Pyridoxine Management of Isoniazid‑Induced Neurotoxicity

Clinical Manifestations Reversed by Pyridoxine

Isoniazid‑induced peripheral neuropathy presents with numbness and paresthesia of the extremities, which can progress to loss of distal sensation; pyridoxine supplementation reverses these symptoms. 1
Motor dysfunction—including ataxia, generalized weakness, and loss of deep‑tendon reflexes—occurs with isoniazid neurotoxicity and improves after pyridoxine administration. 1
Axonal degeneration characterized by mitochondrial swelling and disruption of axoplasmic ground substance is observed in isoniazid‑related neuropathy and is mitigated by pyridoxine therapy. 1
Denervation of muscle fibers, especially those innervated by distal motor neurons, is a feature of isoniazid neurotoxicity that can be reversed with pyridoxine. 1
Seizures may develop in cases of isoniazid overdose; prompt pyridoxine treatment is effective in controlling seizure activity. 2

Standard preventive regimen: 25–50 mg of pyridoxine orally each day for individuals on tuberculosis therapy. 3
If peripheral neuropathy emerges during therapy, the dose should be increased to 100 mg daily. 3

For chronic pyridoxine deficiency causing neuropathy, administer 50–100 mg orally daily for 1–2 weeks to achieve symptom resolution. 2

Give 1 g of pyridoxine intravenously or intramuscularly for each gram of ingested isoniazid, repeating every 30 minutes as needed, up to a maximum total dose of 5 g. 2