Function

Mnemonic

Active forms of Niacin are NAD+ and NADP+.

  • Cofactor for redox reactions (e.g., alcohol dehydrogenase, isocitrate dehydrogenase, G6PD)highresdefault_L26357.jpg

Therapeutic use


Vitamin B3 deficiency

Etiology

  • Malnutrition
  • Heavy drinking
  • Conditions associated with tryptophan deficiency
    • Hartnup disease: decreased renal and intestinal tryptophan absorption
    • Carcinoid syndrome (if metabolically active): increased tryptophan metabolism
  • Vitamin B6 deficiency (e.g., due to treatment with isoniazid): decreased niacin synthesis from tryptophan
  • Chronic consumption of grains that have not been processed by nixtamalization (common cause in developing countries)

Pathophysiology


Clinical features

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  • Glossitis
  • Pellagra (caused by severe deficiency)
    • Characteristic dermatitis
      • Circular broad collar rash on the neck (Casal necklace); affects dermatomes C3 and C4Pasted image 20231104103708.png
      • 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

Diagnostics


Treatment


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