Vitamin B3

Function

Mnemonic

Active forms of Niacin are NAD+ and NADP+.

• Cofactor for redox reactions (e.g., alcohol dehydrogenase, isocitrate dehydrogenase, G6PD)
• Required for the metabolism of fats, carbohydrates, and proteins.
• Synthesized endogenously from the amino acid tryptophan. Requires vitamins B2 (riboflavin) and B6 (pyridoxine) as cofactors.

Therapeutic use

• Dyslipidemia: Niacin lowers VLDL and increases HDL serum levels (See Lipid-lowering agents)

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Vitamin B3 deficiency

Etiology

• Malnutrition: Most common cause worldwide (e.g., alcohol use disorder, diets heavy in corn).
• Hartnup disease: Autosomal recessive disorder causing defective intestinal and renal absorption of neutral amino acids, including tryptophan.
• Malignant carcinoid syndrome: Increased metabolism of tryptophan to serotonin leads to less tryptophan available for niacin synthesis.
• Isoniazid (INH) therapy: INH depletes vitamin B6 (pyridoxine), a required cofactor for niacin synthesis.
• Prolonged diarrhea: Malabsorption.

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Pathophysiology

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Clinical features

• Glossitis
• Pellagra (caused by severe deficiency)
  • Characteristic dermatitis
    • Circular broad collar rash on the neck (Casal necklace); affects dermatomes C3 and C4
    • Hyperpigmented skin lesions in sun-exposed areas (especially on the limbs)
  • Diarrhea and vomiting
  • Neurologic symptoms (e.g, dementia, hallucinations, anxiety, insomnia, encephalopathy)

Mnemonic

• 3 typical features of severe vitamin B₃ Deficiency: Dermatitis, Diarrhea, and Dementia.
• 3 for tree: dermatitis, dementia

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Diagnostics

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Treatment

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Vitamin B3 toxicity

• Facial flushing: due to prostaglandin release and NOT due to histamine (typically seen when niacin therapy is started, can be avoided by coadministration of aspirin)
• Hyperuricemia, podagra
  • Niacin decreases renal uric acid excretion.
• Hyperglycemia