Mechanism:
(1) Glutathione reductase is required to maintain adequate levels of reduced glutathione for red cell metabolism.
(2) Carmustine can bind at the active site of the gluathione reductase within red blood cells, resulting in a complete and irreversible inhibition of the enzyme. The inhibition lasts for the lifespan of the red blood cell. .
(3) An oxidative stress may exhaust the erythrocyte's store of reduced glutathione, and may be followed by hemolysis.
Clinical features:
(1) history of chemotherapy with carmustine
(2) subsequent therapy with an oxidative drug results in a hemolytic anemia
The hemolytic anemia may resemble that seen with G6PD deficiency. The oxidative drugs that cause the hemolysis should be the same (sulfonamides, other antibiotics, antimalarials, acetaminophen or salicylates, and high doses of vitamin C).
The hemolytic anemia may be severe if the exposure to the oxidative drug is soon after carmustine therapy since most erythrocytes would be affected. With time the percent of affected cells is smaller and the hemolytic anemia is less severe.
