isoniazidinduced

Isoniazid-induced adverse effects describe the range of toxicities associated with isoniazid, a first-line antituberculosis medication. The most serious is hepatotoxicity, which can present as asymptomatic transaminase elevations or as acute hepatitis and, rarely, liver failure. Risk factors include older age, alcoholism, preexisting liver disease, use of other hepatotoxic drugs, and slow acetylator status due to NAT2 genetic variation. The mechanism involves formation of toxic metabolites and idiosyncratic reactions that injure liver cells; onset is typically during the first months of therapy.

Isoniazid can cause peripheral neuropathy resulting from depletion of pyridoxine (vitamin B6) and inhibition of pyridoxine-dependent enzymes. Symptoms are symmetric numbness, tingling, and burning pain, usually starting in the feet. Risk factors include malnutrition, diabetes, alcoholism, HIV infection, and advanced age. Routine pyridoxine supplementation (commonly 25–50 mg daily) is recommended in at-risk patients to reduce both neuropathy and related symptoms.

Other adverse effects are less common but may include sideroblastic anemia, optic neuritis, rash, hypersensitivity reactions, and rarely drug-induced lupus erythematosus. Neurologic and hematologic effects are more likely with prolonged use or high doses and in individuals with vitamin deficiencies.

Monitoring and management emphasize baseline and periodic liver function testing, especially in high-risk patients. If hepatotoxicity is suspected, isoniazid should be withheld, and clinical evaluation and supportive care should be provided. Rechallenge or modification of therapy may be considered based on TB risk, with careful monitoring for recurrent toxicity. Pyridoxine supplementation remains a key preventive measure for neurotoxicity in susceptible individuals.