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How can certain drugs trigger red blood cell destruction in people with glucose-6-phosphate dehydrogenase deficiency?

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blood disease Peripheral blood smear revealing histopathologic features indicative of a blast crisis in a case of chronic myelogenous leukemia (CML). Blast crisis occurs when one-fifth to one-third of the cells in the blood or bone marrow are immature blood cells, or blast cells. This phase of CML is characterized by fever, weakness, and an enlarged spleen.

In individuals with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, red blood cell destruction occurs because the deficiency impairs the pentose phosphate pathway, which is essential for protecting cells against oxidative stress.12

Normally, the enzyme G-6-PD helps generate substances that prevent the oxidative destruction of the red blood cell membrane. When a person with this deficiency takes certain drugs—such as sulfonamides or antimalarial compounds like primaquine—these substances are converted within the body into oxidant compounds. Because the affected red blood cells lack sufficient G-6-PD activity to neutralize these oxidants, the cell membranes become vulnerable to oxidative damage, leading to hemolysis, or the premature destruction of red blood cells.12