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Effect of Race/Ethnicity and Genes on Acetaminophen Pharmacokinetics

The recruitment status of this study is unknown because the information has not been verified recently.
Verified October 2008 by Tufts University.
Recruitment status was  Recruiting
Sponsor:
Collaborator:
Information provided by:
Tufts University
ClinicalTrials.gov Identifier:
NCT00768716
First received: October 7, 2008
Last updated: NA
Last verified: October 2008
History: No changes posted

October 7, 2008
October 7, 2008
September 2008
December 2010   (final data collection date for primary outcome measure)
Acetaminophen plasma levels [ Time Frame: 2 days ] [ Designated as safety issue: No ]
Same as current
No Changes Posted
Acetaminophen metabolite levels [ Time Frame: 2 days ] [ Designated as safety issue: No ]
Same as current
Not Provided
Not Provided
 
Effect of Race/Ethnicity and Genes on Acetaminophen Pharmacokinetics
Effect of Race/Ethnicity and Genes on Acetaminophen Pharmacokinetics

Although acetaminophen is the most commonly used nonprescription drug in the USA, little is known regarding the influence of genes and race/ethnicity on acetaminophen disposition. The investigators long-term goal is to understand the causes of differences in acetaminophen disposition between people that are the result of genetic variation and ethnicity and may predispose individuals to a higher risk of acetaminophen hepatotoxicity. The aim of this particular study is to measure the rate of elimination of acetaminophen via the 3 main pathways (glucuronidation, sulfation and oxidation) in self-identified White-Americans (n=100) and African-Americans (n=100). These rates will then be correlated with selected genetic polymorphisms in genes encoding enzymes involved in acetaminophen metabolism. Two main hypotheses will be tested: 1. African-Americans eliminate acetaminophen more rapidly by glucuronidation than do White-Americans. 2. Elimination via glucuronidation, sulfation, and oxidation in subjects will be significantly correlated with the presence of polymorphisms in the UGT1A6, SULT1A1, and CYP2E1 genes, respectively.

Not Provided
Interventional
Phase 4
Allocation: Non-Randomized
Endpoint Classification: Pharmacokinetics Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Basic Science
  • Pain
  • Fever
  • Hepatotoxicity
Drug: Acetaminophen
2 x 500 mg oral once
  • Experimental: White subjects
    Intervention: Drug: Acetaminophen
  • Experimental: Black subjects
    Intervention: Drug: Acetaminophen

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
200
April 2011
December 2010   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • self-declared white/Caucasian
  • self-declared African-American
  • active
  • ambulatory
  • no evidence of medical disease

Exclusion Criteria:

  • alcohol use of 3 or more drinks per day
  • HIV or hepatitis (B or C) infection
  • isoniazid
  • disulfiram
  • phenobarbital
  • phenytoin
  • carbamazepine
  • rifampicin
  • valproic acid
  • probenecid
  • St. John's Wort
Both
18 Years to 64 Years
Yes
Contact: Gina Masse 617-636-2192 gina.masse@tufts.edu
United States
 
NCT00768716
8600, GM061834
No
Dr Michael H. Court, Tufts University
Tufts University
National Institute of General Medical Sciences (NIGMS)
Principal Investigator: Michael H Court, BVSc, PhD Tufts University
Tufts University
October 2008

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP