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Chloramphenicol Toxicity in Liver and Renal Disease
LEIF G. SUHRLAND, MD;
AUSTIN S. WEISBERGER, MD
Arch Intern Med. 1963;112(5):747-754.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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Erythropoietic depression can be detected in patients receiving chloramphenicol before any noticeable decrease occurs in peripheral blood values. Previous studies 1,2 have shown that an increase in serum iron content and an increased saturation of iron-binding globulin precedes the fall in hematocrit by an appreciable interval in patients exhibiting toxic effects. These changes have been correlated with prolonged plasma clearance (T/2) of radioactive iron (Fe59), delayed appearance of Fe59 in circulating erythrocytes, and decreased marrow uptake of Fe59 as detected by external scanning. Utilizing these techniques, it has been shown that erythropoietic depression due to chloramphenicol is more frequent than is generally realized. Early detection permits discontinuation of the drug before irreversible damage to the hematopoietic system occurs.
The mechanism by which chloramphenicol produces erythropoietic depression is unknown. There is evidence that the nitrobenzene moiety may be important since replacement of the nitro group by a methylmercapto,
. . . [Full Text PDF of this Article]
Author Affiliations
CLEVELAND
Assistant Professor of Medicine (Dr. Suhrland); Professor of Medicine (Dr. Weisberger).
From the departments of medicine of Highland View Hospital and the University Hospitals of Cleveland, and from the School of Medicine, Western Reserve University.
Footnotes
Received for publication April 12, 1963; accepted May 10.
Presented in part at 44th annual session of the American College of Physicians, April, 1963.
Supported by USPHS grant He 03952-05.
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