Chloramphenicol toxicity

25 years of research.

Adel A Yunis

Research output: Contribution to journalArticle

96 Citations (Scopus)

Abstract

Significant progress has been made in recent years in the understanding of the pathogenesis of the two types of hematologic toxicity from chloramphenicol. The common, dose-dependent, reversible bone marrow suppression from chloramphenicol is a consequence of mitochondrial injury. The greater erythroid susceptibility to chloramphenicol appears to be a function of the endogenous mitochondrial amino acid pools. The pathogenesis of aplastic anemia from chloramphenicol treatment remains uncertain. A large body of indirect evidence favors a complex mechanism involving metabolic transformation of the p-NO2 group of chloramphenicol by the predisposed subject, leading to the production of a toxic intermediate causing stem cell damage. A concept is presented wherein metabolites of chloramphenicol generated by intestinal bacteria undergo further metabolic transformation in the bone marrow with in situ production of toxic intermediate. This concept of the marrow being both the metabolic site for the offending agent as well as the target for its toxic metabolites will likely apply to other potential myelotoxins.

Original languageEnglish (US)
JournalAmerican Journal of Medicine
Volume87
Issue number3 N
StatePublished - Sep 1989

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Chloramphenicol
Poisons
Research
Bone Marrow
Aplastic Anemia
Stem Cells
Bacteria
Amino Acids
Wounds and Injuries

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Chloramphenicol toxicity : 25 years of research. / Yunis, Adel A.

In: American Journal of Medicine, Vol. 87, No. 3 N, 09.1989.

Research output: Contribution to journalArticle

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