A tuberculosis patient on anti-tubercular treatment presents with a tingling sensation and paresthesia in the lower limbs. He is not a diabetic and occasionally consumes alcohol. Which of the following vitamins must be supplemented to this patient?

Correct Answer: B. Vitamin B6

Isoniazid (INH), a first-line anti-tubercular drug, is a pyridoxine (Vitamin B6) antagonist that inhibits pyridoxal phosphate (the active form of B6) and increases its urinary excretion. This leads to B6 deficiency, which manifests as peripheral neuropathy — presenting with tingling, paresthesia, and numbness in the lower limbs (stocking-glove distribution). The neuropathy is dose-dependent and more common with prolonged INH therapy, especially in slow acetylators (genetically determined). Since the patient is not diabetic and only occasionally consumes alcohol (ruling out alcoholic neuropathy), and presents with classic INH-induced peripheral neuropathy, Vitamin B6 supplementation is mandatory. Indian guidelines (RNTCP/NTEP) recommend prophylactic B6 supplementation (10 mg daily) in all TB patients on INH, particularly those at risk (slow acetylators, malnutrition, alcoholism, diabetes). This prevents the neuropathy entirely. The mechanism is straightforward: B6 is essential for synthesis of neurotransmitters (GABA, serotonin) and myelin formation; its deficiency impairs nerve conduction and causes demyelination.

Why the other options are wrong

A. Vitamin B12 — B12 deficiency causes subacute combined degeneration with posterior column signs (loss of vibration/proprioception), upper motor neuron signs, and megaloblastic anemia — not the acute peripheral neuropathy seen here. While INH can rarely cause B12 malabsorption, it is not a direct B12 antagonist like it is for B6. B12 supplementation is not routine in TB patients unless there is documented deficiency or pernicious anemia. C. Vitamin B2 — Riboflavin (B2) deficiency causes ariboflavinosis with angular cheilitis, glossitis, and seborrheic dermatitis — not peripheral neuropathy. INH does not significantly deplete B2 stores. B2 is not a recognized complication of anti-tubercular therapy and is not routinely supplemented in TB patients. D. Vitamin B3 — Niacin (B3) deficiency causes pellagra (dermatitis, diarrhea, dementia, death) — a systemic condition, not isolated peripheral neuropathy. INH is not a niacin antagonist. While some anti-TB drugs (like rifampicin) may affect B3 metabolism, niacin supplementation is not standard in TB therapy and does not prevent INH-induced neuropathy.

High-Yield Facts

Mnemonics

INH Toxicity — B6 Link Isoniazid → B6 deficiency → Neuropathy. Remember: INH + Neuropathy = B6. The 'I' and 'B6' are phonetically linked in coaching — 'I need B6 for INH.' RNTCP Supplementation Rule All TB patients on INH get B6 prophylaxis (10 mg daily). No exceptions — it's in the national guidelines. If TB + neuropathy symptoms appear, B6 is the answer.

NBE Trap

NBE pairs INH-induced neuropathy with B12 deficiency to trap students who confuse peripheral neuropathy etiologies. While both cause neuropathy, only B6 is directly antagonized by INH; B12 deficiency causes subacute combined degeneration with upper motor neuron signs, not acute paresthesia.

Clinical Pearl

In Indian TB clinics, INH-induced neuropathy is a common complication in slow acetylators and malnourished patients. Routine B6 supplementation (10 mg daily) during the 2-month intensive phase and 4-month continuation phase prevents this entirely — a simple, cost-effective intervention that improves treatment adherence and outcomes.

_Reference: KD Tripathi Pharmacology Ch. 47 (Anti-tubercular drugs); Robbins Pathology Ch. 23 (Nutritional deficiencies); RNTCP Guidelines (Revised National TB Control Programme)_