Abstract
THE major toxic effect of chloramphenicol is the production of bone-marrow arrest and aplastic anemia. Early in the development of chloramphenicol toxicity, vacuoles appear in the erythroid and myeloid precursors of the bone marrow.1 2 3 4 The relation of these early, reversible lesions to later, more serious bone-marrow depression is unknown. Similar cytoplasmic vacuoles in the erythrogones have been reported in erythremic myelosis (Di Guglielmo's syndrome) and acute alcoholism, and in normal infants as well as those with phenylketonuria receiving a phenylalanine-deficient diet.5 6 7 8 The lesions in the infants receiving such diets were reversed by the addition of phenylalanine. Therefore, an attempt was . . .
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