Chloramphenicol Toxicity in Liver and Renal Disease

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Abstract
Erythropoietic depression can be detected in patients receiving chloramphenicol before any noticeable decrease occurs in peripheral blood values. Previous studies 1,2 have shown that an increase in serum iron content and an increased saturation of iron-binding globulin precedes the fall in hematocrit by an appreciable interval in patients exhibiting toxic effects. These changes have been correlated with prolonged plasma clearance (T/2) of radioactive iron (Fe59), delayed appearance of Fe59 in circulating erythrocytes, and decreased marrow uptake of Fe59 as detected by external scanning. Utilizing these techniques, it has been shown that erythropoietic depression due to chloramphenicol is more frequent than is generally realized. Early detection permits discontinuation of the drug before irreversible damage to the hematopoietic system occurs. The mechanism by which chloramphenicol produces erythropoietic depression is unknown. There is evidence that the nitrobenzene moiety may be important since replacement of the nitro group by a methylmercapto,