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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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C1-esterase inhibitor treatment during emergency coronary artery bypass surgery in patients with acute ST-elevation myocardial infarction
From CHEST, 10/1/05 by Matthias Thielmann

PURPOSE: Myocardial inflammatory response including complement activation was demonstrated as an important mechanism of ischemia-reperfusion injury and complement inhibition by CI-esterase-inhibitor (C1-INH) has recently shown cardioprotective effects in experimental and clinical settings.

METHODS: The effects of CI-INH on complement activation, perioperative myocardial cellular damage and patients outcome were studied inpatients undergoing emergency CABG due to acute ST-elevation myocardial infarction (STEMI) with (group 1,n=25) and without (group 2,n=25) bolus administration of C1-INH (40 IU.kg -1) during reperfusion and 6 hours (hrs) postoperatively (20 IU.kg-1) besides the same study protocol. Complement activation fragments (C4), C1-INH, and cardiac troponin I (cTnI) were measured preoperatively, and at 6, 12, 24, and 48 hrs postoperatively. Clinical data, adverse events and patients outcome were recorded prospectively.

RESULTS: Patient characteristics were not different between groups. No drug-related adverse events could be observed in group 1. Constant plasma levels of C1-INH and a reduction of C4 fragments were found in group 1. Preoperative cTnI levels were elevated but not different between the groups. The postoperative release of cTnI was significantly lower (P<0.05;ANOVA) in group 1 with [less than or equal to] 6hrs between symptom onset and reperfusion compared to group 2 at 12 (38.5 [+ or -] 22.1 versus 75.7 [+ or -] 24.6 ng/mL), 24 (65.5 [+ or -] 24.5 versus 95.2 [+ or -] 28.3 ng/mL), and 48hrs (58.3 [+ or -] 37.5 versus 87.5 [+ or -] 41.2 ng/mL) after surgery, but remained unchanged between the groups among patients with a treatment delay of more than 6hrs. Adverse events, ICU and hospital stay, and in-hospital mortality (13.4% versus 14.3%) were not different between the groups.

CONCLUSION: The present study is the first to evaluate the effects of complement inhibition during emergency CABG with STEMI. C1-INH effectively inhibited complement activation and did not cause adverse effects. The reduced release of cTnI was only observed in patients, who were treated within the first 6hrs from symptom onset to reperfusion.

CLINICAL IMPLICATIONS: C1-INH administration during emergency CABG with acute STEMI is safe and effective to inhibit complement activation and may reduce myocardial ischemia-reperfusion injury in patients undergoing CABG within 6hrs between symptom onset and reperfusion.

DISCLOSURE: Matthias Thielmann, None.

Matthias Thielmann MD * Guenter Marggraf MD Parwis Massoudy MD Markus Neuhauser PhD Stephan Knipp MD Markus Kamler MD Jarowit Piotrowski MD Heinz Jakob MD Thoracic and Cardiovascular Surgery, West-German Heart Center Essen, University, Essen, Germany

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