The discovery that primaquine caused hemolytic anemia in persons with glucose-6-phosphate dehydrogenase (G-6-PD) deficient red blood cells provided much impetus to the new discipine of pharmacogenetics. Not only did this discovery and an important widespread X-chromosome-linked inborn error of metabolism to the known list of genetically determined drug-provoked idiosyncratic responses, but it exposed the metabolic error as the culprit responsible for obscure hemolytic reactions to a variety of provocations. These include drugs, such as phenacetin, aspirin, and probenecid; edibles, such as fava beans; bacterial and viral infections and metabolic disturbances, such as ketoacidosis. The discovery also gave rise to speculation about the possible beneficial role of the responsible gene mutation in protecting the heterozygotes from falciparum malaria.
Much interest is currently centered on the role of G-6-PD deficiency in hemolytic anemia complicating viral hepatitis. The occurrence of this complication has been known for some time, but its association with G-6-PD