Physiologic Basis
G6PD is an enzyme in the hexose monophosphate shunt that is essential in generating reduced glutathione and NADPH, which protect hemoglobin from oxidative denaturation. Inherited G6PD deficiency causes neonatal hyperbilirubinemia and chronic hemolytic anemia and exposure to oxidative stressors such as certain drugs or infection, can elicit significant acute hemolysis.
Interpretation
Increased in: Young erythrocytes (reticulocytosis)
Decreased in: G6PD deficiency
Causes of hemolysis in glucose-6- phosphate dehydrogenase deficiency
1. Bacterial and viral infections
2. Drugs:
• Antimalarials: Primaquine, pamaquine
• Antibacterials: Sulfonamides, nalidixic acid, nitrofurantoin, dapsone
• Antipyretics and analgesics
3. Chemicals: Naphthalene balls
Comments
In deficient patients, hemolytic anemia can be triggered by oxidant agents: antimalarial drugs (eg, chloroquine), nalidixic acid, nitrofurantoin, dapsone, phenacetin, vitamin C, and some sulfonamides. Patients from high-risk groups (eg, African American and people from the Mediterranean region) should be screened for G6PD deficiency before taking an oxidant drug. Hemolytic episodes can also occur in deficient patients who eat fava beans (favism), in patients with diabetic acidosis, and in infections. G6PD deficiency may be the cause of hemolytic disease of newborns in Asians and Mediterraneans.
G6PD activity levels may be measured as normal during an acute episode, because only non-hemolyzed young red cells are assessed. If deficiency is still suspected, assay should be repeated in 2–3 months when cells of all ages are present.
Glucose-6-phosphate dehydrogenase report format
( with interpretation )This delves deep into the ideal glucose-6-phosphate dehydrogenase report format with best practices designed for lab owners and technicians. You can download the glucose-6-phosphate dehydrogenase report in MS Word format or create it online.
