Feel free to use our complete database with charts, tables and examples.
|Most common inherited enzyme deficiency affecting red blood cells. G6PD is a critical antioxidant—a deficiency can predispose to oxidation and subsequent hemolysis of the red blood cell.
Common oxidants include:
The degree of hemolysis induced by a drug may be accentuated by the presence of additional factors (infection or disease state etc).The severity of the reaction is dependent on the type of G6PD deficiency (Mediterranean deficiency-Caucasian (most severe) ; Blacks (usually mild to moderate). The sex of the patient is also important—males are at greater risk based on severity compared to females.
Conclusion: G6PD is not an absolute contraindication to the use of oxidizing agents. Decisions should be based on a risk vs benefit analysis (consider severity of disease; sex of patient; availability of other agents; type of deficiency). If therapy is initiated, the patient should be monitored closely for adverse effects. Patients with G6PD deficiency will exhibit signs within 1-3 days of initiation of treatment. Symptoms may include abdominal or back pain in severe cases. The urine of the patient will darken in color.
|1) Aderka D, Garfinkel D, Bograd H, Friedman J, Pinkhas J. Isosorbide dinitrate-induced hemolysis in G6PD-deficient subjects. Acta Haematol. 1983;69(1):63-4.
2) Beutler E. G6PD: population genetics and clinical manifestations. Blood Rev. 1996 Mar;10(1):45-52.
3) Eldad A, Neuman A, Weinberg A, Benmeir P, Rotem M, Wexler MR. Silver sulphadiazine-induced haemolytic anaemia in a glucose-6-phosphate dehydrogenase-deficient burn patient. Burns. 1991 Oct;17(5):430-2.
4) Grossman S, Budinsky R, Jollow D. Dapsone-induced hemolytic anemia: role of glucose-6-phosphate dehydrogenase in the hemolytic response of rat erythrocytes to N-hydroxydapsone. J Pharmacol Exp Ther. 1995 May;273(2):870-7.
5) Herman J, Ben-Meir S. Overt hemolysis in patients with glucose-6-phosphate dehydrogenase deficiency: a survey in general practice. Isr J Med Sci. 1975 Apr;11(4):340-6.
6) Hohl RJ, Kennedy EJ, Frischer H. Defenses against oxidation in human erythrocytes: role of glutathione reductase in the activation of glucose decarboxylation by hemolytic drugs. J Lab Clin Med. 1991 Apr;117(4):325-31.
7) Lavelle KJ, Atkinson KF, Kleit SA. Hyperlactatemia and hemolysis in G6PD deficiency after nitrofurantoin ingestion. Am J Med Sci. 1976 Sep-Oct;272(2):201-4.
8) Magon AM, Leipzig RM, Zannoni VG, Brewer GJ. Interactions of glucose-6-phosphate dehydrogenase deficiency with drug acetylation and hydroxylation reactions. J Lab Clin Med. 1981 Jun;97(6):764-70.
9) Myat-Phone-Kyaw, Myint-Oo, Aung-Naing, Aye-Lwin-Htwe. The use of primaquine in malaria infected patients with red cell glucose-6-phosphate dehydrogenase (G6PD) deficiency in Myanmar. Southeast Asian J Trop Med Public Health. 1994 Dec;25(4):710-3.
10) Reinke CM, Thomas JK, Graves AH. Apparent hemolysis in an AIDS patient receiving trimethoprim/sulfamethoxazole: case report and literature review. J Pharm Technol. 1996 Nov-Dec;11(6):256-62; quiz 293-5.
11) Tabbara IA. Related Articles Hemolytic anemias. Diagnosis and management. Med Clin North Am. 1992 May;76(3):649-68.
12) Vanella A, Campisi A, Castorina C, Sorrenti V, Attaguile G, Samperi P, Azzia N, Di Giacomo C, Schiliro G. Antioxidant enzymatic systems and oxidative stress in erythrocytes with G6PD deficiency: effect of deferoxamine. Pharmacol Res. 1991