A 58-year-old man with a history of tuberculosis treated with isoniazid and rifampin for 6 months presents with a new-onset seizure. He also reports peripheral neuropathy developing during TB treatment that never fully resolved. Current medications include only a multivitamin. Neurological examination confirms distal sensory loss and absent ankle reflexes. EEG shows focal epileptiform activity. MRI brain is unremarkable. Laboratory studies including glucose, electrolytes, and kidney function are normal. Considering his medication history and current presentation, which biochemical mechanism best explains the relationship between his previous treatment and current neurological manifestations?
Fat-soluble vitamins (A, D, E, K)
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Water-soluble vitamins - B complex
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Vitamin C (ascorbic acid)
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Macrominerals (Na, K, Ca, Mg, P, Cl)
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Trace minerals (Fe, Zn, Cu, Se, I)
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Vitamin cofactor functions in metabolism
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Deficiency syndromes of fat-soluble vitamins
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Deficiency syndromes of water-soluble vitamins
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Mineral deficiency disorders
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Vitamin toxicity syndromes
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Dietary sources and requirements
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Assessment of vitamin/mineral status
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