Pharmacokinetics of isoniazid: The good, the bad, and the alternatives

Emily R. Erwin, Angela P. Addison, Sarah Finney John, Omonike Arike Olaleye, Rosemarie C. Rosell

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

Although isoniazid (INH) has been successful in treating Tuberculosis (TB) since its introduction in 1952, there has been continual reports of drug-associated hepatotoxicity in TB patients. These toxic side effects may reveal more about the recipient of the drug, than the drug itself. A combination of pharmacogenetic and pharmacokinetic studies have identified polymorphisms within enzymes involved in INH metabolism and detoxification. These essential metabolic enzymes include N-acetyltransferase 2, Cytochrome P450 2E1, and glutathione S transferases. Different phenotypes of these enzymes can affect the rate of INH metabolism, resulting in production of hepatotoxic metabolites. This review is intended to elucidate the pharmacokinetics of INH by examining its Administration, Distribution, Metabolism, and Elimination, while suggesting potential alternatives within INH personalized treatment to help reduce hepatotoxicity.

Original languageEnglish (US)
Pages (from-to)S66-S70
JournalTuberculosis
Volume116
DOIs
StatePublished - May 2019

Keywords

  • Hepatotoxicity
  • Isoniazid
  • Isoniazid metabolism
  • Pharmacokinetics
  • Tuberculosis

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases

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