Isoniazid metabolism and hepatotoxicity

被引：171

作者：

Wang, Pengcheng ^{[1
]}

Pradhan, Komal ^{[1
]}

Zhong, Xiao-bo ^{[2
]}

Ma, Xiaochao ^{[1
]}

机构：

[1] Univ Pittsburgh, Sch Pharm, Dept Pharmaceut Sci, Ctr Pharmacogenet, Pittsburgh, PA 15261 USA

[2] Univ Connecticut, Sch Pharm, Dept Pharmaceut Sci, Storrs, CT 06269 USA

来源：

ACTA PHARMACEUTICA SINICA B | 2016年 / 6卷 / 05期

关键词：

Isoniazid; Metabolism; Hepatotoxicity; Anti-tuberculosis; N-Acetyltransferase; 2; Amidase; ARYLAMINE N-ACETYLTRANSFERASES; INDUCED LIVER-INJURY; TOXIC HYDRAZINO METABOLITES; ISONICOTINIC-ACID HYDRAZIDE; DRUG-INDUCED HEPATOTOXICITY; S-TRANSFERASE M1; OXIDATIVE STRESS; ANTITUBERCULOSIS DRUGS; GENETIC POLYMORPHISMS; PLASMA-CONCENTRATIONS;

D O I：

10.1016/j.apsb.2016.07.014

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Isoniazid (INH) is highly effective for the management of tuberculosis. However, it can cause liver injury and even liver failure. INH metabolism has been thought to be associated with INH-induced liver injury. This review summarized the metabolic pathways of INH and discussed their associations with INH-induced liver injury. (C) 2016 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.

引用

页码：384 / 392

页数：9

共 138 条

[1]

Andersson C, 1994, Adv Pharmacol, V27, P19, DOI 10.1016/S1054-3589(08)61028-5

[2] Isoniazid Inhibits the Heme-Based Reactivity of Mycobacterium tuberculosis Truncated Hemoglobin N [J].

Ascenzi, Paolo ;

Coletta, Andrea ;

Cao, Yu ;

Trezza, Viviana ;

Leboffe, Loris ;

Fanali, Gabriella ;

Fasano, Mauro ;

Pesce, Alessandra ;

Ciaccio, Chiara ;

Marini, Stefano ;

Coletta, Massimo .

PLOS ONE, 2013, 8 (08)

[3] NAT2 genotype guided regimen reduces isoniazid-induced liver injury and early treatment failure in the 6-month four-drug standard treatment of tuberculosis: A randomized controlled trial for pharmacogenetics-based therapy [J].

Azuma, Junichi ;

Ohno, Masako ;

Kubota, Ryuji ;

Yokota, Soichiro ;

Nagai, Takayuki ;

Tsuyuguchi, Kazunari ;

Okuda, Yasuhisa ;

Takashima, Tetsuya ;

Kamimura, Sayaka ;

Fujio, Yasushi ;

Kawase, Ichiro .

EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY, 2013, 69 (05) :1091-1101

[4] Pharmacokinetics, tissue distribution and relative bioavailability of isoniazid-solid lipid nanoparticles [J].

Bhandari, Rohit ;

Kaur, Indu Pal .

INTERNATIONAL JOURNAL OF PHARMACEUTICS, 2013, 441 (1-2) :202-212

[5] Pharmacological evidence for anandamide amidase in human cardiac and vascular tissues [J].

Bilfinger, TV ;

Salzet, M ;

Fimiani, C ;

Deutsch, DG ;

Tramu, G ;

Stefano, GB .

INTERNATIONAL JOURNAL OF CARDIOLOGY, 1998, 64 :S15-S22

[6]

BLACK M, 1975, GASTROENTEROLOGY, V69, P289

[7] PLASMA HYDRAZINE CONCENTRATIONS IN MAN AFTER ISONIAZID AND HYDRALAZINE ADMINISTRATION [J].

BLAIR, IA ;

TINOCO, RM ;

BRODIE, MJ ;

CLARE, RA ;

DOLLERY, CT ;

TIMBRELL, JA ;

BEEVER, IA .

HUMAN TOXICOLOGY, 1985, 4 (02) :195-202

[8] HUMAN ARYLAMINE N-ACETYLTRANSFERASE GENES - ISOLATION, CHROMOSOMAL LOCALIZATION, AND FUNCTIONAL EXPRESSION [J].

BLUM, M ;

GRANT, DM ;

MCBRIDE, W ;

HEIM, M ;

MEYER, UA .

DNA AND CELL BIOLOGY, 1990, 9 (03) :193-203

[9] Mechanisms of isoniazid-induced idiosyncratic liver injury: Emerging role of mitochondrial stress [J].

Boelsterli, Urs A. ;

Lee, Kang Kwang .

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, 2014, 29 (04) :678-687

[10] EFFECT OF ISONIAZID ON VITAMIN-D METABOLISM AND HEPATIC MONO-OXYGENASE ACTIVITY [J].

BRODIE, MJ ;

BOOBIS, AR ;

HILLYARD, CJ ;

ABEYASEKERA, G ;

MACINTYRE, I ;

PARK, BK .

CLINICAL PHARMACOLOGY & THERAPEUTICS, 1981, 30 (03) :363-367

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