Kimberly D. Clay, MD, MPH; John S. Hanson, MD; Scott D. Pope, PharmD; Richard W. Rissmiller, MD; Preston P. Purdum, MD; Peter M. Banks, MD
Clay KD, Hanson JS, Pope SD, Rissmiller RW, Purdum PP, Banks PM. Brief Communication: Severe Hepatotoxicity of Telithromycin: Three Case Reports and Literature Review. Ann Intern Med. 2006;144:415-420. doi: 10.7326/0003-4819-144-6-200503210-00121
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Published: Ann Intern Med. 2006;144(6):415-420.
Telithromycin is the first ketolide antibacterial agent approved by the U.S. Food and Drug Administration. Physicians sometimes use it to treat common respiratory tract infections.
This brief report describes 3 previously healthy patients who developed severe hepatotoxicity within a few days of taking telithromycin. One patient required orthotopic liver transplantation, and 1 died.
The authors judged the cases as probably but not definitely related to telithromycin. Case reports cannot establish how often telithromycin-related severe hepatotoxicity occurs.
Telithromycin should be used cautiously pending further postmarketing surveillance data.
The liver is only about one third of the normal size (480 g) and consists predominantly of diffuse collapse. Islands of surviving intact lobular parenchyma consist of regenerative nodules ( ).
A conventional hematoxylin–eosin stain shows only rare islands of surviving regenerative lobular cellularity ( ). (Original magnification, ×5.) Reticulin silver staining demonstrates dense condensation of fibers surrounding persisting ducts without any intervening lobules, except in the regenerative nodule ( ). (Original magnification, × 5.) Immunohistochemical stain for cytokeratin cocktail AE1/AE3 highlights the dense aggregates of ducts ( ) uninterrupted by lobular elements. (Original magnification, ×5.)
The figure shows total lobular necrosis, with pink hepatocytes lacking nuclei ( ). Portal triads are densely infiltrated by lymphoid cells. (Hematoxylin–eosin; original magnification, ×10).
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Emergency Medicine, Gastroenterology/Hepatology, Liver Disease.
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