Isoniazid (INH) causes peripheral neuropathy as a dose-related adverse effect. The mechanism is:
- A Direct axonal membrane toxicity via reactive nitrogen intermediates
- B Interference with thiamine (B1) metabolism causing Wernicke-like neuropathy
- C INH competes with pyridoxal phosphate (activated vitamin B6) for enzyme binding sites, causing functional pyridoxine deficiency ✓
- D Inhibition of vitamin B12 absorption in the ileum
Correct answer: C. INH competes with pyridoxal phosphate (activated vitamin B6) for enzyme binding sites, causing functional pyridoxine deficiency
Explanation
INH is structurally similar to pyridoxine and forms hydrazones with pyridoxal phosphate, depleting its active coenzyme form. Pyridoxal phosphate is essential for transamination reactions and synthesis of GABA and other neurotransmitters. Supplementation with pyridoxine (25–50 mg/day) prevents INH-induced peripheral neuropathy, especially in malnourished patients, diabetics, alcoholics, and slow acetylators. This is not related to thiamine or B12 deficiency.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.