This review is limited to a discussion on the pathogenesis of chloramphenicol (CAP) toxicity. Classification of hematologic toxicity from CAP into two types with distinct clinical features was suggested from a detailed analysis of a large number of cases of incidental CAP toxicity collected from the literature. Current evidence has reinforced the validity of this classification and supports the concept of a lack of relationship between reversible erythroid suppression and aplastic anemia from CAP. Ample data are available to indicate that reversible bone marrow suppression from CAP is a pharmacologic effect and results from inhibition of mitochondrial protein synthesis and consequent mitochondrial injury. Although some evidence has been provided to suggest that bone marrow aplasia occurs on the basis of a genetically determined biochemical predisposition involving the pathway of DNA synthesis, this concept cannot be considered conclusive at present. The difference in the inhibitory capacity of CAP and thiamphenicol (TAP) on DNA synthesis is of considerable interest, but its significance awaits definitive clinical data on TAP and more experimental work on the various CAP analogues. Whether the impression that TAP does not cause bone marrow aplasia will be confirmed from clinical studies now in progress remains to be seen.
|Original language||English (US)|
|Number of pages||10|
|Journal||Seminars in Hematology|
|State||Published - Dec 1 1973|
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