Chloramphenicol, Acute Leukemia and Chromosomal Vacuolizations

Ko, Goh

doi:10.1097/00007611-197107000-00008

Cited by 7 publications

(2 citation statements)

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“…One type, usually reversible upon discontinuation of the drug, is dose-related and is characterized by anemia and a normocellular marrow. Examination of bone marrow cells in two cases of ANLL presumed to have been caused by chloramphenicol ingestion has revealed abnormal chromosome morphology (124) and an abnormal karyotype with a large telocentric marker chromosome (125) Wallenstein et al (120) have estimated that the risk of developing blood disorders after chloramphenicol treatment lies somewhere between 1 in 24,500 and 1 in 40,800.…”

Section: Chloramphenicolmentioning

confidence: 99%

Chemically Induced Leukemia in Humans

Adamson¹,

Seiber²

1981

Environmental Health Perspectives

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JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.The human population may be exposed to potentially leukemogenic agents, either in the form of drugs and food additives or as environmental contaminants and pollutants. However, in spite of the large number and diversity of these chemicals, only a few have been implicated as human leukemogens. One such agent is benzene, a known bone marrow depressant. A number of case reports have associated chronic exposure to this agent with the development of acute leukemia, as have several epidemiologic surveys. Treatment with various antitumor agents, including procarbazine, melphalan, thio-TEPA, chlorambucil, and cyclophosphamide, has also been associated with the development of acute leukemia. In addition, chloramphenicol and phenylbutazone have been implicated as human leukemogens, but the association between exposure to these two agents and acute leukemia appears at present to be weaker than it is for benzene and antitumor agent exposure. Despite such associations between exposure to chemicals and acute leukemia, several important problems exist with regard to implicating specific agents in the development of this neoplasm in man, including the paucity of animal models for chemically induced leukemia, and the frequent necessity to rely on single case reports or clusters of cases in which chemical exposures are associated with acute leukemia. Future efforts should be directed at performing properly designed and well executed epidemiologic studies, and at developing new in vitro and in vivo models for the study of this neoplasm.

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Section: Chloramphenicolmentioning

confidence: 99%

Chemically Induced Leukemia in Humans

Adamson¹,

Seiber²

1981

Environmental Health Perspectives

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“…In contrast chloramphenicol(CAP)-induced bone marrow aplasia rarely constitutes a preleukemic state evolv ing into acute leukemia. Since Brauer and Dameshek [2] described the appearance of ANLL following aplastic anemia after CAP therapy in 1967, a small number of similar cases have been published [3][4][5][6][7]10], indi cating a low incidence of this complication. We report an additional case, in which a re lation of CAP to secondary leukemia must be taken into consideration.…”

mentioning

confidence: 99%