Isoniazid: Antibacterial agent used primarily as a tuberculostatic. It remains the treatment of choice for tuberculosis.Antitubercular Agents: Drugs used in the treatment of tuberculosis. They are divided into two main classes: "first-line" agents, those with the greatest efficacy and acceptable degrees of toxicity used successfully in the great majority of cases; and "second-line" drugs used in drug-resistant cases or those in which some other patient-related condition has compromised the effectiveness of primary therapy.Rifampin: A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)Mycobacterium tuberculosis: A species of gram-positive, aerobic bacteria that produces TUBERCULOSIS in humans, other primates, CATTLE; DOGS; and some other animals which have contact with humans. Growth tends to be in serpentine, cordlike masses in which the bacilli show a parallel orientation.Pyrazinamide: A pyrazine that is used therapeutically as an antitubercular agent.Ethambutol: An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863)Antibiotics, Antitubercular: Substances obtained from various species of microorganisms that are, alone or in combination with other agents, of use in treating various forms of tuberculosis; most of these agents are merely bacteriostatic, induce resistance in the organisms, and may be toxic.Tuberculosis, Multidrug-Resistant: Tuberculosis resistant to chemotherapy with two or more ANTITUBERCULAR AGENTS, including at least ISONIAZID and RIFAMPICIN. The problem of resistance is particularly troublesome in tuberculous OPPORTUNISTIC INFECTIONS associated with HIV INFECTIONS. It requires the use of second line drugs which are more toxic than the first line regimens. TB with isolates that have developed further resistance to at least three of the six classes of second line drugs is defined as EXTENSIVELY DRUG-RESISTANT TUBERCULOSIS.Tuberculosis: Any of the infectious diseases of man and other animals caused by species of MYCOBACTERIUM.Tuberculosis, Pulmonary: MYCOBACTERIUM infections of the lung.Ethionamide: A second-line antitubercular agent that inhibits mycolic acid synthesis.Streptomycin: An antibiotic produced by the soil actinomycete Streptomyces griseus. It acts by inhibiting the initiation and elongation processes during protein synthesis.Aminosalicylic Acids: A group of 2-hydroxybenzoic acids that can be substituted by amino groups at any of the 3-, 4-, 5-, or 6-positions.Aminosalicylic Acid: An antitubercular agent often administered in association with ISONIAZID. The sodium salt of the drug is better tolerated than the free acid.Microbial Sensitivity Tests: Any tests that demonstrate the relative efficacy of different chemotherapeutic agents against specific microorganisms (i.e., bacteria, fungi, viruses).Drug Resistance, Bacterial: The ability of bacteria to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).Isonicotinic Acids: Heterocyclic acids that are derivatives of 4-pyridinecarboxylic acid (isonicotinic acid).Catalase: An oxidoreductase that catalyzes the conversion of HYDROGEN PEROXIDE to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in ACATALASIA.Thioacetazone: A thiosemicarbazone that is used in association with other antimycobacterial agents in the initial and continuation phases of antituberculosis regimens. Thiacetazone containing regimens are less effective than the short-course regimen recommended by the International Union Against Tuberculosis and are used in some developing countries to reduce drug costs. (From Martindale, The Extra Pharmacopoeia, 30th ed, p217)Mycolic AcidsMycobacterium: A genus of gram-positive, aerobic bacteria. Most species are free-living in soil and water, but the major habitat for some is the diseased tissue of warm-blooded hosts.Drug Resistance, Multiple, Bacterial: The ability of bacteria to resist or to become tolerant to several structurally and functionally distinct drugs simultaneously. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).Latent Tuberculosis: The dormant form of TUBERCULOSIS where the person shows no obvious symptoms and no sign of the causative agent (Mycobacterium tuberculosis) in the SPUTUM despite being positive for tuberculosis infection skin test.Drug Resistance, Microbial: The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).Mycobacteriophages: Viruses whose host is one or more Mycobacterium species. They include both temperate and virulent types.Drug Therapy, Combination: Therapy with two or more separate preparations given for a combined effect.Bacterial Proteins: Proteins found in any species of bacterium.Aza CompoundsSputum: Material coughed up from the lungs and expectorated via the mouth. It contains MUCUS, cellular debris, and microorganisms. It may also contain blood or pus.Tuberculin Test: One of several skin tests to determine past or present tuberculosis infection. A purified protein derivative of the tubercle bacilli, called tuberculin, is introduced into the skin by scratch, puncture, or interdermal injection.Mycobacterium smegmatis: A rapid-growing, nonphotochromogenic species of MYCOBACTERIUM originally isolated from human smegma and found also in soil and water. (From Dorland, 28th ed)Clofazimine: A fat-soluble riminophenazine dye used for the treatment of leprosy. It has been used investigationally in combination with other antimycobacterial drugs to treat Mycobacterium avium infections in AIDS patients. Clofazimine also has a marked anti-inflammatory effect and is given to control the leprosy reaction, erythema nodosum leprosum. (From AMA Drug Evaluations Annual, 1993, p1619)Arylamine N-Acetyltransferase: An enzyme that catalyzes the transfer of acetyl groups from ACETYL-COA to arylamines. It can also catalyze acetyl transfer between arylamines without COENZYME A and has a wide specificity for aromatic amines, including SEROTONIN. However, arylamine N-acetyltransferase should not be confused with the enzyme ARYLALKYLAMINE N-ACETYLTRANSFERASE which is also referred to as SEROTONIN ACETYLTRANSFERASE.Rifamycins: A group of ANTI-BACTERIAL AGENTS characterized by a chromophoric naphthohydroquinone group spanned by an aliphatic bridge not previously found in other known ANTI-BACTERIAL AGENTS. They have been isolated from fermentation broths of Streptomyces mediterranei.HydrazinesOxidoreductases: The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)Colony Count, Microbial: Enumeration by direct count of viable, isolated bacterial, archaeal, or fungal CELLS or SPORES capable of growth on solid CULTURE MEDIA. The method is used routinely by environmental microbiologists for quantifying organisms in AIR; FOOD; and WATER; by clinicians for measuring patients' microbial load; and in antimicrobial drug testing.

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IsoniazidMycobacterium tuberculosis complex: Mycobacterium tuberculosis complex refers to a genetically related group of Mycobacterium species that can cause tuberculosis in humans or other organisms.Pyrazinoic acidMulti-drug-resistant tuberculosis: Multi-drug-resistant tuberculosis (MDR-TB) is defined as a form of TB infection caused by bacteria that are resistant] to treatment with at least two of the most powerful [[Therapy#Lines of therapy|first-line anti-TB drugs, isoniazid (INH) and rifampicin (RMP).Tuberculosis managementTuberculosis radiology: Radiology is used in the diagnosis of tuberculosis.StreptomycinATC code J04: ==J04A Drugs for treatment of tuberculosis==Glen Lake Sanatorium: Glen Lake Sanatorium, a tuberculosis treatment center serving Hennepin County in Minnesota, opened on January 4, 1916, with a capacity of 50 patients. In 1909, the Minnesota State Legislature had passed a bill authorizing the appointment of county sanatorium boards and appropriating money for the construction of county sanatoriums.Resistome: The resistome is a proposed expression by Gerard D. Wright for the collection of all the antibiotic resistance genes and their precursors in both pathogenic and non-pathogenic bacteria.MethylpyridiniumCatalase: Catalase is a common enzyme found in nearly all living organisms exposed to oxygen (such as bacteria, plants, and animals). It catalyzes the decomposition of hydrogen peroxide to water and oxygen.Mycobacterium frederiksbergense: Mycobacterium frederiksbergense is a species of the phylum actinobacteria (Gram-positive bacteria with high guanine and cytosine content, one of the dominant phyla of all bacteria), belonging to the genus mycobacterium.Mycobacterium indicus pranii: Mycobacterium indicus pranii (MIP),Mycobacterium indicus pranii earlier known as Mw, is a non-pathogenic mycobacterial species, which, based on its growth characteristics and metabolic properties,Rahman SA, Singh Y, Kohli S, Ahmad J, Ehtesham NZ, Tyagi AK, Hasnain SE. 2014.QuantiFERON: Interferon-gamma release assays (IGRAs) are diagnostic tools for latent tuberculosis infection (LTBI). They are surrogate markers of Mycobacterium tuberculosis infection and indicate a cellular immune response to M.Combination therapy: Combination therapy or polytherapy is therapy that uses more than one medication or modality (versus monotherapy, which is any therapy taken alone). Typically, these terms refer to using multiple therapies to treat a single disease, and often all the therapies are pharmaceutical (although it can also involve non-medical therapy, such as the combination of medications and talk therapy to treat depression).Ferric uptake regulator family: In molecular biology, the ferric uptake regulator (FUR) family of proteins includes metal ion uptake regulator proteins. These are responsible for controlling the intracellular concentration of iron in many bacteria.AmitifadineSputumMantoux test: The Mantoux test or Mendel-Mantoux test (also known as the Mantoux screening test, tuberculin sensitivity test, Pirquet test, or PPD test for purified protein derivative) is a screening tool for tuberculosis (TB). It is one of the major tuberculin skin tests used around the world, largely replacing multiple-puncture tests such as the Tine test.Cooperstown cocktail: The Cooperstown cocktailStreetman D, Bleakley J et al. Combined phenotypic assessment of CYP1A2, CYP2C19, CYP2D6, CYP3A, N-acetyltransferase-2, and xanthine oxidase with the "Cooperstown cocktail".Rifamycin: The rifamycins are a group of antibiotics that are synthesized either naturally by the bacterium Amycolatopsis rifamycinica or artificially. They are a subclass of the larger family of ansamycins.Hydrazine sulfateGlucose-methanol-choline oxidoreductase family: In molecular biology, the glucose-methanol-choline oxidoreductase family (GMC oxidoreductase) is a family of enzymes with oxidoreductase activity.

(1/1316) Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.

Three Mycobacterium smegmatis mutants selected for resistance to triclosan each had a different mutation in InhA, an enoyl reductase involved in fatty acid synthesis. Two expressed some isoniazid resistance. A mutation originally selected on isoniazid also mediated triclosan resistance, as did the wild-type inhA gene on a multicopy plasmid. Replacement of the mutant chromosomal inhA genes with wild-type inhA eliminated resistance. These results suggest that M. smegmatis InhA, like its Escherichia coli homolog FabI, is a target for triclosan.  (+info)

(2/1316) Use of site-directed mutagenesis to probe the structure, function and isoniazid activation of the catalase/peroxidase, KatG, from Mycobacterium tuberculosis.

A series of mutants bearing single amino acid substitutions often encountered in the catalase/peroxidase, KatG, from isoniazid-resistant isolates of Mycobacterium tuberculosis has been produced by site-directed mutagenesis. The resultant enzymes were overexpressed, purified and characterized. Replacing Cys-20 by Ser abolished disulphide-bridge formation, but did not affect either dimerization of the enzyme or catalysis. The substitution of Thr-275, which is probably involved in electron transfer from the haem, by proline resulted in a highly unstable enzyme with insignificant enzyme activities. The most commonly occurring substitution in drug-resistant clinical isolates is the replacement of Ser-315 by Thr; this lowered catalase and peroxidase activities by 50% and caused a significant decrease in the KatG-mediated inhibition of the activity of the NADH-dependent enoyl-[acyl-carrier protein] reductase, InhA, in vitro. The ability of this enzyme to produce free radicals from isoniazid was severely impaired, as judged by its loss of NitroBlue Tetrazolium reduction activity. Replacement of Leu-587 by Pro resulted in marked instability of KatG, indicating that the C-terminal domain is also important for structural and functional integrity.  (+info)

(3/1316) Molecular evidence for heterogeneity of the multiple-drug-resistant Mycobacterium tuberculosis population in Scotland (1990 to 1997).

Multiple-drug-resistant Mycobacterium tuberculosis (MDR-MTB) has been well studied in hospitals or health care institutions and in human immunodeficiency virus-infected populations. However, the characteristics of MDR-MTB in the community have not been well investigated. An understanding of its prevalence and circulation within the community will help to estimate the problem and optimize the strategies for control and prevention of its development and transmission. In this study, MDR-MTB isolates from Scotland collected between 1990 and 1997 were characterized, along with non-drug-resistant isolates. The results showed that they were genetically diverse, suggesting they were unrelated to each other and had probably evolved independently. Several new alleles of rpoB, katG, and ahpC were identified: rpoB codon 525 (ACC-->AAC; Thr525Asn); katG codon 128 (CGG-->CAG; Arg128Gln) and codon 291 (GCT-->CCT; Ala291Pro); and the ahpC synonymous substitution at codon 6 (ATT-->ATC). One of the MDR-MTB isolates from an Asian patient had an IS6110 restriction fragment length polymorphism pattern very similar to that of the MDR-MTB W strain and had the same drug resistance-related alleles but did not have any epidemiological connection with the W strains. Additionally, a cluster of M. tuberculosis isolates was identified in our collection of 715 clinical isolates; the isolates in this cluster had genetic backgrounds very similar to those of the W strains, one of which had already developed multiple drug resistances. The diverse population of MDR-MTB in Scotland, along with a low incidence of drug-resistant M. tuberculosis, has implications for the control of the organism and prevention of its spread.  (+info)

(4/1316) Rapid film-based determination of antibiotic susceptibilities of Mycobacterium tuberculosis strains by using a luciferase reporter phage and the Bronx Box.

Detecting antibiotic resistance in Mycobacterium tuberculosis is becoming increasingly important with the global recognition of drug-resistant strains and their adverse impact on clinical outcomes. Current methods of susceptibility testing are either time-consuming or costly; rapid, reliable, simple, and inexpensive methods would be highly desirable, especially in the developing world where most tuberculosis is found. The luciferase reporter phage is a unique reagent well-suited for this purpose: upon infection with viable mycobacteria, it produces quantifiable light which is not observed in mycobacterial cells treated with active antimicrobials. In this report, we describe a modification of our original assay, which allows detection of the emitted light with a Polaroid film box designated the Bronx Box. The technique has been applied to 25 M. tuberculosis reference and clinical strains, and criteria are presented which allow rapid and simple discrimination among strains susceptible or resistant to isoniazid and rifampin, the major antituberculosis agents.  (+info)

(5/1316) EPR spin trapping and 2-deoxyribose degradation studies of the effect of pyridoxal isonicotinoyl hydrazone (PIH) on *OH formation by the Fenton reaction.

The search for effective iron chelating agents was primarily driven by the need to treat iron-loading refractory anemias such as beta-thalassemia major. However, there is a potential for therapeutic use of iron chelators in non-iron overload conditions. Iron can, under appropriate conditions, catalyze the production of toxic oxygen radicals which have been implicated in numerous pathologies and, hence, iron chelators may be useful as inhibitors of free radical-mediated tissue damage. We have developed the orally effective iron chelator pyridoxal isonicotinoyl hydrazone (PIH) and demonstrated that it inhibits iron-mediated oxyradical formation and their effects (e.g. 2-deoxyribose oxidative degradation, lipid peroxidation and plasmid DNA breaks). In this study we further characterized the mechanism of the antioxidant action of PIH and some of its analogs against *OH formation from the Fenton reaction. Using electron paramagnetic resonance (EPR) with 5, 5-dimethyl-1-pyrroline-N-oxide (DMPO) as a spin trap for *OH we showed that PIH and salicylaldehyde isonicotinoyl hydrazone (SIH) inhibited Fe(II)-dependent production of *OH from H2O2. Moreover, PIH protected 2-deoxyribose against oxidative degradation induced by Fe(II) and H2O2. The protective effect of PIH against both DMPO hydroxylation and 2-deoxyribose degradation was inversely proportional to Fe(II) concentration. However, PIH did not change the primary products of the Fenton reaction as indicated by EPR experiments on *OH-mediated ethanol radical formation. Furthermore, PIH dramatically enhanced the rate of Fe(II) oxidation to Fe(III) in the presence of oxygen, suggesting that PIH decreases the concentration of Fe(II) available for the Fenton reaction. These results suggest that PIH and SIH deserve further investigation as inhibitors of free-radical mediated tissue damage.  (+info)

(6/1316) Potentiation of isoniazid activity against Mycobacterium tuberculosis by melatonin.

The limited number of effective antituberculosis drugs available necessitates optimizing current treatments. We show that melatonin, which is synthesized in the pineal gland, can cause at least a threefold increase in the efficacy of isoniazid. This suggests that tuberculosis chemotherapy can be improved by innate molecules such as melatonin.  (+info)

(7/1316) A five-year assessment of controlled trials of in-patient and out-patient treatment and of plaster-of-Paris jackets for tuberculosis of the spine in children on standard chemotherapy. Studies in Masan and Pusan, Korea. Fifth report of the Medical Research Council Working Party on tuberculosis of the spine.

In two centres in Korea 350 patients with a diagnosis of tuberculosis of the thoracic and/or lumbar spine were allocated at random: in Masan to in-patient rest in bed (IP) for six months followed by out-patient treatment or to ambulatory out-patient treatment (OP) from the start; in Pusan to out-patient treatment with a plaster-of-Paris jacket (J) for nine months or to ambulatory treatment without any support (No J). All patients recieved chemotherapy with PAS with isoniazid for eighteen months, either supplemented with streptomycin for the first three months (SPH) or without this supplement (PH), by random allocation. The main analysis of this report concerns 299 patients (eighty-three IP, eighty-three OP, sixty-three J, seventy No J; 143 SPH, 156 PH). Pre-treatment factors were similar in both centres except that the patients in Pusan had, on average, less extensive lesions although in a greater proportion the disease was radiographically active. One patient (J/SPH) died with active spinal disease and three (all No J/SPH) with paraplegia. A fifth patient (IP/PH) who died from cardio respiratory failure also had pulmonary tuberculosis. Twenty-three patients required operation and/or additional chemotherapy for the spinal lesion. A sinus or clinically evident abscess was either present initially or developed during treatment in 41 per cent of patients. Residual lesions persisted in ten patients (four IP, two OP, one J, three No J; six SPH, four PH) at five years. Thirty-two patients had paraparesis on admission or developing later. Complete resolution occurred in twenty on the allocated regimen and in eight after operation or additional chemotherapy or both. Of the remaining four atients, all of whom had operation and additional chemotherapy, three died and one still had paraparesis at five years. Of 295 patients assessed at five years 89 per cent had a favourable status. The proportions of the patients responding favourably were similar in the IP (91 per cent) and OP (89 per cent) series, in the J (90 per cent) and No J (84 per cent) series and in the SPH (86 per cent) and PH (92 per cent) series.  (+info)

(8/1316) Inhibition of isoniazid-induced hepatotoxicity in rabbits by pretreatment with an amidase inhibitor.

Isoniazid (INH), a widely used drug in the prophylaxis and treatment of tuberculosis, is associated with a 1 to 2% risk of severe and potentially fatal hepatotoxicity. There is evidence that the INH metabolite hydrazine plays an important role in the mechanism of this toxicity. Metabolism of INH leads to the production of hydrazine via both direct and indirect pathways. In both cases, the activity of an INH amidase is required to hydrolyze an amide bond. In the present study, using a model of INH-induced hepatotoxicity in rabbits, pretreatment of rabbits with the amidase inhibitor bis-p-nitrophenyl phosphate 30 min before injection of INH inhibited the formation of INH-derived hydrazine and decreased measures of hepatocellular damage, hepatic triglyceride accumulation, and hypertriglyceridemia. Bis-p-nitrophenyl phosphate also potently inhibited the production of hydrazine from INH in in vitro microsomal incubations (IC50 2 microM). Although hepatic glutathione stores are decreased, they are not depleted in animals with INH-induced hepatotoxicity. Significant effects on hepatic microsomal cytochrome P-450 1A1/2 and cytochrome P-450 2E1 activities suggest that these isozymes may be involved in the mechanism of the toxicity. In conclusion, this study demonstrates the importance of amidase activity in this rabbit model of hepatotoxicity and provides additional evidence in support of the role of hydrazine in the mechanism of INH-induced hepatotoxicity.  (+info)


  • Isoniazid is an antibiotic that is used to treat tuberculosis (TB). (
  • The exact mechanism of action of isoniazid is unknown, but it is thought to prevent the tuberculosis bacteria from making substances called mycolic acids, which are needed to form the cell walls of the bacteria. (
  • Used for the treatment of tuberculosis, isoniazid can interfere with the absorption or metabolism of numerous nutrients. (
  • Isoniazid and rifampin is a combination medicine used to treat tuberculosis (TB). (
  • Isoniazid is used for treating or preventing tuberculosis. (
  • Isoniazid is used for the treatment and prevention of tuberculosis, including the treatment of latent tuberculosis infection (LTBI). (

take isoniazid

  • Individuals who take isoniazid may develop nerve problems such as tingling or numbness in the arms, hands, legs, and feet. (
  • Take isoniazid and rifampin on an empty stomach, at least 1 hour before or 2 hours after a meal. (
  • If nausea occurs, ask your doctor if you can take Isoniazid with food. (
  • It is important to take Isoniazid regularly to get the most benefit. (


  • What is Rifamate (isoniazid and rifampin)? (
  • Isoniazid and rifampin are antibiotics that fight bacteria. (
  • Isoniazid and rifampin may also be used for purposes not listed in this medication guide. (
  • What is the most important information I should know about Rifamate (isoniazid and rifampin)? (
  • You should not use isoniazid and rifampin if you have active liver disease (including hepatitis or cirrhosis), or a history of liver problems caused by taking isoniazid. (
  • Serious and sometimes fatal liver problems may occur during treatment with isoniazid and rifampin or after you stop taking this medication, even months after stopping. (
  • It may increase your risk of liver damage while you are taking isoniazid and rifampin. (
  • What should I discuss with my healthcare provider before taking Rifamate (isoniazid and rifampin)? (
  • You should not use this medicine if you are allergic to isoniazid or rifampin, or if you have active liver disease (including hepatitis or cirrhosis), or a history of liver problems caused by taking isoniazid. (
  • It is not known whether isoniazid and rifampin will harm an unborn baby. (
  • Isoniazid and rifampin can make birth control pills less effective. (
  • Ask your doctor about using non hormonal birth control (condom, diaphragm with spermicide) to prevent pregnancy while taking isoniazid and rifampin. (
  • Isoniazid and rifampin can pass into breast milk and may harm a nursing baby. (
  • How should I take Rifamate (isoniazid and rifampin)? (
  • Your doctor will perform blood tests to make sure you do not have conditions that would prevent you from safely using isoniazid and rifampin. (
  • Your doctor may have you take extra vitamin B6 while you are taking isoniazid and rifampin. (
  • Isoniazid and rifampin will not treat a viral infection such as the common cold or flu. (
  • Isoniazid and rifampin is usually given until lab tests show that the infection has cleared. (
  • Tell any doctor who treats you that you are using isoniazid and rifampin. (
  • What should I avoid while taking Rifamate (isoniazid and rifampin)? (
  • Do not wear soft contact lenses while taking isoniazid and rifampin. (


  • Immediate isoniazid/pyridoxine and cotrimoxazole, plus 12 weeks fluconazole, 5 days azithromycin and a single dose of albendazole compared with immediate cotrimoxazole (if not already taking this) in all patients plus (not malawi)isoniazid/pyridoxine after 12 weeks. (
  • An initial cohort of patients receive isoniazid (with pyridoxine) daily for 5 days. (



  • After this time some of the medicines are stopped and the others (usually rifampicin and isoniazid) are continued for a further four months to kill any remaining bacteria. (

nerve problems

  • If you have a history of alcohol abuse, you may also be at increased risk of developing nerve problems from Isoniazid. (


  • Influence of polymorphic N-acetyltransferase phenotype on the inhibition and induction of acetaminophen bioactivation with long-term isoniazid. (
  • Inhibition and induction of cytochrome P4502E1-catalyzed oxidation by isoniazid in humans. (
  • Inhibition of the metabolism of paracetamol by isoniazid. (


  • Ask your health care provider if Isoniazid may interact with other medicines that you take. (
  • Isoniazid (brand names include: Laniazid / Nydrazid / Isokin / Isonex / Isoniazid / Isozid / Pycazide / Rimifon / Tibinil-I) belongs to a group of medicines known as antitubercular agents. (


  • To prevent these complications, it may make sense to take vitamin B 6 supplements at a dose of 15 to 30 mg per day when using isoniazid. (
  • If you miss a dose of Isoniazid, use it as soon as possible. (


  • Isoniazid may cause vitamin B6 deficiency, particularly in certain groups of people, including pregnant women and people with diabetes, alcohol dependence, chronic kidney failure, malnutrition or HIV infection. (
  • Isoniazid (INH) preventive therapy (IPT) is effective for HIV-infected adults, but the safety of IPT in pregnant women is unknown. (
  • Pregnant women may be enrolled in the isoniazid cohort only. (


  • 1,2 In fact, use of isoniazid is one cause of the few occasions in which vitamin B 6 deficiency is seen in the developed world. (
  • According to animal studies, isoniazid can interfere with the body's ability to produce vitamin B 3 (niacin) by blocking a key enzyme. (


  • Isoniazid is used in both stages of treatment. (
  • Isoniazid can also be used in the treatment of a BCG-oma. (
  • Your doctor may want you to have blood tests or other medical evaluations during treatment with isoniazid to monitor progress and side effects. (


  • Severe acetaminophen toxicity in a patient receiving isoniazid. (





  • Isoniazid tablets are usually taken once a day. (
  • if you are older than 35 years old, you have recently given birth, or you have previously taken Isoniazid. (



  • If you are using Isoniazid to treat TB, it should always be used along with another medicine. (


  • Isoniazid may also be given by injection in situations when tablets are unsuitable. (


  • Store Isoniazid between 68 and 77 degrees F (20 and 25 degrees C). Brief storage at temperatures between 59 and 86 degrees F (15 and 30 degrees C) is permitted. (


  • Therefore several anti-TB drugs with different mechanisms of action are used at the same time (usually rifampicin, pyrazinamide, isoniazid and ethambutol). (