The commonest manifestations of G6PD deficiency, neonatal jaundice and acute hemolytic anemia, are largely preventable or controllable by screening, surveillance and avoidance of triggering factors, particularly fava beans, by G6PD-deficient subjects. When a patient presents with acute hemolytic anemia, and once the cause is diagnosed, no specific treatment may be needed if the episode is mild. At the other end of the spectrum, and especially in children, acute hemolytic anemia may be a medical emergency requiring immediate blood transfusion. The management of neonatal jaundice does not differ from that of neonatal jaundice due to causes other than G6PD deficiency and, in order to prevent neurological damage, treatment with phototherapy and/or exchange blood transfusion may be required. The management of CNSHA is similar to that of CNSHA due to glycolytic enzymopathies, but in addition it is important to avoid exposure to potentially hemolytic drugs. Again, although there is no evidence of selective red cell destruction in the spleen (as seen in hereditary spherocytosis), splenectomy has proven beneficial in severe cases.

Recently, life-long expression of human G6PD at therapeutic levels has been obtained in red blood cells and in white blood cells of mice through retroviral-mediated transfer into hematopoietic stem cells.

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