Document Detail


Glucuronidation of 3'-azido-3'-deoxythymidine (zidovudine) by human liver microsomes: relevance to clinical pharmacokinetic interactions with atovaquone, fluconazole, methadone, and valproic acid.
MedLine Citation:
PMID:  9660989     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Zidovudine (3'-azido-3'-deoxythymidine [AZT]), an antiviral nucleoside analog effective in the treatment of human immunodeficiency virus infection, is primarily metabolized to an inactive glucuronide form, GAZT, via uridine-5'-diphospho-glucuronosyltransferase (UGT) enzymes. UGT enzymes exist as different isoforms, each exhibiting substrate specificity. Published clinical studies have shown that atovaquone, fluconazole, methadone, and valproic acid decreased GAZT formation, presumably due to UGT inhibition. The effect of these drugs on AZT glucuronidation was assessed in vitro by using human hepatic microsomes to begin understanding in vitro-in vivo correlations for UGT metabolism. The concentrations of each drug studied were equal to those reported with the usual clinical doses and at concentrations at least 10 times higher than would be expected with these doses. High-performance liquid chromatography was used to assess the respective metabolism and formation of AZT and GAZT. All four drugs exhibited concentration-dependent inhibition of AZT glucuronidation. The respective concentrations of atovaquone and methadone which caused 50% inhibition of GAZT were > 100 and 8 micrograms/ml, well above their usual clinical concentrations. Fluconazole and valproic acid exhibited 50% inhibition of GAZT at 50 and 100 micrograms/ml, which are within the clinical ranges of 10 to 100 and 50 to 100 micrograms/ml, respectively. These data suggest that inhibition of AZT glucuronidation may be more clinically significant with concomitant fluconazole and valproic acid. Factors such as inter- and intraindividual pharmacokinetic variability and changes in AZT intracellular concentrations should be considered as other mechanisms responsible for changes in AZT pharmacokinetics with concomitant therapies.
Authors:
C B Trapnell; R W Klecker; C Jamis-Dow; J M Collins
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Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Antimicrobial agents and chemotherapy     Volume:  42     ISSN:  0066-4804     ISO Abbreviation:  Antimicrob. Agents Chemother.     Publication Date:  1998 Jul 
Date Detail:
Created Date:  1998-10-08     Completed Date:  1998-10-08     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  0315061     Medline TA:  Antimicrob Agents Chemother     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1592-6     Citation Subset:  IM; X    
Affiliation:
Center for Biologics Evaluation and Research, Food and Drug Administration, Rockville, Maryland 20852, USA. trapnelc@globomax.com
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MeSH Terms
Descriptor/Qualifier:
Anti-HIV Agents / metabolism*
Anticonvulsants / pharmacology
Antifungal Agents / pharmacology
Atovaquone
Drug Interactions
Fluconazole / pharmacology
Glucuronates / metabolism
Humans
Methadone / pharmacology
Microsomes, Liver / drug effects,  metabolism*
Naphthoquinones / pharmacology
Narcotics / pharmacology
Valproic Acid / pharmacology
Zidovudine / metabolism,  pharmacology*
Chemical
Reg. No./Substance:
0/Anti-HIV Agents; 0/Anticonvulsants; 0/Antifungal Agents; 0/Glucuronates; 0/Naphthoquinones; 0/Narcotics; 30516-87-1/Zidovudine; 76-99-3/Methadone; 86386-73-4/Fluconazole; 94015-53-9/Atovaquone; 99-66-1/Valproic Acid
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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