Glucose-6-phosphate Dehydrogenase Deficiency: A Case Report

Abstract

Abstract:Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common hereditary enzyme disorder and more than 200 million people have a deficiency in this enzyme. G6PD deficiency is an X-linked enzyme defect, and one of its main signs is the presence of hemolytic anemia. It is a worldwide important cause of neonatal jaundice and causes life threatening hemolytic crisis in childhood. At later ages, certain drugs such as anti-malarial drugs and fava beans cause hemolysis among G6PD deficiency patients. The frequency and severity is influenced by genetic and cultural factors. It is common in Mediterranean, African and some East Asian populations but rare in Bangladeshi peoples. Genetic counseling may be of benefit for patients and their families. Other treatment is symptomatic and supportive.

Cell and Gene Therapy for Anemia: Hematopoietic Stem Cells and Gene Editing

“…Therefore, the optimal management for G6PD deficiency is the avoidance of substances that can trigger hemolysis, although this strategy is not feasible in parasitic endemic areas in certain regions. G6PD deficiency affects more than 400 million people worldwide [78][79][80]. A deficiency that occurs secondary to the mutation of the G6PD gene on the X chromosome was discovered in the 1950s, when American soldiers experienced acute hemolytic anemia due to antimalarial treatment; this deficiency is known as primaquine sensitivity syndrome [81,82].…”