TY - JOUR
T1 - Pharmacokinetics of isoniazid
T2 - The good, the bad, and the alternatives
AU - Erwin, Emily R.
AU - Addison, Angela P.
AU - John, Sarah Finney
AU - Olaleye, Omonike Arike
AU - Rosell, Rosemarie C.
N1 - Funding Information:
This work was supported by the U.S. DOE, Hispanic-Serving Institutions, STEM Articulation Grant P031C110128, Gulf Coast Consortium/Welch Foundation Computational Chemistry Research Group R-11-0059 under Prime Award H-E-0035, National Institute on Minority Health and Health Disparities of the National Institute of Health under Award Number 5G12MD007605, Cullen-Smith Foundation, and the University of Saint Thomas Biology Department.Publication of this supplement was supported by The University of Texas Health Science Center at Houston.This work was presented in part at the Texas Tuberculosis Research Symposium (TTRS) 2018, El Paso, Texas, USA, sponsored by the Texas Tech University Health Sciences Center El Paso.
Funding Information:
This work was presented in part at the Texas Tuberculosis Research Symposium (TTRS) 2018, El Paso, Texas, USA, sponsored by the Texas Tech University Health Sciences Center El Paso .
Funding Information:
This work was supported by the U.S. DOE, Hispanic-Serving Institutions , STEM Articulation Grant P031C110128 , Gulf Coast Consortium/Welch Foundation Computational Chemistry Research Group R-11-0059 under Prime Award H-E-0035 , National Institute on Minority Health and Health Disparities of the National Institute of Health under Award Number 5G12MD007605 , Cullen-Smith Foundation, and the University of Saint Thomas Biology Department .
Funding Information:
This work was supported by the U.S. DOE, Hispanic-Serving Institutions, STEM Articulation Grant P031C110128, Gulf Coast Consortium/Welch Foundation Computational Chemistry Research Group R-11-0059 under Prime Award H-E-0035, National Institute on Minority Health and Health Disparities of the National Institute of Health under Award Number 5G12MD007605, Cullen-Smith Foundation, and the University of Saint Thomas Biology Department.Each article needs to have a financial disclosure line, usually within the author bio section. Publication of this supplement was supported by The University of Texas Health Science Center at Houston.This work was presented in part at the Texas Tuberculosis Research Symposium (TTRS) 2018, El Paso, Texas, USA, sponsored by the Texas Tech University Health Sciences Center El Paso.
Funding Information:
Each article needs to have a financial disclosure line, usually within the author bio section. Publication of this supplement was supported by The University of Texas Health Science Center at Houston .
Publisher Copyright:
© 2019 Elsevier Ltd
PY - 2019/5
Y1 - 2019/5
N2 - 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.
AB - 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.
KW - Hepatotoxicity
KW - Isoniazid
KW - Isoniazid metabolism
KW - Pharmacokinetics
KW - Tuberculosis
UR - http://www.scopus.com/inward/record.url?scp=85065140629&partnerID=8YFLogxK
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U2 - 10.1016/j.tube.2019.04.012
DO - 10.1016/j.tube.2019.04.012
M3 - Article
C2 - 31076322
AN - SCOPUS:85065140629
SN - 1472-9792
VL - 116
SP - S66-S70
JO - Tuberculosis
JF - Tuberculosis
ER -