Chloramphenicol is a bacteriostatic agent that binds to the 50 S ribosome of bacteria and inhibits protein synthesis. Despite broad antimicrobial activity, chloramphenicol is rarely used in the United States secondary to potential adverse effects at therapeutic doses. Chloramphenicol may result in hypersensitivity reactions, neurologic abnormalities, and hematologic toxicity. The most notorious is a symptom complex of vomiting, poor sucking, cyanosis, and diarrhea in neonates and children. The syndrome (gray baby syndrome) is seen after several days of high-dose chloramphenicol administration and often progresses to obtundation, palor, hypotension, hypothermia, and death. The toxicity of chloramphenicol in neonates is believed to result from inability to metabolize the drug.

Chloramphenicol is responsible for two types of hematologic toxicity: the most common is reversible myelosuppression, and the second is aplastic anemia. Reversible bone marrow suppression appears to be related to mitochondria injury in bone marrow. This inhibition is reversed with cessation of use of the drug. Aplastic anemia is a rare complication, occurring in from 1:24,000 to 1:40,500 recipients of the drug. The mechanism of toxicity is hypothesized to be a toxic metabolite resulting in stem cell damage.15 Aplastic anemia with chloramphenicol is not dose related and does not typically resolve with cessation of the drug.

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