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Article
April 1981

ChloramphenicolA 1981 View

Author Affiliations

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

Arch Intern Med. 1981;141(5):573-574. doi:10.1001/archinte.1981.00340050025007
Abstract

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

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