See also congenital nonspherocytic hemolytic anemia, favism.

a blood test to diagnose G6PD deficiency in suspected individuals.

Deficiency of this enzyme causes precipitation of hemoglobin and cellular membrane changes, possibly resulting in hemolysis of variable severity, a sex-linked trait carried on the X chromosome.

There are three G6PD variants of high frequency in different ethnic groups.

G6PD A–is more common in African Americans (10% of males) than in other populations.

G6PD Mediterranean is especially common in Iraqis, Kurds, Sephardic Jews, and Lebanese and less common in Greeks, Italians, Turks, North Africans, Spaniards, Portuguese, and Ashkenazi Jews.