A patient on anti-TB treatment develops peripheral neuropathy. Investigation reveals pyridoxine deficiency induced by a first-line drug. Which mechanism explains why this drug causes pyridoxine deficiency?
- A Isoniazid competes with pyridoxal phosphate for binding to pyridoxal kinase, accelerating its excretion ✓
- B Rifampicin induces CYP450 enzymes, increasing pyridoxine metabolism
- C Ethambutol chelates zinc, impairing pyridoxine-dependent enzymes
- D Pyrazinamide inhibits pyridoxal phosphate synthesis from pyridoxine
Explanation
Isoniazid (INH) has structural similarity to pyridoxal and competes with it; INH reacts with pyridoxal to form INH-pyridoxal hydrazones that are excreted in urine, depleting pyridoxal phosphate (the active form of B6); pyridoxine supplementation (25-50 mg/day) is given prophylactically. Rifampicin induces CYP450 and can affect many drugs but does not specifically cause pyridoxine deficiency. Ethambutol causes optic neuritis by chelating zinc in retinal ganglion cells, not pyridoxine depletion. Pyrazinamide causes hyperuricemia by inhibiting tubular secretion of urate.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
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