Effects of genetic variability on rifampicin and isoniazid pharmacokinetics in South African patients with recurrent tuberculosis.


Journal

Pharmacogenomics
ISSN: 1744-8042
Titre abrégé: Pharmacogenomics
Pays: England
ID NLM: 100897350

Informations de publication

Date de publication:
03 2019
Historique:
pubmed: 16 2 2019
medline: 19 3 2020
entrez: 16 2 2019
Statut: ppublish

Résumé

We report the prevalence and effect of genetic variability on pharmacokinetic parameters of isoniazid and rifampicin. Genotypes for SLCO1B1, NAT2, PXR, ABCB1 and UGT1A genes were determined using a TaqMan Among 172 patients, 18, 43 and 34% were classified as rapid, intermediate and slow NAT2 acetylators, respectively. Of the 58 patients contributing drug concentrations, rapid and intermediate acetylators had 2.3- and 1.6-times faster isoniazid clearance than slow acetylators. No association was observed between rifampicin pharmacokinetics and SLCO1B1, ABCB1, UGT1A or PXR genotypes. Clinical relevance of the effects of genetic variation on isoniazid concentrations and low first-line tuberculosis drug exposures observed require further investigation.

Identifiants

pubmed: 30767706
doi: 10.2217/pgs-2018-0166
pmc: PMC6562923
doi:

Substances chimiques

ABCB1 protein, human 0
ATP Binding Cassette Transporter, Subfamily B 0
Liver-Specific Organic Anion Transporter 1 0
SLCO1B1 protein, human 0
Arylamine N-Acetyltransferase EC 2.3.1.5
NAT2 protein, human EC 2.3.1.5
UGT1A1 enzyme EC 2.4.1.-
Glucuronosyltransferase EC 2.4.1.17
Isoniazid V83O1VOZ8L
Rifampin VJT6J7R4TR

Banques de données

ClinicalTrials.gov
['NCT02114684']

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

225-240

Subventions

Organisme : Wellcome Trust
ID : 206379/Z/17/Z
Pays : United Kingdom

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Auteurs

Anushka Naidoo (A)

Centre for the AIDS Programme of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa.

Maxwell Chirehwa (M)

Division of Clinical Pharmacology, Department of Medicine, University of Cape Town, Cape Town, South Africa.

Veron Ramsuran (V)

Centre for the AIDS Programme of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa.
KwaZulu-Natal Research Innovation & Sequencing Platform (KRISP), School of Laboratory Medicine & Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.

Helen McIlleron (H)

Division of Clinical Pharmacology, Department of Medicine, University of Cape Town, Cape Town, South Africa.

Kogieleum Naidoo (K)

Centre for the AIDS Programme of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa.
MRC-CAPRISA HIV-TB Pathogenesis & Treatment Research Unit, Doris Duke Medical Research Institute, University of KwaZulu-Natal, Durban, South Africa.

Nonhlanhla Yende-Zuma (N)

Centre for the AIDS Programme of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa.

Ravesh Singh (R)

Department of Microbiology, National Health Laboratory Services, KZN Academic Complex, Inkosi Albert Luthuli Central Hospital, Durban, South Africa.

Sinaye Ncgapu (S)

Centre for the AIDS Programme of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa.

John Adamson (J)

Pharmacology Core, Africa Health Research Institute (AHRI), Durban, South Africa.

Katya Govender (K)

Pharmacology Core, Africa Health Research Institute (AHRI), Durban, South Africa.

Paolo Denti (P)

Division of Clinical Pharmacology, Department of Medicine, University of Cape Town, Cape Town, South Africa.

Nesri Padayatchi (N)

Centre for the AIDS Programme of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa.
MRC-CAPRISA HIV-TB Pathogenesis & Treatment Research Unit, Doris Duke Medical Research Institute, University of KwaZulu-Natal, Durban, South Africa.

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Classifications MeSH