Niacin Deficiency (Pellagra): Dermatitis (Skin)

The skin rash of pellagra is one of the most distinctive in all of medicine, because it follows a rule almost no other rash obeys: it appears only where the sun touches. The backs of the hands, the forearms, the face, the V of the chest, and a band around the neck turn red, then rough, dark, and scaly — while skin under clothing stays perfectly normal. That sharp, symmetric line between sun-exposed and covered skin is the fingerprint of niacin (vitamin B3) deficiency. This page explains why too little niacin makes skin unable to withstand ordinary daylight, how to recognize the classic “Casal’s necklace” across the throat, why this rash is so often mistaken for sunburn or eczema, and how quickly it heals once niacin is restored.

Table of Contents

1. What the Pellagra Rash Looks and Feels Like
2. The Mechanism: Why Low Niacin Lets Sunlight Burn the Skin
3. Casal’s Necklace and the Sun-Exposed Pattern
4. Honest Differential: Other Causes of a Sun-Sensitive Rash
5. Clues That Point to Niacin Deficiency
6. What Causes the Niacin Deficiency Behind It
7. Getting Diagnosed
8. Correcting the Deficiency and Healing the Skin
9. When to Seek Care / Red Flags
10. Key Research Papers
11. Connections
12. Featured Videos

What the Pellagra Rash Looks and Feels Like

The pellagra rash does not look like most rashes. It is not scattered, not patchy, and not random — it is symmetric, sharply bordered, and confined to sun-exposed skin. If you drew the rash on a body outline, it would map almost exactly onto the parts of the body that catch daylight: the backs of both hands and the forearms up to where a short sleeve ends, the face (especially the cheeks, nose, and forehead), the front and back of the neck, and the upper chest. Skin that stays covered — the belly, the upper arms, anything under clothing — is typically spared, producing an almost drawn-on line where covered skin meets exposed skin.

The rash usually evolves through a recognizable sequence over days to weeks:

• It starts looking like a bad sunburn. The exposed skin turns red, warm, and tender, sometimes with a burning or itching sensation. People very often blame the sun, a new soap, or a detergent — and because it genuinely is triggered by sun, mild cases can come and go with the seasons.
• Then it darkens. Instead of fading like a sunburn, the redness gives way to a deepening brown or bronze hyperpigmentation. This darkening is a hallmark that separates pellagra from an ordinary burn that would heal and lighten.
• The skin thickens, dries, and cracks. Over time the affected skin becomes rough, leathery, and scaly, and may fissure painfully — the backs of the hands can look almost “glove-like,” with a sharp cut-off at the wrist. In more severe cases, blisters (bullae) can form and break, leaving raw, weeping, or crusted areas that are vulnerable to infection.

The rash is classically bilateral and symmetric — both hands, both forearms, both cheeks — because both sides of the body get equal sun. That symmetry, plus the hard border at the edge of clothing, is what makes an experienced clinician think of pellagra rather than a one-sided contact rash or a localized skin infection. The skin changes are also often accompanied by a sore, red, swollen tongue and mouth, because the same niacin-starved, fast-turnover surfaces line the mouth and gut.

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The Mechanism: Why Low Niacin Lets Sunlight Burn the Skin

Niacin (vitamin B3, in the forms nicotinic acid and nicotinamide) is the raw material the body uses to build NAD and NADP — two coenzymes that are absolutely central to how every cell makes and spends energy and repairs itself. NAD-dependent reactions run hundreds of steps in metabolism, and NADPH (the reduced form of NADP) powers the cell’s repair and antioxidant machinery. When niacin is in short supply, NAD and NADP levels fall, and the tissues that suffer first are the ones that divide and renew the fastest: the skin, the lining of the mouth and gut, and the nervous system. That is why pellagra famously hits three systems — skin (dermatitis), gut (diarrhea), and brain (dementia and mental changes) — the classic “three Ds.”

But why sunlight specifically? The skin is constantly bombarded by ultraviolet (UV) light, which damages DNA and generates reactive, oxidizing molecules. Healthy skin shrugs this off using NAD- and NADPH-powered repair systems — including DNA-repair enzymes and antioxidant defenses that neutralize the damage before it accumulates. When niacin is deficient and NAD/NADP run low, that repair capacity is depleted. Researchers have proposed several overlapping reasons the skin then becomes photosensitive: a relative shortage of urocanic acid (a natural sunscreen molecule made in the skin from the amino acid histidine), a build-up of kynurenic acid and other tryptophan-pathway byproducts that act as photosensitizers, and the simple fact that NAD-dependent DNA repair can no longer keep up with everyday UV injury. The net effect is that an ordinary, non-harmful dose of daylight now causes real, visible damage.

An analogy. Think of your skin as a road surface that takes constant wear from traffic (the UV light of normal daylight). A well-funded road crew (NAD- and NADPH-powered repair) patches the cracks as fast as they form, so the road always looks fine. Niacin deficiency is a budget cut that lays off the road crew. The traffic hasn’t changed — the sun is no stronger than it was — but now the small daily cracks never get repaired, so they widen into potholes. That is the pellagra rash: not abnormal sun, but a skin that can no longer fix the ordinary damage sun always causes. Restore the “budget” (the niacin) and the crew goes back to work; new skin grows in healthy, which is why the rash heals once treatment begins.

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Casal’s Necklace and the Sun-Exposed Pattern

The single most famous sign of pellagra is Casal’s necklace (also called Casal’s collar) — a broad, well-demarcated band of the characteristic dark, scaly rash that wraps around the front and sides of the neck, dipping down onto the upper chest in a V. It is named after Gaspar Casal, the 18th-century Spanish physician who first described pellagra in detail and recognized this collar of skin disease as its signature. The reason the rash forms a necklace is simply geometry: the neckline and the open collar of a shirt expose a ring of skin to the sun while the rest of the chest stays covered, so the photosensitive damage stops exactly where the clothing begins.

Several named patterns of the pellagra rash recur often enough that each has its own description:

• Casal’s necklace — the collar of rash around the neck and upper chest, described above. When present, it is close to diagnostic.
• The “gauntlet” or glove pattern — rash covering the backs of the hands and forearms with a sharp cut-off at the wrist or mid-forearm, matching the edge of a sleeve.
• The “boot” pattern — the same changes on the tops of the feet and lower legs in people who go barefoot or wear sandals.
• Butterfly distribution on the face — redness across the cheeks and bridge of the nose, which can be mistaken for the “butterfly” rash of lupus or for rosacea.

The unifying theme is that the rash traces the borders of clothing and the angle of the sun. This is the most useful single observation for recognizing pellagra: a symmetric, dark, scaly eruption that respects the line between covered and uncovered skin, sparing the skin folds and shaded areas (under the chin, behind the ears) that daylight never reaches.

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Honest Differential: Other Causes of a Sun-Sensitive Rash

It is important to be candid: a rash on sun-exposed skin is not proof of niacin deficiency. Photosensitivity — skin that reacts abnormally to light — is far more often caused by something other than pellagra, and most people with a sun-aggravated rash are not niacin-deficient. The honest differential includes several much more common possibilities:

• Drug-induced photosensitivity — by far the most common cause. Many widely used medications make skin sun-reactive, including some antibiotics (doxycycline and other tetracyclines, certain fluoroquinolones, sulfonamides), the diuretic hydrochlorothiazide, some anti-inflammatories, retinoids, and amiodarone. A new sun-sensitive rash should always prompt a careful look at the medication list.
• Polymorphous light eruption (PMLE) — a common, itchy rash that erupts on sun-exposed skin in spring and early summer, especially in younger women. It is benign and unrelated to nutrition.
• Lupus and other autoimmune disease — systemic and cutaneous lupus classically produce a photosensitive facial (“butterfly”) rash. Dermatomyositis also causes a sun-aggravated rash.
• Porphyria cutanea tarda — a metabolic disorder causing skin fragility and blistering on sun-exposed skin, particularly the backs of the hands, which can closely mimic pellagra.
• Phototoxic plant and fragrance reactions (phytophotodermatitis) — contact with lime juice, certain plants, or fragrances followed by sun can produce a streaky, dark, sun-pattern rash.
• Ordinary eczema or contact dermatitis — including eczema on the hands and face that happens to be aggravated by sun and irritants, which is why pellagra is frequently misdiagnosed as a stubborn dermatitis.

Because these look-alikes are common and pellagra (in well-nourished countries) is rare, a clinician weighs the rash together with the rest of the picture — diet, alcohol use, medications, weight loss, diarrhea, and mental changes — before concluding that niacin deficiency is the cause. The point of this page is not to encourage self-diagnosis but to explain when a sun-pattern rash should make niacin deficiency part of the conversation.

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Clues That Point to Niacin Deficiency

A few features tip the balance toward pellagra rather than the more common look-alikes above. Any one of them is a clue; several together make the case strong:

• The rash is on the skin, but the symptoms are body-wide. Pellagra rarely travels alone. A photosensitive rash plus ongoing diarrhea, a sore beefy-red tongue, and new confusion, memory trouble, depression, or irritability is the classic constellation. The dermatitis is often the most visible of the “three Ds,” but the others are the giveaway.
• The skin darkens rather than fades. A sunburn heals and lightens; the pellagra rash deepens into brown, scaly, thickened skin and is slow to resolve without treatment.
• There is a clear reason for poor niacin status. Heavy alcohol use, a very restricted or corn-based diet, recent bariatric surgery, a malabsorption condition such as inflammatory bowel disease, anorexia, or a relevant medication (see below) all raise the prior probability of niacin deficiency dramatically.
• It improves strikingly with niacin. One of the most telling clues is the response to treatment: the rash and the systemic symptoms typically begin to improve within days of starting niacin (nicotinamide), which is both diagnostic and curative.

If your sun-pattern rash exists in isolation — no gut symptoms, no mental changes, a normal diet, no heavy drinking, and no culprit drug — niacin deficiency is unlikely, and a clinician will look harder at the common causes in the section above. Pellagra is, fundamentally, a disease of context.

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What Causes the Niacin Deficiency Behind It

The body gets niacin in two ways: directly from food, and indirectly by converting the amino acid tryptophan into niacin (roughly 60 mg of dietary tryptophan yields about 1 mg of niacin). Because there are two supply routes, true pellagra usually requires both to be compromised. The main causes fall into a few groups:

• Dietary deficiency, classically corn-based. Historically, pellagra swept regions where maize (corn) was the staple, because the niacin in untreated corn is bound up in a form the body cannot absorb, and corn is also low in tryptophan. Cultures that soaked corn in lime water (nixtamalization, as in traditional tortilla-making) released the niacin and were protected; those that did not were not. Today, dietary pellagra is seen mainly in famine, refugee, and food-insecurity settings — a 1990 outbreak among Mozambican refugees in Malawi is a well-documented modern example.
• Alcohol use disorder — the most common cause in wealthy countries. Heavy drinking displaces food, impairs absorption of niacin and other B vitamins, and damages the gut and liver, so chronic alcohol use is the classic modern setting for pellagra.
• Malabsorption and gut disease — Crohn’s disease, chronic diarrhea, celiac disease, and the aftermath of bariatric (weight-loss) surgery can all reduce niacin absorption.
• Medications that block the niacin or tryptophan pathway. The tuberculosis drug isoniazid interferes with vitamin B6 (which is a required cofactor for converting tryptophan to niacin) and is a recognized cause of drug-induced pellagra. Other implicated drugs include 5-fluorouracil (a chemotherapy agent), pyrazinamide, and some anticonvulsants and azathioprine/6-mercaptopurine.
• Conditions that steal tryptophan. In carcinoid syndrome, hormone-secreting tumors divert large amounts of tryptophan into making serotonin, leaving too little to make niacin — producing pellagra. In Hartnup disease, an inherited defect impairs absorption of tryptophan and other amino acids, causing a pellagra-like rash.

The thread connecting these is that niacin deficiency severe enough to cause the rash is almost always a sign of something larger — a diet, an addiction, a gut disorder, a medication, or a metabolic condition. Treating the skin without finding and fixing that root cause only buys time.

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Getting Diagnosed

Pellagra is, to a large degree, a clinical diagnosis — meaning it is recognized from the pattern (the symmetric sun-exposed rash, often with gut and mental symptoms) and the context (diet, alcohol, medications), rather than from a single definitive blood test. Direct measurement of niacin in blood is not routine, is not widely available, and does not reliably reflect tissue stores. Most often, clinicians measure niacin’s breakdown products in the urine — chiefly N1-methylnicotinamide and a related metabolite — with low levels supporting the diagnosis.

In practice, the workup usually includes:

• A careful history and skin examination — the cornerstone. The distribution of the rash (sun-exposed, symmetric, Casal’s necklace), plus questions about diet, alcohol, weight loss, bowel habits, mood and memory, and a full medication review.
• General bloodwork — a Comprehensive Metabolic Panel and complete blood count to assess overall nutrition, liver and kidney function, and to screen for co-existing deficiencies. People with pellagra commonly lack several nutrients at once (other B vitamins, zinc, protein), because the underlying problem is rarely selective for niacin alone.
• The therapeutic trial. Because niacin treatment is safe, inexpensive, and fast-acting, a striking improvement after starting nicotinamide is often used to confirm the diagnosis — a dramatic response within days strongly supports pellagra.

A skin biopsy is sometimes done when the diagnosis is uncertain, but the changes it shows are suggestive rather than specific. The most reliable “test” remains a clinician who recognizes the pattern and asks the right questions about how the person has been eating and living.

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Correcting the Deficiency and Healing the Skin

The good news is that pellagra is one of medicine’s most rewarding conditions to treat: the right vitamin, in adequate dose, reverses it, and the skin heals. Treatment has a few components:

• Niacin replacement, usually as nicotinamide. Clinicians typically treat established pellagra with nicotinamide (also called niacinamide) rather than nicotinic acid, because nicotinamide does not cause the uncomfortable skin flushing that high-dose nicotinic acid produces. Treatment doses are well above the ordinary dietary requirement and are continued for several weeks; the exact dose and route (oral or, if the gut is failing, by injection) are set by the treating clinician. The systemic symptoms and the rash usually begin improving within days, and the skin re-epithelializes over the following weeks.
• A nutrient-rich diet and the other B vitamins. Because pellagra rarely comes alone, treatment includes restoring overall nutrition and often replacing other B vitamins (including vitamin B6, which the body needs to convert tryptophan to niacin) and protein. Niacin-rich and tryptophan-rich foods rebuild stores: liver and other organ meats, tuna, salmon and other fish, poultry, eggs, legumes, peanuts, and whole or fortified grains. (See the food sources of vitamin B3 for more.)
• Protect the skin from the sun while it heals. Because the skin is photosensitive, sun protection — shade, covering clothing, and sunscreen — helps prevent further damage during recovery. This is supportive care, not the cure; the cure is the niacin.
• Fix the underlying cause. This is the part that prevents relapse: treating alcohol use disorder, correcting a malabsorption condition, changing or supplementing around a culprit medication (for example, adding vitamin B6 and/or niacin for someone who must stay on isoniazid), or addressing carcinoid syndrome. Replacing niacin without addressing why it ran out invites the deficiency — and the rash — to return.

For everyday prevention in well-nourished people, the recommended dietary allowance for niacin is modest — on the order of 14–16 mg of niacin equivalents per day for adult women and men — and is easily met by a varied diet, which is why dietary pellagra is rare where food is abundant. The disease is essentially a marker of poverty, addiction, or illness rather than of any need for high-dose supplements in healthy people.

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When to Seek Care / Red Flags

A persistent, symmetric, darkening rash on sun-exposed skin always deserves medical evaluation — both to confirm or rule out pellagra and to catch the more common look-alikes. Certain features mean you should be seen promptly rather than waiting:

• The rash comes with diarrhea, a sore red tongue, weight loss, or new mental changes — confusion, memory loss, depression, agitation, or disorientation. This combination raises real concern for pellagra and, untreated, advanced pellagra can be life-threatening.
• Blistering, raw, weeping, or rapidly spreading skin, or signs of skin infection (increasing pain, pus, fever, red streaking) — broken skin can become infected.
• A sun-sensitive rash after starting a new medication — this needs review, since the drug may be the cause and may need to be changed.
• Heavy alcohol use with poor eating, or a known malabsorption condition, plus any new rash or neurological symptoms — this is the classic high-risk setting for pellagra and other vitamin deficiencies.
• Confusion, severe weakness, dehydration, or inability to eat or drink — advanced niacin deficiency with marked dementia, diarrhea, and dermatitis is a medical emergency and warrants urgent care.

The reassuring counterpoint is that, once recognized, the condition responds quickly and completely to treatment. The danger of pellagra lies almost entirely in not recognizing it — in mistaking the rash for a stubborn sunburn or eczema while the deficiency quietly affects the gut and brain. When the dots are connected, the cure is a vitamin.

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Key Research Papers

1. Wan P, Moat S, Anstey A (2011). Pellagra: a review with emphasis on photosensitivity. British Journal of Dermatology;164(6):1188-1200. — DOI: 10.1111/j.1365-2133.2010.10163.x
2. Hegyi J, Schwartz RA, Hegyi V (2004). Pellagra: Dermatitis, dementia, and diarrhea. International Journal of Dermatology;43(1):1-5. — DOI: 10.1111/j.1365-4632.2004.01959.x
3. Prabhu D, Dawe RS, Mponda K (2021). Pellagra a review exploring causes and mechanisms, including isoniazid-induced pellagra. Photodermatology, Photoimmunology & Photomedicine;37(2):99-104. — DOI: 10.1111/phpp.12659
4. Rajakumar K (2000). Pellagra in the United States: a historical perspective. Southern Medical Journal;93(3):272-277. — DOI: 10.1097/00007611-200093030-00005
5. Centers for Disease Control and Prevention (1991). Outbreak of Pellagra Among Mozambican Refugees—Malawi, 1990. Archives of Dermatology;127(6):791. — DOI: 10.1001/archderm.1991.01680050029002
6. Goldberger J, Wheeler GA (1923). Pellagra Prevention by Diet among Institutional Inmates. Public Health Reports (1896-1970);38(41):2361-2368. — DOI: 10.2307/4576901
7. Crook MA (2014). The importance of recognizing pellagra (niacin deficiency) as it still occurs. Nutrition;30(6):729-730. — DOI: 10.1016/j.nut.2014.03.004
8. Meyer-Ficca M, Kirkland JB (2016). Niacin. Advances in Nutrition;7(3):556-558. — DOI: 10.3945/an.115.011239
9. Feuz MB, Meyer-Ficca ML, Meyer RG (2023). Beyond Pellagra—Research Models and Strategies Addressing the Enduring Clinical Relevance of NAD Deficiency in Aging and Disease. Cells;12(3):500. — DOI: 10.3390/cells12030500
10. Darvay A, Basarab T, McGregor JM, Russell-Jones R (1999). Isoniazid induced pellagra despite pyridoxine supplementation. Clinical and Experimental Dermatology;24(3):167-169. — DOI: 10.1046/j.1365-2230.1999.00444.x
11. Freundlich E, Statter M, Yatziv S (1981). Familial pellagra-like skin rash with neurological manifestations. Archives of Disease in Childhood;56(2):146-148. — DOI: 10.1136/adc.56.2.146
12. Wolf R, Wolf D, Ruocco V (2002). Miscellaneous treatments, II: niacin and heparin: unapproved uses, dosages, or indications. Clinics in Dermatology;20(5):547-557. — DOI: 10.1016/s0738-081x(02)00268-7

PubMed Topic Searches

• PubMed — Pellagra, photosensitivity, and dermatitis
• PubMed — Casal’s necklace and niacin deficiency
• PubMed — Treatment of pellagra with nicotinamide
• PubMed — Drug-induced pellagra (isoniazid, 5-fluorouracil)
• PubMed — Tryptophan–niacin–NAD pathway in pellagra

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Connections

• Niacin Deficiency (Pellagra) Hub
• Pellagra: Diarrhea & Digestive Symptoms
• Pellagra: Dementia & Mental Changes
• Pellagra: Fatigue & Weakness
• Niacin Toxicity (High Intake)
• Vitamin B3 (Niacin) Overview
• Pellagra and Niacin Deficiency
• Food Sources of Vitamin B3
• Vitamin B6 (Pyridoxine)
• Tryptophan
• Dermatology
• Eczema
• Gastroenterology
• Comprehensive Metabolic Panel
• Zinc
• Beef Liver
• Tuna
• Eggs

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