An antibiotic pill for tuberculosis (TB). It is combined with other TB drugs to treat active disease and is also used to prevent TB in people at high risk. It can cause severe, sometimes fatal liver injury and nerve damage felt as tingling in the hands and feet.
Isoniazid and other antituberculosis drugs are not on the ISMP acute care high-alert list.
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The label does not describe a narrow therapeutic index or direct dosing by measured blood levels of the drug.
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Severe and sometimes fatal hepatitis can occur, even after many months of therapy. Risk is age related (about 23 per 1,000 at ages 50 to 64) and higher with daily alcohol use, chronic liver disease, injection drug use, and in women, particularly Black and Hispanic women and after delivery. Interview patients monthly; for those 35 and older, measure AST and ALT before starting and periodically. Strongly consider stopping if liver tests rise beyond 3 to 5 times the normal upper limit, stop promptly for symptoms of liver injury, and defer preventive therapy in acute liver disease.
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Pyridoxine (vitamin B6) given IV. If the amount ingested is known, give pyridoxine gram for gram equal to the isoniazid dose as a slow IV bolus over 3 to 5 minutes; if unknown, start with 5 g in adults or 80 mg/kg in children, and repeat if seizures continue. Add diazepam for seizures that do not respond, support ventilation, and correct metabolic acidosis. Symptoms start 30 minutes to 3 hours after ingestion, and 80 to 150 mg/kg can be fatal if untreated.
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Doses come from the FDA label. Study tool, not for clinical decisions.
No dose table. Monitor carefully in severe renal dysfunction. Most reported cases of cerebellar syndrome occurred in chronic kidney disease.
Inhibits synthesis of mycolic acids, an essential component of the mycobacterial cell wall, and kills actively growing M. tuberculosis both inside and outside cells. Peak levels occur 1 to 2 hours after an oral dose; it distributes into all body fluids including CSF, crosses the placenta, and 50% to 70% of a dose is excreted in urine within 24 hours. It is inactivated mainly by acetylation, which is genetically determined; slow acetylators reach higher levels and more toxicity. Resistance comes from mutations in katG, inhA, kasA, and ahpC and develops rapidly with monotherapy.