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INH

Isoniazid is a first-line antituberculous medication used in the prevention and treatment of tuberculosis. It is often prescribed under the name INH. The chemical name is isonicotinyl hydrazine or isonicotinic acid hydrazide. more...

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It is available in tablet, syrup, and injectable forms (given via intramuscular injection), available world-wide, inexpensive to produce, and is generally well tolerated.

Mechanism of action

Isoniazid is a prodrug and must be activated by bacterial catalase. The active form inhibits the synthesis of mycolic acid in the mycobacterial cell wall.

Isoniazid reaches therapeutic concentrations in serum, cerebrospinal fluid (CSF), and within caseous granulomas. Isoniazid is metabolized in the liver via acetylation. There are two forms of the enzyme responsible for acetylation, so that some patients metabolize the drug quicker than others. Hence, the half-life is bimodal with peaks at 1 hour and 3 hours in the US population. The metabolites are excreted in the urine. Doses do not usually have to be adjusted in case of renal failure.

Isoniazid is bactericidal to rapidly-dividing mycobacteria, but is bacteriostatic if the mycobacterium is slow-growing.

Side effects

Adverse reactions include rash, abnormal liver function tests, hepatitis, peripheral neuropathy, mild central nervous system (CNS) effects, and drug interactions resulting in increased phenytoin (Dilantin) or disulfiram (Antabuse) levels.

Peripheral neuropathy and CNS effects are associated with the use of isoniazid and is due to pyridoxine (vitamin B6) depletion, but is uncommon at doses of 5 mg/kg. Persons with conditions in which neuropathy is common (e.g., diabetes, uremia, alcoholism, malnutrition, HIV-infection), as well as pregnant women and persons with a seizure disorder, may be given pyridoxine (vitamin B6) (10-50 mg/day) with isoniazid.

Reference

Core Curriculum on Tuberculosis (2000) Division of Tuberculosis Elimination, Centers for Disease Control and Prevention

See Chapter 6, Treatment of LTBI Regimens - Isoniazid
See Chapter 7 - Treatment of TB Disease Monitoring - Adverse Reactions to First-Line TB Drugs - Isoniazid
See Table 5 First-Line Anti-TB Medications

Isoniazid Overdose: Recognition and Management American Family Physician 1998 Feb 15

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ANALYSIS OF MUTATIONS IN GENES ASSOCIATED WITH RESISTANCE TO ISONIAZID (INH) IN Mycobacterium tuberculosis BRAZILIAN CLINICAL ISOLATES
From Revista do Instituto de Medicina Tropical de Sao Paulo, 1/1/04 by Cardoso, Rosilene Frenatti

In the present study the mutations frequencies in the katG, kasA, inhA genes and oxyR-ahpC intergenic region of 97 resistant and 60 sensitive Mycobacterium tuberculosis clinical isolates from Brazil were investigated. The mutations screening were carried out by PCR-SSCP and confirmed by automated sequencing. The minimal inhibitory concentration for INH was done by the microplate Alamar Blue Assay (MABA). The molecular differentiation of INH resistant and sensitive isolates was carried out by Spoligotyping of the locus DR. We found 40 different Spoligotyping patterns when analyzing 97 INH resistant clinical isolates and 30 in 60 INH sensitive isolates. Our data showed no resistant isolates had a complete deletion of the katG gene. However, one resistant isolate that had a deletion at region 3' in katG gene was found and a high percentage of mutation in this gene (85.6%) mainly at codon 315 (61.9%). Twenty-five new mutations previously not described in the literature, were detected in katG gene in all resistant isolates studied and 25.8% had mutation in inhA promoter region, 5.82% had mutation in inhA structural region and 10.3% at oxyR-ahpC intergenic region where one of this is a new mutation (-48) previously not described in the literature. It was observed in kasA gene mutation in resistant and sensitive isolates. The most frequent mutation observed in kasA gene was at codon 269 that will cause alteration G269S (23.7%). Other silent mutations were detected only in INH sensitive isolates, however with a low frequency. PCR-SSCP showed good sensibility (90.7%) to detect mutations in INH resistant isolates, analyzing 5 genic regions (315 codon region of katG gene, inhA promoter and inhA structural region and oxyR-ahpC intergenic region) by PCR-SSCP. PCR-SSCP showed agreement in 100% when compared to sequencing. We can thus conclude that mutation screening by PCR-SSCP can be used to detect resistance to INH in M. tuberculosis.

* This thesis is available at the Library of the Instituto de Medians Tropical de Sao Paulo

CARDOSO, Rosilene Fressatti - Analise de mutacoes nos genes relacionados coin resistencia a isoniazida (INH) cm isolados clinicos de Mycobacterium tuberculosis de origem brasileira. Sao Paulo, 2003. (Tese de Doutorado - Faculdade de Ciencias Famaceuticas da Universidade de Sao Paulo).

Rosilene Frenatti Cardoso

Laboratorio de Bacteriologia Clinica

Univorsidade Estadual de Maringa

Bloco J-90 - Sala 05

87000-000 MARINGA - PARANA

e-mail: rfcardoso@uem.br

mfressatti@uol.com.br

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