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Picture niacin as the fuel additive every cell needs to run its energy factories (NAD/NADP); when supply runs out, the tissues that burn through energy fastest and renew themselves quickest — skin exposed to sunlight, the gut lining, and the brain — are the first to break down, giving the classic skin-gut-brain triad.

• Pellagra is caused by deficiency of niacin (vitamin B3) or its amino acid precursor tryptophan.
• Niacin is a precursor for NAD and NADP, essential coenzymes for cellular energy metabolism and DNA repair across rapidly dividing and metabolically active tissues (skin, gut mucosa, neurons).
• Classic causes, chronic alcohol misuse, generalised malnutrition, maize-based diets (niacin is bound/unavailable and tryptophan-poor), prolonged isoniazid therapy (competes with pyridoxine, a cofactor for niacin synthesis), and carcinoid syndrome (tryptophan diverted to serotonin synthesis).
• Deficiency produces the classic triad of dermatitis, diarrhoea and dementia — often summarised as the '3 D's', with death as a fourth if untreated.

• Watch for a symmetrical, photosensitive, hyperpigmented rash on sun-exposed areas (hands, neck, face) alongside chronic diarrhoea and confusion or irritability.
• Risk factors in the stem include chronic alcohol dependence, generalised malnutrition, a maize-dependent diet, or long-term isoniazid therapy.
• Carcinoid syndrome plus this triad points to secondary pellagra via tryptophan diversion into serotonin synthesis.
• The combination of skin, gut and brain findings together (not any single feature alone) is the key recognition pattern for niacin deficiency.

• Pellagra vs Wernicke's encephalopathyAn acute brain condition from thiamine deficiency causing confusion, ataxia, and abnormal eye movements.Read more → — pellagra causes a photosensitive symmetrical dermatitis plus diarrhoea and dementia; Wernicke's (thiamine deficiency) causes the acute triad of confusion, ataxiaLoss of full control of body movements, causing an unsteady, uncoordinated gait or actions.Read more → and ophthalmoplegiaWeakness or paralysis of the muscles that move the eyes.Read more → without a characteristic rash.
• Pellagra vs vitamin B12 deficiency — pellagra's cognitive change accompanies dermatitis and diarrhoea; B12 deficiency instead produces subacute combined degeneration (dorsal column and corticospinal signs) and macrocytic anaemia, without the sun-exposed rash.
• Pellagra vs pyridoxine (B6) deficiency — B6 deficiency causes peripheral neuropathy and sideroblastic anaemia (classically with isoniazid), not the specific photosensitive dermatitis of pellagra, though isoniazid can precipitate both deficiencies together.
• Dietary vs secondary pellagra — dietary pellagra follows maize-dependent or generally deficient diets; secondary pellagra follows conditions that divert or block tryptophan/niacin metabolism, such as carcinoid syndrome or prolonged isoniazid use.

• Assuming any dermatitis in a malnourished patient is pellagra — confirm the photosensitive, symmetrical distribution (hands, neck — 'Casal's necklace') plus diarrhoea and cognitive change before committing to niacin deficiency.
• Forgetting that maize-based diets cause pellagra even without alcohol misuse — dietary tryptophan/niacin bioavailabilityThe proportion of a dose of a drug that actually reaches the bloodstream in an active form.Read more → is the key mechanism, not alcohol alone.
• Missing carcinoid syndrome as a cause of secondary pellagra — tryptophan diversion into serotonin synthesis can starve the niacin pathway even with a normal diet.
• Confusing the B-vitamin deficiencies with overlapping neuropsychiatric features — always anchor on the specific accompanying systemic clue (rash for niacin, ataxiaLoss of full control of body movements, causing an unsteady, uncoordinated gait or actions.Read more →/ophthalmoplegiaWeakness or paralysis of the muscles that move the eyes.Read more → for thiamine, neuropathy for pyridoxine, subacute combined degeneration for B12).

• Localise the clue to the relevant anatomical level, cell type, pathway or molecular process.
• Map that structure or process to its normal function.
• Predict the deficit or clinical sign produced when it is disrupted.
• Reject options that belong to a neighbouring structure, pathway or level of explanation.