JCHOR

The Journal of Current Hematology & Oncology Research regularly publishes internationally qualified research in hematology and oncology within the current scholarly knowledge. This journal is indexed by indices that are considered international scientific journal indices (DRJI, ESJI, OAJI, etc.). According to the current Associate Professorship criteria, it is within the scope of International Article 1-d. Each article published in this journal corresponds to 5 points.

EndNote Style
Index
Case Report
A case of dapsone-induced hemolytic anemia related to G6PD enzyme deficiency
Hemolytic anemia is characterized by a decrease in the number of circulating erythrocytes due to an increase in their hemolysis. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common erythrocyte enzyme defects related to hemolysis. The G6PD enzyme abrogates the hemolysis of erythrocytes by protecting them against oxidative stress due to its involvement in the glutathione metabolism. G6PD enzyme deficiency-related hemolytic anemia may present as neonatal jaundice or become manifest due to exposure to infections, favism and medications later in life. Dapsone is a medication that is preferred by doctors in the treatment of many dermatological disorders such as pemphigus vulgaris, and leads to hemolysis in the presence of G6PD enzyme deficiency. In this type of non-immune hemolysis, haptoglobulin is low and Coombs' tests are negative. Hemolytic anemia, a serious complication that may appear subsequent to dapsone use, can be prevented by testing G6PD enzyme levels prior to dapsone therapy. In this case, we emphasized that the hemolytic anemia in the patient using dapsone may be due to G6PD enzyme deficiency.


1. Lee GR, Foerster J, Lukens J, Paraskevas F, Greer JP, Rodgers GM,Eds. Wintrobe’s Clinical Hematology. 10th edition. Mass PublishingCo.1999;17(2):84-91.
2. Reclos GJ, Hatzidakis CJ, Schulpis KH. Glucose-6-phosphatedehydrogenase deficiency neonatal screening: preliminary evidencethat a high percentage of partially deficient female neonates are missedduring routine screening. J Med Screen. 2000;7(1):46-51. doi:10.1136/jms.7.1.46
3. Saunders WB. Glucose-6-phosphate dehydrogenase deficiency andhemolytic anemia. Kın: Nathan DG, Orkin SH, eds. Nathan and ASKİHematolog of Infancy and Childhood. 7th ed. Philadelphia; 2009. p.883-900.
4. Beutler E. Glucose-6-phosphate dehydrogenase deficiency: a historicalperspective. Blood. 2008;111(1):16-24. doi:10.1182/blood-2007-04-077412
5. Glucose-6-phosphate dehydrogenase deficiency and hemolytic anemia.In: Nathan DG, Orkin SH, eds. Nathan and Oski’s hematology ofinfancy and childhood. 7th ed. Philadelphia: W. B. Saunders; 2009.p.883-900.
6. Glader BE. Glucose-6-phosphate dehydrogenase deficiency and relateddisorders of hexose monophosphate shunt and glutathione metabolism.In: Wintrobe’s clinical hematology. 10th ed. Baltimore: Williams &Wilkins; 2008.p. 1176-90.
7. Ashurst JV, Wasson MN, Hauger W, Fritz WT. Pathophysiologicmechanisms, diagnosis, and management of dapsone-inducedmethemoglobinemia. J Am Osteopath Assoc. 2010;110(1):16-20.
8. Lechner K, Jäger U. How I treat autoimmune hemolytic anemias inadults. Blood. 2010;116(11):1831-1838. doi:10.1182/blood-2010-03-259325
9. Büyükokuroğlu ME, Süleyman H. Glukoz 6-fosfat dehidrogenazeksikliği. Turkiye Klinikleri J Med Sci. 2001;(21): 415-419.
10. Garratty G. Immune hemolytic anemia associated with drug therapy.Blood Rev. 2010;24(4-5):143-150. doi:10.1016/j.blre.2010.06.004
Volume 1, Issue 1, 2023
Page : 15-17
_Footer