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A 1981 View

Dieter W. Gump, MD

Arch Intern Med. 1981;141(5):573-574.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

After chloramphenicol was marketed in 1949, its broad spectrum of activity and therapeutic efficacy were quickly appreciated and led to widespread use. However, from 1950 to 1952, numerous reports appeared suggesting a causal relationship between its use and the development of aplastic anemia and pancytopenia. In 1955, Krakoff et al¹ showed that large dosages (6 to 12 g/day) of chloramphenicol led to a disappearance of reticulocytes and anemia in all four patients to whom they administered the drug and vacuolation of erythrocyte precursors and a reversible pancytopenia in one of these patients. Subsequently, it became clear that chloramphenicol somtimes caused a dose-related depression of bone marrow function in patients who received the drug. Rarely, an idiosyncratic aplasia of the marrow occurred.² The former is reversible, whereas the latter is usually fatal. Other than bone marrow toxicity, chloramphenicol has been shown to cause the gray baby syndrome,³ depression . . . [Full Text PDF of this Article]

Author Affiliations
Infectious Disease Unit University of Vermont College of Medicine Burlington, VT 05405

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