Isoniazid

Last updated
Isoniazid
Isoniazid skeletal.svg
Isoniazid 3d.png
Clinical data
Trade names Hydra, Hyzyd, Isovit, others
Other namesisonicotinic acid hydrazide, isonicotinyl hydrazine, INH, INAH, INHA
AHFS/Drugs.com Monograph
MedlinePlus a682401
License data
Pregnancy
category
Routes of
administration
By mouth, intramuscular, intravenous
ATC code
Legal status
Legal status
Pharmacokinetic data
Protein binding Very low (0–10%)
Metabolism liver; CYP450: 2C19, 3A4 inhibitor
Elimination half-life 0.5–1.6h (fast acetylators), 2-5h (slow acetylators)
Excretion urine (primarily), feces
Identifiers
  • Pyridine-4-carbohydrazide
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
NIAID ChemDB
CompTox Dashboard (EPA)
ECHA InfoCard 100.000.195 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C6H7N3O
Molar mass 137.142 g·mol−1
3D model (JSmol)
  • C1=CN=CC=C1C(=O)NN
  • InChI=1S/C6H7N3O/c7-9-6(10)5-1-3-8-4-2-5/h1-4H,7H2,(H,9,10) Yes check.svgY
  • Key:QRXWMOHMRWLFEY-UHFFFAOYSA-N Yes check.svgY
   (verify)

Isoniazid, also known as isonicotinic acid hydrazide (INH), is an antibiotic used for the treatment of tuberculosis. [4] For active tuberculosis, it is often used together with rifampicin, pyrazinamide, and either streptomycin or ethambutol. [5] For latent tuberculosis, it is often used alone. [4] It may also be used for atypical types of mycobacteria, such as M. avium , M. kansasii , and M. xenopi . [4] It is usually taken by mouth, but may be used by injection into muscle. [4]

Contents

History

First synthesis was described in 1912. [6] A. Kachugin invented the drug against tuberculosis under name Tubazid in 1949. Three pharmaceutical companies unsuccessfully attempted to patent the drug at the same time, [7] the most prominent one being Roche, which launched its version, Rimifon, in 1952. [8]

The drug was first tested at Many Farms, a Navajo community in Arizona, due to the Navajo reservation's tuberculosis problem and because the population had not previously been treated with streptomycin, the main tuberculosis treatment at the time. [9] The research was led by Walsh McDermott, an infectious disease researcher with an interest in public health, who had previously taken isoniazid to treat his own tuberculosis. [10]

Isoniazid and a related drug, iproniazid, were among the first drugs to be referred to as antidepressants. [11]

It is on the World Health Organization's List of Essential Medicines. [12] The World Health Organization classifies isoniazid as critically important for human medicine. [13] Isoniazid is available as a generic medication. [4]

Medical uses

Tuberculosis

Isoniazid is often used to treat latent and active tuberculosis infections. In persons with isoniazid-sensitive Mycobacterium tuberculosis infection, drug regimens based on isoniazid are usually effective when persons adhere to the prescribed treatment. However, in persons with isoniazid-resistant Mycobacterium tuberculosis infection, drug regimens based on isoniazid have a high rate of failure. [14]

Isoniazid has been approved as prophylactic therapy for the following populations:

Isoniazid can be used alone or in combination with Rifampin for treatment of latent tuberculosis, or as part of a four-drug regimen for treatment of active tuberculosis. [17] The drug regimen typically requires daily or weekly oral administration for a period of three to nine months, often under Directly Observed Therapy (DOT) supervision. [17]

Non-tuberculous mycobacteria

Isoniazid was widely used in the treatment of Mycobacterium avium complex as part of a regimen including rifampicin and ethambutol. [18] Evidence suggests that isoniazid prevents mycolic acid synthesis in M. avium complex as in M. tuberculosis [19] and although this is not bactericidal to M. avium complex, it greatly potentiates the effect of rifampicin. The introduction of macrolides led to this use greatly decreasing. However, since rifampicin is broadly underdosed in M. avium complex treatment, this effect may be worth re-investigating. [20]

Special populations

It is recommended that women with active tuberculosis who are pregnant or breastfeeding take isoniazid. Preventive therapy should be delayed until after giving birth. [21] Nursing mothers excrete a relatively low and non-toxic concentration of INH in breast milk, and their babies are at low risk for side effects. Both pregnant women and infants being breastfed by mothers taking INH should take vitamin B6 in its pyridoxine form to minimize the risk of peripheral nerve damage. [22] Vitamin B6 is used to prevent isoniazid-induced B6 deficiency and neuropathy in people with a risk factor, such as pregnancy, lactation, HIV infection, alcoholism, diabetes, kidney failure, or malnutrition. [23]

People with liver dysfunction are at a higher risk for hepatitis caused by INH, and may need a lower dose. [21]

Levels of liver enzymes in the bloodstream should be frequently checked in daily alcohol drinkers, pregnant women, IV drug users, people over 35, and those who have chronic liver disease, severe kidney dysfunction, peripheral neuropathy, or HIV infection since they are more likely to develop hepatitis from INH. [21] [24]

Side effects

Up to 20% of people taking isoniazid experience peripheral neuropathy when taking daily doses of 6 mg/kg of body weight or higher. [25] Gastrointestinal reactions include nausea and vomiting. [15] Aplastic anemia, thrombocytopenia, and agranulocytosis due to lack of production of red blood cells, platelets, and white blood cells by the bone marrow respectively, can also occur. [15] Hypersensitivity reactions are also common and can present with a maculopapular rash and fever. [15] Gynecomastia may occur. [17]

Asymptomatic elevation of serum liver enzyme concentrations occurs in 10% to 20% of people taking INH, and liver enzyme concentrations usually return to normal even when treatment is continued. [26] Isoniazid has a boxed warning for severe and sometimes fatal hepatitis, which is age-dependent at a rate of 0.3% in people 21 to 35 years old and over 2% in those over age 50. [15] [27] Symptoms suggestive of liver toxicity include nausea, vomiting, abdominal pain, dark urine, right upper quadrant pain, and loss of appetite. [15] Black and Hispanic women are at higher risk for isoniazid-induced hepatotoxicity. [15] When it happens, isoniazid-induced liver toxicity has been shown to occur in 50% of patients within the first 2 months of therapy. [28]

Some recommend that liver function should be monitored carefully in all people receiving it, [21] but others recommend monitoring only in certain populations. [26] [29] [30]

Headache, poor concentration, weight gain, poor memory, insomnia, and depression have all been associated with isoniazid use. [31] All patients and healthcare workers should be aware of these serious side effects, especially if suicidal ideation or behavior are suspected. [31] [32] [33]

Isoniazid is associated with pyridoxine (vitamin B6) deficiency because of its similar structure. Isoniazid is also associated with increased excretion of pyridoxine. Pyridoxal phosphate (a derivative of pyridoxine) is required for δ-aminolevulinic acid synthase, the enzyme responsible for the rate-limiting step in heme synthesis. Therefore, isoniazid-induced pyridoxine deficiency causes insufficient heme formation in early red blood cells, leading to sideroblastic anemia. [23]

Isoniazid was found to significantly elevate the in vivo concentration of GABA and homocarnosine in a single subject via magnetic resonance spectroscopy. [34]

Drug interactions

People taking isoniazid and acetaminophen are at risk of acetaminophen toxicity. Isoniazid is thought to induce a liver enzyme which causes a larger amount of acetaminophen to be metabolized to a toxic form. [35] [36]

Isoniazid decreases the metabolism of carbamazepine, thus slowing down its clearance from the body. People taking carbamazepine should have their carbamazepine levels monitored and, if necessary, have their dose adjusted accordingly. [37]

It is possible that isoniazid may decrease the serum levels of ketoconazole after long-term treatment. This is seen with the simultaneous use of rifampin, isoniazid, and ketoconazole. [38]

Isoniazid may increase the amount of phenytoin in the body. The doses of phenytoin may need to be adjusted when given with isoniazid. [39] [40]

Isoniazid may increase the plasma levels of theophylline. There are some cases of theophylline slowing down isoniazid elimination. Both theophylline and isoniazid levels should be monitored. [41]

Valproate levels may increase when taken with isoniazid. Valproate levels should be monitored and its dose adjusted if necessary. [39]

Mechanism of action

Isoniazid is a prodrug that inhibits the formation of the mycobacterial cell wall. Isoniazid must be activated by KatG, a bacterial catalase-peroxidase enzyme in Mycobacterium tuberculosis . [42] KatG catalyzes the formation of the isonicotinic acyl radical, which spontaneously couples with NADH to form the nicotinoyl-NAD adduct. This complex binds tightly to the enoyl-acyl carrier protein reductase InhA, thereby blocking the natural enoyl-AcpM substrate and the action of fatty acid synthase. This process inhibits the synthesis of mycolic acids, which are required components of the mycobacterial cell wall. A range of radicals are produced by KatG activation of isoniazid, including nitric oxide, [43] which has also been shown to be important in the action of another antimycobacterial prodrug pretomanid. [44]

Activation of isoniazid with NAD.jpg

Isoniazid is bactericidal to rapidly dividing mycobacteria, but is bacteriostatic if the mycobacteria are slow-growing. [45] It inhibits the cytochrome P450 system and hence acts as a source of free radicals. [46]

Isoniazid is a mild non-selective monoamine oxidase inhibitor(MAO-I). [47]

Metabolism

Isoniazid reaches therapeutic concentrations in serum, cerebrospinal fluid, and within caseous granulomas. It is metabolized in the liver via acetylation into acetylhydrazine. Two forms of the enzyme are responsible for acetylation, so some patients metabolize the drug more quickly than others. Hence, the half-life is bimodal, with "slow acetylators" and "fast acetylators". A graph of number of people versus time shows peaks at one and three hours. The height of the peaks depends on the ethnicities of the people being tested. The metabolites are excreted in the urine. Doses do not usually have to be adjusted in case of renal failure.[ citation needed ]


Preparation

Isoniazid is an isonicotinic acid derivative. It is manufactured using 4-cyanopyridine and hydrazine hydrate. [48] In another method, isoniazid was claimed to have been made from citric acid starting material. [49]

It can in theory be made from methyl isonicotinate, which is labelled a semiochemical.

Brand names

Hydra, Hyzyd, Isovit, Laniazid, Nydrazid, Rimifon, and Stanozide. [50]

Other uses

Chromatography

Isonicotinic acid hydrazide is also used in chromatography to differentiate between various degrees of conjugation in organic compounds barring the ketone functional group. [51] The test works by forming a hydrazone which can be detected by its bathochromic shift.[ citation needed ]

Dogs

Isoniazid may be used for dogs, but there have been concerns it can cause seizures. [52]

Related Research Articles

<span class="mw-page-title-main">Tuberculosis</span> Infectious disease

Tuberculosis (TB), also known colloquially as the "white death", or historically as consumption, is an infectious disease usually caused by Mycobacterium tuberculosis (MTB) bacteria. Tuberculosis generally affects the lungs, but it can also affect other parts of the body. Most infections show no symptoms, in which case it is known as latent tuberculosis. Around 10% of latent infections progress to active disease which, if left untreated, kill about half of those affected. Typical symptoms of active TB are chronic cough with blood-containing mucus, fever, night sweats, and weight loss. Infection of other organs can cause a wide range of symptoms.

<i>Mycobacterium tuberculosis</i> Species of pathogenic bacteria that causes tuberculosis

Mycobacterium tuberculosis, also known as Koch's bacillus, is a species of pathogenic bacteria in the family Mycobacteriaceae and the causative agent of tuberculosis. First discovered in 1882 by Robert Koch, M. tuberculosis has an unusual, waxy coating on its cell surface primarily due to the presence of mycolic acid. This coating makes the cells impervious to Gram staining, and as a result, M. tuberculosis can appear weakly Gram-positive. Acid-fast stains such as Ziehl–Neelsen, or fluorescent stains such as auramine are used instead to identify M. tuberculosis with a microscope. The physiology of M. tuberculosis is highly aerobic and requires high levels of oxygen. Primarily a pathogen of the mammalian respiratory system, it infects the lungs. The most frequently used diagnostic methods for tuberculosis are the tuberculin skin test, acid-fast stain, culture, and polymerase chain reaction.

<i>Mycobacterium</i> Genus of bacteria

Mycobacterium is a genus of over 190 species in the phylum Actinomycetota, assigned its own family, Mycobacteriaceae. This genus includes pathogens known to cause serious diseases in mammals, including tuberculosis and leprosy in humans. The Greek prefix myco- means 'fungus', alluding to this genus' mold-like colony surfaces. Since this genus has cell walls with a waxy lipid-rich outer layer that contains high concentrations of mycolic acid, acid-fast staining is used to emphasize their resistance to acids, compared to other cell types.

<span class="mw-page-title-main">Rifampicin</span> Antibiotic medication

Rifampicin, also known as rifampin, is an ansamycin antibiotic used to treat several types of bacterial infections, including tuberculosis (TB), Mycobacterium avium complex, leprosy, and Legionnaires' disease. It is almost always used together with other antibiotics with two notable exceptions: when given as a "preferred treatment that is strongly recommended" for latent TB infection; and when used as post-exposure prophylaxis to prevent Haemophilus influenzae type b and meningococcal disease in people who have been exposed to those bacteria. Before treating a person for a long period of time, measurements of liver enzymes and blood counts are recommended. Rifampicin may be given either by mouth or intravenously.

<span class="mw-page-title-main">Management of tuberculosis</span> Disease treatment

Management of tuberculosis refers to techniques and procedures utilized for treating tuberculosis (TB), or simply a treatment plan for TB.

<span class="mw-page-title-main">Miliary tuberculosis</span> Medical condition

Miliary tuberculosis is a form of tuberculosis that is characterized by a wide dissemination into the human body and by the tiny size of the lesions (1–5 mm). Its name comes from a distinctive pattern seen on a chest radiograph of many tiny spots distributed throughout the lung fields with the appearance similar to millet seeds—thus the term "miliary" tuberculosis. Miliary TB may infect any number of organs, including the lungs, liver, and spleen. Miliary tuberculosis is present in about 2% of all reported cases of tuberculosis and accounts for up to 20% of all extra-pulmonary tuberculosis cases.

<span class="mw-page-title-main">Pyrazinamide</span> Medication

Pyrazinamide is a medication used to treat tuberculosis. For active tuberculosis, it is often used with rifampicin, isoniazid, and either streptomycin or ethambutol. It is not generally recommended for the treatment of latent tuberculosis. It is taken by mouth.

<span class="mw-page-title-main">Ethambutol</span> Chemical compound

Ethambutol is a medication primarily used to treat tuberculosis. It is usually given in combination with other tuberculosis medications, such as isoniazid, rifampicin and pyrazinamide. It may also be used to treat Mycobacterium avium complex, and Mycobacterium kansasii. It is taken by mouth.

<span class="mw-page-title-main">4-Aminosalicylic acid</span> Anti-tuberculosis and anti-inflammatory drug

4-Aminosalicylic acid, also known as para-aminosalicylic acid (PAS) and sold under the brand name Paser among others, is an antibiotic primarily used to treat tuberculosis. Specifically it is used to treat active drug resistant tuberculosis together with other antituberculosis medications. It has also been used as a second line agent to sulfasalazine in people with inflammatory bowel disease such as ulcerative colitis and Crohn's disease. It is typically taken by mouth.

<span class="mw-page-title-main">Iproniazid</span> Antidepressant

Iproniazid is a non-selective, irreversible monoamine oxidase inhibitor (MAOI) of the hydrazine class. It is a xenobiotic that was originally designed to treat tuberculosis, but was later most prominently used as an antidepressant drug. However, it was withdrawn from the market because of its hepatotoxicity. The medical use of iproniazid was discontinued in most of the world in the 1960s, but remained in use in France until its discontinuation in 2015.

<span class="mw-page-title-main">Clofazimine</span> Medication

Clofazimine, sold under the brand name Lamprene, is a medication used together with rifampicin and dapsone to treat leprosy. It is specifically used for multibacillary (MB) leprosy and erythema nodosum leprosum. Evidence is insufficient to support its use in other conditions though a retrospective study found it 95% effective in the treatment of Mycobacterium avium complex (MAC) when administered with a macrolide and ethambutol, as well as the drugs amikacin and clarithromycin. However, in the United States, clofazimine is considered an orphan drug, is unavailable in pharmacies, and its use in the treatment of MAC is overseen by the Food and Drug Administration. It is taken orally.

<i>Mycobacterium avium-intracellulare</i> infection Medical condition

Mycobacterium avium-intracellulare infection (MAI) is an atypical mycobacterial infection, i.e. one with nontuberculous mycobacteria or NTM, caused by Mycobacterium avium complex (MAC), which is made of two Mycobacterium species, M. avium and M. intracellulare. This infection causes respiratory illness in birds, pigs, and humans, especially in immunocompromised people. In the later stages of AIDS, it can be very severe. It usually first presents as a persistent cough. It is typically treated with a series of three antibiotics for a period of at least six months.

Latent tuberculosis (LTB), also called latent tuberculosis infection (LTBI) is when a person is infected with Mycobacterium tuberculosis, but does not have active tuberculosis (TB). Active tuberculosis can be contagious while latent tuberculosis is not, and it is therefore not possible to get TB from someone with latent tuberculosis. The main risk is that approximately 10% of these people will go on to develop active tuberculosis. This is particularly true, and there is added risk, in particular situations such as medication that suppresses the immune system or advancing age.

<span class="mw-page-title-main">Tuberculous meningitis</span> Medical condition

Tuberculous meningitis, also known as TB meningitis or tubercular meningitis, is a specific type of bacterial meningitis caused by the Mycobacterium tuberculosis infection of the meninges—the system of membranes which envelop the central nervous system.

<span class="mw-page-title-main">Ethionamide</span> Chemical compound

Ethionamide is an antibiotic used to treat tuberculosis. Specifically it is used, along with other antituberculosis medications, to treat active multidrug-resistant tuberculosis. It is no longer recommended for leprosy. It is taken by mouth.

Mycobacterium avium complex is a group of mycobacteria comprising Mycobacterium intracellulare and Mycobacterium avium that are commonly grouped because they infect humans together; this group, in turn, is part of the group of nontuberculous mycobacteria. These bacteria cause Mycobacterium avium-intracellulare infections or Mycobacterium avium complex infections in humans. These bacteria are common and are found in fresh and salt water, in household dust and in soil. MAC bacteria usually cause infection in those who are immunocompromised or those with severe lung disease.

<span class="mw-page-title-main">Multidrug-resistant tuberculosis</span> Medical condition

Multidrug-resistant tuberculosis (MDR-TB) is a form of tuberculosis (TB) infection caused by bacteria that are resistant to treatment with at least two of the most powerful first-line anti-TB medications (drugs): isoniazid and rifampicin. Some forms of TB are also resistant to second-line medications, and are called extensively drug-resistant TB (XDR-TB).

Delamanid is sold under the brand name Deltyba, is a medication used to treat tuberculosis. Specifically it is used, along with other antituberculosis medications, for active multidrug-resistant tuberculosis. It is taken by mouth.

Ethambutol/isoniazid/pyrazinamide/rifampicin, also known as ethambutol/isoniazid/pyrazinamide/rifampin, is a medication used for tuberculosis. It is a fixed dose combination of ethambutol, isoniazid, pyrazinamide, and rifampicin. It is used either alone or with other antituberculosis medication. It is taken by mouth.

References

  1. "Isoniazid (Nydrazid) Use During Pregnancy". Drugs.com. 7 October 2019. Retrieved 24 January 2020.
  2. "Drug and medical device highlights 2018: Helping you maintain and improve your health". Health Canada . 14 October 2020. Retrieved 17 April 2024.
  3. "FDA-sourced list of all drugs with black box warnings (Use Download Full Results and View Query links.)". nctr-crs.fda.gov. FDA . Retrieved 22 Oct 2023.
  4. 1 2 3 4 5 "Isoniazid". The American Society of Health-System Pharmacists. Archived from the original on 20 December 2016. Retrieved 8 December 2016.
  5. World Health Organization (2009). Stuart MC, Kouimtzi M, Hill SR (eds.). WHO Model Formulary 2008. World Health Organization. p. 136. hdl: 10665/44053 . ISBN   9789241547659.
  6. Saygin D, Tabib T, Bittar HE, Valenzi E, Sembrat J, Chan SY, et al. (1912-04-01). "Transcriptional profiling of lung cell populations in idiopathic pulmonary arterial hypertension". Pulmonary Circulation (in German). 10 (1): 393–414. doi:10.1177/2045894020908782. PMC   7052475 . PMID   32166015.
  7. Rieder HL (April 2009). "Fourth-generation fluoroquinolones in tuberculosis". Lancet. 373 (9670): 1148–1149. doi:10.1016/S0140-6736(09)60559-6. PMID   19345815. S2CID   43789954.
  8. "History". rocheusa.com. Roche USA. Archived from the original on 2007-12-12.
  9. Jones DS (2002). "The health care experiments at Many Farms: the Navajo, tuberculosis, and the limits of modern medicine, 1952-1962". Bulletin of the History of Medicine. 76 (4): 749–790. doi:10.1353/bhm.2002.0186. PMID   12446978. S2CID   30166423.
  10. Beeson PB (1990). "Walsh McDermott". Biographical Memoirs. Vol. 59. National Academies Press. pp. 282–307. doi:10.17226/1652. ISBN   978-0-309-04198-0.
  11. Moncrieff J (June 2008). "The creation of the concept of an antidepressant: an historical analysis" (PDF). Social Science & Medicine. 66 (11): 2346–2355. doi:10.1016/j.socscimed.2008.01.047. PMID   18321627.
  12. Organization WH (2019). World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization. hdl: 10665/325771 . WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
  13. Critically important antimicrobials for human medicine (6th revision ed.). Geneva: World Health Organization. 2019. hdl: 10665/312266 . ISBN   9789241515528.
  14. Gegia M, Winters N, Benedetti A, van Soolingen D, Menzies D (February 2017). "Treatment of isoniazid-resistant tuberculosis with first-line drugs: a systematic review and meta-analysis". The Lancet. Infectious Diseases. 17 (2): 223–234. doi:10.1016/S1473-3099(16)30407-8. PMID   27865891.
  15. 1 2 3 4 5 6 7 "Isoniazid (package insert)". 30 March 2023.
  16. "The Use of Preventive Therapy for Tuberculosis Infection in the United States – Recommendations of the Advisory Committee for Elimination of Tuberculosis". Morbidity and Mortality Weekly Report. 39 (RR-8): 9–12. May 18, 1990. Archived from the original on 2 March 2016. Retrieved 22 February 2016.
  17. 1 2 3 Lewis SM, Dirksen SR, Heitkemper MM, Bucher L, Harding M (5 December 2013). Medical-surgical nursing : assessment and management of clinical problems (Ninth ed.). St. Louis, Missouri. ISBN   978-0-323-10089-2. OCLC   228373703.{{cite book}}: CS1 maint: location missing publisher (link)
  18. Research Committee Of The British Thoracic Society (March 2001). "First randomised trial of treatments for pulmonary disease caused by M avium intracellulare, M malmoense, and M xenopi in HIV negative patients: rifampicin, ethambutol and isoniazid versus rifampicin and ethambutol". Thorax. 56 (3): 167–172. doi:10.1136/thorax.56.3.167. PMC   1758783 . PMID   11182006.
  19. Mdluli K, Swanson J, Fischer E, Lee RE, Barry CE (March 1998). "Mechanisms involved in the intrinsic isoniazid resistance of Mycobacterium avium". Molecular Microbiology. 27 (6): 1223–1233. doi: 10.1046/j.1365-2958.1998.00774.x . PMID   9570407. S2CID   13764717.
  20. van Ingen J, Egelund EF, Levin A, Totten SE, Boeree MJ, Mouton JW, et al. (September 2012). "The pharmacokinetics and pharmacodynamics of pulmonary Mycobacterium avium complex disease treatment". American Journal of Respiratory and Critical Care Medicine. 186 (6): 559–565. doi:10.1164/rccm.201204-0682OC. PMID   22744719.
  21. 1 2 3 4 "Isoniazid tablet". DailyMed. 18 October 2018. Archived from the original on 13 March 2019. Retrieved 24 January 2020.
  22. Bothamley G (2001). "Drug treatment for tuberculosis during pregnancy: safety considerations". Drug Safety. 24 (7): 553–565. doi:10.2165/00002018-200124070-00006. PMID   11444726. S2CID   10479433.
  23. 1 2 Steichen O, Martinez-Almoyna L, De Broucker T (April 2006). "[Isoniazid induced neuropathy: consider prevention]". Revue des Maladies Respiratoires. 23 (2 Pt 1): 157–160. doi:10.1016/S0761-8425(06)71480-2. PMID   16788441.
  24. Saukkonen JJ, Cohn DL, Jasmer RM, Schenker S, Jereb JA, Nolan CM, et al. (October 2006). "An official ATS statement: hepatotoxicity of antituberculosis therapy". American Journal of Respiratory and Critical Care Medicine. 174 (8): 935–952. doi:10.1164/rccm.200510-1666ST. PMID   17021358. S2CID   36384722.
  25. Alldredge B (February 12, 2013). Applied Therapeutics. Lippincott Williams & Wilkins. ISBN   9781609137137.
  26. 1 2 "Latent Tuberculosis Infection: A Guide for Primary Health Care Providers". cdc.gov. Center for Disease Control. Archived from the original on 25 March 2016. Retrieved 25 March 2016.
  27. Trevor, A. & Katzung, B. (2013). Katzung & Trevor's Pharmacology: examination & board review (10th ed., p. 417). New York. McGraw-Hill Medical, Lange.
  28. "Isoniazid UpToDate". Archived from the original on 2015-10-25.
  29. "Treatment of Tuberculosis – Guidelines (4th ed.)" (PDF). who.int. World Health Organization. Archived (PDF) from the original on 4 April 2016. Retrieved 25 March 2016.
  30. Joint T (July 1998). "Chemotherapy and management of tuberculosis in the United Kingdom: recommendations 1998. Joint Tuberculosis Committee of the British Thoracic Society". Thorax. 53 (7): 536–548. doi:10.1136/thx.53.7.536. PMC   1745276 . PMID   9797751.
  31. 1 2 Alao AO, Yolles JC (September 1998). "Isoniazid-induced psychosis". The Annals of Pharmacotherapy. 32 (9): 889–891. doi:10.1345/aph.17377. PMID   9762376. S2CID   73122253.
  32. Iannaccone R, Sue YJ, Avner JR (February 2002). "Suicidal psychosis secondary to isoniazid". Pediatric Emergency Care. 18 (1): 25–27. doi: 10.1097/00006565-200202000-00008 . PMID   11862134. S2CID   31383347.
  33. Pallone KA, Goldman MP, Fuller MA (February 1993). "Isoniazid-associated psychosis: case report and review of the literature". The Annals of Pharmacotherapy. 27 (2): 167–170. doi:10.1177/106002809302700205. PMID   8439690. S2CID   28637999.
  34. Landheer K, Prinsen H, Petroff OA, Rothman DL, Juchem C (June 2020). "Elevated homocarnosine and GABA in subject on isoniazid as assessed through 1H MRS at 7T". Analytical Biochemistry. 599: 113738. doi:10.1016/j.ab.2020.113738. PMID   32302606. S2CID   215809029.
  35. Murphy R, Swartz R, Watkins PB (November 1990). "Severe acetaminophen toxicity in a patient receiving isoniazid". Annals of Internal Medicine. 113 (10): 799–800. doi:10.7326/0003-4819-113-10-799. PMID   2240884.
  36. Burk RF, Hill KE, Hunt RW, Martin AE (July 1990). "Isoniazid potentiation of acetaminophen hepatotoxicity in the rat and 4-methylpyrazole inhibition of it". Research Communications in Chemical Pathology and Pharmacology. 69 (1): 115–118. PMID   2218067.
  37. Fleenor ME, Harden JW, Curtis G (June 1991). "Interaction between carbamazepine and antituberculosis agents". Chest. 99 (6): 1554. doi: 10.1378/chest.99.6.1554a . PMID   2036861.
  38. Baciewicz AM, Baciewicz FA (September 1993). "Ketoconazole and fluconazole drug interactions". Archives of Internal Medicine. 153 (17): 1970–1976. doi:10.1001/archinte.153.17.1970. PMID   8357281.
  39. 1 2 Jonville AP, Gauchez AS, Autret E, Billard C, Barbier P, Nsabiyumva F, et al. (1991). "Interaction between isoniazid and valproate: a case of valproate overdosage". European Journal of Clinical Pharmacology. 40 (2): 197–198. doi:10.1007/BF00280078. PMID   2065702. S2CID   22218366.
  40. Bass JB, Farer LS, Hopewell PC, O'Brien R, Jacobs RF, Ruben F, et al. (May 1994). "Treatment of tuberculosis and tuberculosis infection in adults and children. American Thoracic Society and The Centers for Disease Control and Prevention". American Journal of Respiratory and Critical Care Medicine. 149 (5): 1359–1374. doi:10.1164/ajrccm.149.5.8173779. PMID   8173779.
  41. Höglund P, Nilsson LG, Paulsen O (February 1987). "Interaction between isoniazid and theophylline". European Journal of Respiratory Diseases. 70 (2): 110–116. PMID   3817069.
  42. Suarez J, Ranguelova K, Jarzecki AA, Manzerova J, Krymov V, Zhao X, et al. (March 2009). "An oxyferrous heme/protein-based radical intermediate is catalytically competent in the catalase reaction of Mycobacterium tuberculosis catalase-peroxidase (KatG)". The Journal of Biological Chemistry. 284 (11): 7017–7029. doi: 10.1074/jbc.M808106200 . PMC   2652337 . PMID   19139099.
  43. Timmins GS, Master S, Rusnak F, Deretic V (August 2004). "Nitric oxide generated from isoniazid activation by KatG: source of nitric oxide and activity against Mycobacterium tuberculosis". Antimicrobial Agents and Chemotherapy. 48 (8): 3006–3009. doi:10.1128/AAC.48.8.3006-3009.2004. PMC   478481 . PMID   15273113.
  44. Singh R, Manjunatha U, Boshoff HI, Ha YH, Niyomrattanakit P, Ledwidge R, et al. (November 2008). "PA-824 kills nonreplicating Mycobacterium tuberculosis by intracellular NO release". Science. 322 (5906): 1392–1395. Bibcode:2008Sci...322.1392S. doi:10.1126/science.1164571. PMC   2723733 . PMID   19039139.
  45. Ahmad Z, Klinkenberg LG, Pinn ML, Fraig MM, Peloquin CA, Bishai WR, et al. (October 2009). "Biphasic kill curve of isoniazid reveals the presence of drug-tolerant, not drug-resistant, Mycobacterium tuberculosis in the guinea pig". The Journal of Infectious Diseases. 200 (7): 1136–1143. doi: 10.1086/605605 . PMID   19686043.
  46. Harvey RA, Howland RD, Mycek MJ, Champe PC (2006). Harvey RA, Champe PC (eds.). Pharmacology. Vol. 864 (4th ed.). Lippincott Williams & Wilkins. ISBN   9780781741187.
  47. Judd FK, Mijch AM, Cockram A, Norman TR (1994). "Isoniazid and antidepressants: is there cause for concern?". International Clinical Psychopharmacology. 9 (2): 123–125. doi:10.1097/00004850-199400920-00009. PMID   8056994.
  48. William Andrew Publishing (2008). Pharmaceutical Manufacturing Encyclopedia (3rd ed.). Norwich, NY: Elsevier Science. pp. 1968–1970. ISBN   9780815515265.
  49. Baizer MM, Dub M, Gister S, Steinberg NG (July 1956). "Synthesis of isoniazid from citric acid". Journal of the American Pharmaceutical Association. 45 (7): 478–480. doi:10.1002/jps.3030450714. PMID   13345683.
  50. "Drugs@FDA". fda.gov. United States Food and Drug Administration. Archived from the original on 14 August 2012. Retrieved 22 August 2016.
  51. Saygin D, Tabib T, Bittar HE, Valenzi E, Sembrat J, Chan SY, et al. (1959). "Transcriptional profiling of lung cell populations in idiopathic pulmonary arterial hypertension". Pulmonary Circulation. 10 (1): 102–105. doi:10.1021/ac60145a020. PMC   7052475 . PMID   32166015.
  52. Sykes JE (2013). Canine and Feline Infectious Diseases (E-Book). Elsevier Health Sciences. p. 425. ISBN   978-0323241946 via Google Books.

Further reading