A patient with pulmonary tuberculosis develops peripheral neuropathy and sideroblastic anaemia after 2 months of anti-TB treatment. These adverse effects are most likely attributable to which drug and which mechanism?
- A Isoniazid causing pyridoxine (vitamin B6) deficiency by competing with pyridoxal phosphate ✓
- B Rifampicin causing enzyme induction and vitamin K depletion
- C Pyrazinamide causing hyperuricaemia and tubular toxicity
- D Ethambutol causing optic neuritis by chelating copper
Explanation
Isoniazid (INH) is a structural analogue of pyridoxine; it inhibits pyridoxal kinase and competes with pyridoxal phosphate, depleting active B6. Pyridoxine deficiency causes peripheral sensory neuropathy (symmetrical stocking-glove) and sideroblastic anaemia (B6-dependent ALA synthase in haem synthesis is impaired, causing iron accumulation in ring sideroblasts). Prophylactic pyridoxine 10–25 mg/day is co-administered in at-risk patients (diabetics, alcoholics, elderly). Ethambutol causes optic neuritis (retrobulbar). Pyrazinamide causes hyperuricaemia. Rifampicin causes hepatotoxicity and induces CYP450 enzymes.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
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