Chest ACCP Member Benefits
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nolan, C. M.
Right arrow Articles by Nelson, S. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nolan, C. M.
Right arrow Articles by Nelson, S. D.

Chest, Vol 105, 408-411, Copyright © 1994 by American College of Chest Physicians


ARTICLES

Hepatotoxicity associated with acetaminophen usage in patients receiving multiple drug therapy for tuberculosis

CM Nolan, RE Sandblom, KE Thummel, JT Slattery and SD Nelson
Tuberculosis Control Program, Seattle-King County, Department of Public Health, Seattle.

We report three patients who experienced hepatotoxic reactions in association with acetaminophen ingestion while undergoing treatment for active tuberculosis with isoniazid, rifampin, and other agents. All were young adult women. One patient intentionally took a large amount of acetaminophen and had typical signs and symptoms of acetaminophen overdosage; another took acetaminophen in combination form for a minor upper respiratory illness. She experienced no symptoms. The remaining patient took acetaminophen to ameliorate the symptoms of fever and malaise that were subsequently attributed to tuberculosis. She had the rapid onset of signs and symptoms of isoniazid hepatotoxicity. The patterns of liver function abnormalities were similar: each patient experienced pronounced serum elevations of hepatocellular enzymes with at most only modest rises in those of bilirubin. All antituberculous drugs were withheld until symptoms resolved and laboratory values became normal; then treatment for tuberculosis was resumed without isoniazid and was successfully completed in all three patients. These cases plus similar reports in the literature suggest that isoniazid or rifampin, or both, may potentiate the hepatotoxicity of acetaminophen, perhaps by induction of cytochrome P450 isozymes that oxidize acetaminophen to its toxic metabolites.


This article has been cited by other articles:


Home page
PediatricsHome page
Committee on Drugs
Acetaminophen Toxicity in Children
Pediatrics, October 1, 2001; 108(4): 1020 - 1024.
[Abstract] [Full Text] [PDF]


Home page
Antimicrob. Agents Chemother.Home page
Z. Desta, N. V. Soukhova, and D. A. Flockhart
Inhibition of Cytochrome P450 (CYP450) Isoforms by Isoniazid: Potent Inhibition of CYP2C19 and CYP3A
Antimicrob. Agents Chemother., February 1, 2001; 45(2): 382 - 392.
[Abstract] [Full Text]


Home page
Clin. Chem.Home page
S. White and S. H. Y. Wong
Standards of laboratory practice: analgesic drug monitoring
Clin. Chem., May 1, 1998; 44(5): 1110 - 1123.
[Abstract] [Full Text] [PDF]


Home page
Clin. Chem.Home page
M. G. Sturgill and G. H. Lambert
Xenobiotic-induced hepatotoxicity: mechanisms of liver injury and methods of monitoring hepatic function
Clin. Chem., August 1, 1997; 43(8): 1512 - 1526.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1994 by the American College of Chest Physicians.