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PubMed2002

Isoniazid-resistant cavitary tuberculosis in a physician following isoniazid prophylaxis.

Single-drug prophylaxis is recommended after tuberculin skin test conversion, but not when there is active disease on chest radiograph because resistance develops frequently. Isoniazid-resistant tuberculosis developed in a physician receiving prophylaxis despite "faint left upper lobe soft tissue density" on chest radiograph. Ignoring active disease on chest x-ray renders this strategy counterproductive and cost ineffective.

Adult↗
PubMed1982

Isoniazid disposition, comparison of isoniazid phenotyping methods in and acetylator distribution of Japanese patients with idiopathic systemic lupus erythematosus and control subjects.

1 Plasma levels of isoniazid (INH) and acetyl INH in plasma were measured with a spectrofluorometric method, and INH and its metabolites (acetyl INH, mono-acetylhydrazine, diacetylhydrazine and free hydrazine) excreted in urine were measured with a gas chromatography-mass spectrometry, respectively, after an oral dose of INH 10 mg/kg in 19 Japanese patients with idiopathic systemic lupus erythematosus (SLE) and in the same number of healthy controls. 2 When phenotyped according to various methods previously reported, 16 to 18 of the SLE and 17 to 19 of the control group were rapid acetylators. Regardless of the phenotyping methods applied, the distribution of acetylator phenotype of SLE patients was not significantly different from the control group or from the data previously reported among normal Japanese population. 3 By phenotyping our subjects with an INH T 1/2 of 110 min or less as rapid acetylators, and more slow acetylators, 3 of SLE patients and 2 of the controls were slow, while the remainder were all rapid. When this antimode was used, the mean apparent kinetic variables of INH and acetyl INH estimated from the plasma concentration-time data and the mean values for the 24-h urinary amount of INH and its metabolites, except for monoacetylhydrazine (P less than 0.05), did not significantly differ between the rapid acetylators of SLE and control groups. 4 The distribution of INH T 1/2, acetyl INH to INH ratios in plasma and urine, values in urine for log10 (diacetylhydrazine to monoacetylhydrazine) and for diacetylhydrazine to INH or acetyl INH was similar between the two groups except for one patient who was definitely classified as a slow acetylator regardless of whichever phenotyping methods were used. The excretory patterns of hydrazine compounds reflect, in general, the inactivating ability of INH in each individual. 5 The data suggest that phenotyping by using plasma samples is, in general, better than by using urine samples. The plasma T 1/2 alone is the most satisfactory criterion. 6 We conclude that neither INH disposition nor phenotype distribution assessed by the reported methods using INH as the test compound are altered in idiopathic SLE, and that a search for racial and/or geographical factor(s) likely to result in autoimmune disease may give a clue to the pathogenesis in addition to further exploration for the possible interrelation between idiopathic SLE and genetic slow acetylation.

Acetylation↗
PubMed1977

Differentiation of catalases in Mycobacterium phlei on the basis of susceptibility to isoniazid: association with peroxidase and acquired resistance to isoniazid.

Mycobacterium phlei contains two catalase activities and a single peroxidase activity. The latter is associated with one of the catalases. The single catalase-peroxidase enzyme accounted for 75% of the total catalase activity and was lost upon acquisition of resistance to the antitubercular drug isoniazid (INH). Heat-treated (68 degrees C) wild-type cells showed similar decreases in catalase activity as well as complete loss of peroxidase activity. Catalase activity in the INH-resistant strain of M. phlei (Inh(r)) was unaffected by heating. The heat-sensitive catalase of the wild-type M. phlei was completely inhibited by 0.1 M INH, and Cu(2+) enhanced this inhibitory effect by 100-fold. No inhibition of activity was found with the heat-stable enzyme. Equivalent inhibition of catalase was also observed with nicotinic acid hydrazide and benzoic acid hydrazide. Peroxidase activity was also completely inhibited by any one of the three hydrazides, either INH, benzoic acid hydrazide, or nicotinic acid hydrazide at 10(-3) M. The presence of two catalase activities and the loss of one (catalase-peroxidase) on acquiring INH resistance or heating wild-type cells was confirmed by acrylamide gel electrophoresis of the cell-free extracts.

Bacterial Proteins↗
PubMed1999

High-dose isoniazid therapy for isoniazid-resistant murine Mycobacterium tuberculosis infection.

The use of isoniazid (INH) for the treatment of INH-resistant Mycobacterium tuberculosis infection has been controversial. The purpose of the present studies was to determine if there is a dose response with INH for INH-susceptible M. tuberculosis Erdman (ATCC 35801), and whether high-dose INH (100 mg/kg of body weight) was more effective than standard-dose INH (25 mg/kg) for therapy of tuberculosis infections caused by INH-resistant mutants of M. tuberculosis Erdman. Six-week-old CD-1 mice were infected with approximately 10(7) viable mycobacteria. Early control groups of infected but untreated mice were euthanized by CO(2) inhalation 1 week later when treatment was initiated. INH (25, 50, 75, and 100 mg/kg) was given by gavage 5 days/week for 4 weeks. Late control groups of untreated mice and treated mice were sacrificed 2 days after the last dose of drug. Spleens and right lungs were removed aseptically and homogenized, and viable cell counts were determined by titration on 7H10 agar plates. In the next study, INH at 100 mg/kg was compared to INH at 25 mg/kg against an isogenic mutant of M. tuberculosis Erdman (INH MIC, 2 microg/ml) and the parent strain. This mutant was found to have a mutation in the KatG protein (Phe to Leu at position 183). In the first study, there was no dose response with increasing doses of INH. In the second study, there was no significant difference between the reduction of viable cell counts for mice treated with INH at 100 mg/kg and that for mice treated with INH at 25 mg/kg (parent or INH-resistant mutant). These preliminary results suggest that INH may be useful in combination therapy of M. tuberculosis infections caused by low-level INH-resistant organisms (INH MICs, 0.2 to 5 microg/ml) and that higher doses of INH are unlikely to be more efficacious than the standard 300-mg/day dose.

Animals↗
PubMed1997

Rifampicin and isoniazid increase acetaminophen and isoniazid cytotoxicity in human HepG2 hepatoma cells.

Acetaminophen (APAP) induced a concentration-dependent (0-30 mM) cytotoxic effect in human HepG2 hepatoma cells which was significantly increased when intracellular reduced glutathione (GSH) content was decreased. The cytotoxic effect of APAP (0-30 mM) was significantly lower in a day 3-treated compared to day 1-treated HepG2 cells. A 3-day preincubation of HepG2 cells with 5 microM 3-methylcholanthrene (3MC), 50 microM rifampicin (RFP) or 1 mM isoniazid (INH) significantly increased 15-30 mM APAP cytotoxicity, of about 15-20% for INH and RFP and 35-50% for 3MC. The cytotoxicity of 10 mM APAP was also increased (about 20%) by a 3-day preincubation with INH but was not affected by 3MC and RFP. INH induced a concentration-dependent (0-40 mM) cytotoxic effect in day-1 treated HepG2 cells and not significantly affected by decreases in intracellular GSH concentrations. INH was not cytotoxic in day 3-treated HepG2 cells. A 3-day preincubation of HepG2 cells with 50 mM RFP or 1 mM INH significantly increased 10-40 mM INH cytotoxicity, respectively of about 10% and 10-25%. A 3-day preincubation with 3MC did not modify the cytotoxic effect of INH at these concentrations. This is to our knowledge the first report of increases by INH and RFP of APAP of INH cytotoxicity in vitro in hepatocellular cells of human origin. It is in accordance with clinical observations of severe hepatotoxicity associated with APAP or INH usage in patients receiving multiple drug therapy (INH, RFP) for tuberculosis or in alcoholics.

Acetaminophen↗
PubMedDate not supplied

[Decreased resistance of multiresistant mycobacteria to isoniazid during the treatment of experimental tuberculosis with ozone and isoniazid].

Mycobacteria (MB) of the clinical strain resistant to streptomycin, isoniazid (IN), rifampicin and kanamycin were injected intravenously into 68 BALB/c mice. The animals were divided into 5 groups: two control groups 0 and 1 (intact and infected without subsequent treatment), group 2 (treated with IN), group 3 (treated with IN and injected intraperitoneally with dissolved ozone, or dO3), group 4 (injected with dO3). The animals started to die by month 4 after the infection. By month 5 all mice died with the exception of intact mice and those treated with dO3). By month 4 the study of MB cultures isolated from the lungs revealed a decrease in their resistance to IN in the groups undergoing treatment with dO3. Hepatic and splenic lesions were observed after treatment with IN only were greater than in the absence of treatment. After the use of IN + dO3 such lesions were the least. The mechanism of a decrease in the medicinal resistance of MB under the action of dO3 and the expediency of the simultaneous use IN and dO3 in cases of the unknown medicinal resistance of MB are discussed.

Administration, Oral↗