PellagraMANAGEMENT

ENDOCRINE AND METABOLIC PRESENTATIONS · 12 SECTIONS

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718 items

☷ Legend

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

Acute Porphyria Adrenal crisis Adrenal Insufficiency (Addisonian Crisis)Dehydration Diabetes Insipidus Diabetic Ketoacidosis (DKA)Euglycemic DKA (SGLT2 inhibitor)Galactosemia GLP-1 receptor agonist complications (retained gastric contents, aspiration risk)Homocystinuria Hypercalcemia Hyperkalemia Hypermagnesemia Hypernatremia Hyperosmolar Hyperglycemic State (HHS)Hypertensive emergency Hypertensive urgency Hypocalcemia Hypoglycemia Hypogonadism (Acute Presentation)Hypokalemia Hypomagnesemia Hyponatremia Hypoparathyroidism (Tetany)Insulin pump failure Maple Syrup Urine Disease (Crisis)Medium-Chain Acyl-CoA Dehydrogenase Deficiency (MCAD)Metabolic Acidosis Metabolic Alkalosis Myasthenia gravis crisis Myxedema coma Pellagra Pheochromocytoma (Crisis)Pituitary Apoplexy Pompe Disease (GSD II)Respiratory Acidosis Respiratory Alkalosis Scurvy SIADH Starvation Ketosis Tarui Disease (GSD VII)Thyroid storm Tyrosinemia Vitamin D Deficiency (Severe-Rickets)Von Gierke Disease (GSD I)

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp54

Immediate priorities

›Altered mental status triage

›Encephalopathy, delirium, stupor, or coma from severe niacin deficiency

›Medical emergency requiring urgent IV/IM niacin

›Mortality if untreated

›Concurrent Wernicke's encephalopathy in alcoholic patients

›Co-occurs in approximately 26% of alcoholic pellagra cases

›Thiamine 500 mg IV before glucose administration

›If GCS < 13, initiate parenteral thiamine and niacin empirically

›Do not delay treatment waiting for confirmatory labs

›Pellagra encephalopathy may be irreversible if treatment delayed

›Airway and aspiration risk

›Dysphagia from glossitis and mucositis

›High aspiration risk in encephalopathic patients

›Nil per os until airway protective reflexes confirmed

›Seizure risk in alcohol-dependent patients

›Reported in 16% of alcoholic pellagra cases

›Benzodiazepine protocol for concurrent alcohol withdrawal

›Fluid and electrolyte stabilization

›Severe dehydration from high-output diarrhea

›IV crystalloid resuscitation

›Electrolyte panel with replacement

›Severe malnutrition

›BMI below 18.5 in 54% of alcoholic pellagra patients

›Nutritional support team early involvement

Monitoring and targets

›Vital sign targets

›Heart rate and blood pressure trend

02History/hx84

Presentation pattern

›Cardinal symptom complex

›Photosensitive dermatitis

›Symmetric erythema on sun-exposed areas

›Casal's necklace pattern around neck

›Dorsal hand and forearm involvement

›Gastrointestinal symptoms

›Diarrhea (watery, occasionally bloody or mucoid)

›Glossitis and stomatitis

›Dysphagia and nausea

›Neuropsychiatric symptoms

›Insomnia and fatigue as early features

›Depression, anxiety, and irritability

›Confusion, hallucinations, and memory loss in advanced disease

›Alarm features

›Encephalopathy or delirium

›Confusion, disorientation, hallucinations, or stupor

›Indicates severe or advanced disease requiring admission

›Altered mental status not responding to thiamine

›Key diagnostic clue for concurrent pellagra in alcoholics

›Progressive worsening despite multivitamins lacking niacin

›New seizures

›Occurs in 16% of alcohol-dependent patients with pellagra

Risk factors

›Dietary and nutritional causes

›Maize or corn-dependent diet without nixtamalization

›Niacin in corn is bound and not bioavailable without alkali processing

›Primary driver globally; 85% of cases attributable to dietary deficiency

›Food insecurity and poverty

›64.5% of pellagra patients from low-income groups

›93% in humanitarian crisis settings

›Tryptophan-poor diet

›Sorghum-based diets

›Severe protein restriction

›Alcohol use disorder

›Chronic alcoholism

›9.6–35% of cases depending on population studied

›Impairs niacin absorption and increases metabolic demand

›Quantity, frequency, and duration of alcohol use

›Heavy daily use most significant risk

›Concurrent nutritional neglect amplifies risk

›Medication causes

›Isoniazid

›Leading drug cause; 14.3% of cases in systematic review

›aOR 42.6 for pellagra risk; inhibits tryptophan-to-niacin conversion

›Onset median 5–9 months after initiation

›Other anti-TB drugs

›Pyrazinamide and ethionamide

›Chemotherapy agents

›5-fluorouracil and 6-mercaptopurine

›Anticonvulsants

›Phenytoin and phenobarbital

›Parkinson's medications

›Carbidopa and benserazide; biochemical evidence of niacin depletion

›Malabsorption conditions

›Gastrointestinal disorders

›Celiac disease, IBD, bariatric surgery

›Chronic GI surgery with short bowel

›HIV infection

›Independent risk factor; often co-occurs with isoniazid use

›Chronic liver disease

›Impaired NAD metabolism in cirrhosis

›Social and contextual risk factors

›Homelessness

›Key risk factor; assess housing and meal access

›Anorexia nervosa or restrictive eating disorders

›Lactation

›Increased niacin requirements in breastfeeding women

Symptom timeline

›Onset and progression

›Seasonal worsening in spring and summer

›Increased sun exposure precipitates or worsens dermatitis

›Classic seasonal pattern in endemic regions

›Neuropsychiatric progression stages

›Early: insomnia, fatigue, apathy

›Intermediate: depression, anxiety, irritability, memory loss

›Late: confusion, hallucinations, psychosis, stupor, coma

›GI symptom timing

›Diarrhea may precede or follow dermatitis

›Full classic triad present in minority of cases

›Collateral history

›Housing status and food access

›Shelter-based meal programs

›Social isolation and caregiver neglect

›Family history

›Hartnup disease (autosomal recessive tryptophan transport disorder)

›Carcinoid syndrome diverts tryptophan to serotonin synthesis

03Physical Exam/exam60

Skin findings

›Pathognomonic and characteristic patterns

›Casal's necklace

›Broad band of hyperpigmented scaling dermatitis encircling the neck

›Pathognomonic finding when present

›Gauntlet distribution

›Symmetric well-demarcated erythema or hyperpigmentation on dorsal hands and forearms

›Sharp border distinguishing sun-exposed from protected skin

›Photosensitive distribution

›Face, neck, and chest V-sign

›Dorsal feet and extensor surfaces

›Acute versus chronic skin changes

›Acute phase

›Erythema resembling sunburn

›Vesicles or bullae in severe cases

›Chronic phase

›Hyperpigmentation and hyperkeratosis

›Thickened leathery skin with sharp demarcation

›Scaling and fissuring

Oral and mucosal findings

›Glossitis and stomatitis

›Tongue appearance

›Bright red beefy tongue

›Swelling and fissuring

›Oral mucosal changes

›Angular cheilitis

›Stomatitis with painful lesions

›Vaginal mucosa

04Differential Diagnosis/ddx51

Dermatologic mimics

›Photodermatitis and phototoxic reactions

›Drug-induced phototoxicity

›ICD-10: L56.0

›Lacks GI and neuropsychiatric features

›Medication history key differentiator

›Systemic lupus erythematosus

›ICD-10: M32.9

›Malar rash with different distribution

›ANA and complement levels to differentiate

›Dermatomyositis

›ICD-10: M33.10

›Heliotrope rash and Gottron's papules

›Proximal muscle weakness differentiating feature

›Other nutritional and metabolic dermatoses

›Zinc deficiency (acrodermatitis enteropathica)

›ICD-10: E60

›Periorificial and acral distribution

›Serum zinc levels to differentiate

›Porphyria cutanea tarda

›ICD-10: E80.1

›Blistering on sun-exposed areas

›Urine porphyrins elevated

›Hartnup disease

›ICD-10: E72.02

›Pellagra-like rash with aminoaciduria

›Consider in children or young adults with recurrent episodes

05Laboratory Tests/lt51

Basic metabolic workup

›Complete blood count

›Anemia assessment

›Nutritional anemia common in pellagra

›Macrocytosis if concurrent folate or B12 deficiency

›White cell count

›Leukocytosis suggests secondary skin infection or sepsis

›Comprehensive metabolic panel

›Electrolyte abnormalities

›Hyponatremia, hypokalemia, hypomagnesemia from diarrhea

›Correction required before nutritional repletion

›Hepatic function

›Baseline before high-dose niacin (hepatotoxicity risk)

›Elevated in chronic liver disease as pellagra risk factor

›Creatinine and BUN

›Dehydration assessment

›Renal function before electrolyte replacement

Nutritional biomarkers

›Niacin-specific testing

›Urinary N1-methylnicotinamide (1-MN) and 2-pyridone ratio

›Low levels support niacin deficiency

›Not widely available; diagnosis primarily clinical

›Serum niacin and NAD levels

›Blood levels are unreliable measures of deficiency

›Do not withhold treatment pending these results

›Concurrent deficiency assessment

›Thiamine level

›Rule out concurrent Wernicke's encephalopathy

06Diagnostic Tests/dt68

Scoring Systems

›Severity stratification for pellagra

›Mild pellagra

›Dermatitis only without GI or neuropsychiatric involvement

›Suitable for outpatient oral niacin therapy

›Moderate pellagra

›Dermatitis plus GI symptoms (diarrhea, glossitis, dysphagia)

›Monitor for progression; may require hospital observation

›Severe pellagra

›Neuropsychiatric involvement: encephalopathy, psychosis, delirium

›Medical emergency requiring parenteral niacin and admission

›Clinical Assessment Tool for Malnutrition (MUST)

›BMI score component

›BMI less than 18.5: score 2

›BMI 18.5–20: score 1

›Unintentional weight loss component

›Greater than 10% in 3–6 months: score 2

›5–10%: score 1

›Acute disease effect component

›Acutely ill and no nutritional intake greater than 5 days: score 2

›Glasgow Coma Scale

›Encephalopathy severity tracking

›Serial GCS to monitor treatment response

›Improvement within 24–48 hours of parenteral niacin expected

MRI

›Brain MRI indications in pellagra

›Encephalopathic patient not improving with empirical treatment

›Rule out structural lesion, Wernicke's, or alternative encephalopathy

07Disposition/dispo46

Admission criteria

›Indications for inpatient admission

›Neuropsychiatric involvement

›Encephalopathy, delirium, psychosis, or seizures

›Requires parenteral niacin and close monitoring

›Severe dehydration from diarrhea

›Unable to maintain oral hydration

›Electrolyte disturbances requiring IV replacement

›Inability to tolerate oral intake

›Severe glossitis or dysphagia preventing medication intake

›Parenteral nutrition consideration

›Concurrent Wernicke's encephalopathy

›Requires inpatient parenteral thiamine protocol

›Severe malnutrition with hemodynamic instability

›BMI below 18.5 with tachycardia or hypotension

›Refeeding syndrome risk monitoring required

›ICU admission triggers

›Stupor or coma

›Airway management required

›Continuous neurological monitoring

›Refractory seizures

›Hemodynamic compromise from severe dehydration

Discharge criteria

›Safe for outpatient management when

›Isolated dermatitis without neuropsychiatric or severe GI involvement

›Able to tolerate oral niacin and adequate diet

›Reliable follow-up arranged within 1–2 weeks

›Mild confusion with oral medication tolerance

08Treatment/t75

Parenteral niacin (severe or encephalopathic)

›Nicotinamide IV or IM for severe pellagra

›Dosing

›100–500 mg IV or IM three times daily

›Mean total dose approximately 1,500 mg per day in alcoholic encephalopathy

›Duration of parenteral phase

›7–10 days of parenteral therapy

›Transition to oral once able to tolerate

›Monitoring

›Neurological status reassessment every 24–48 hours

›Hepatic function monitoring with high doses

›Concurrent thiamine supplementation in alcohol-related cases

›Thiamine 500 mg IV three times daily for 2–3 days

›Then 250 mg IV or IM daily for 5 days

›Transition to oral thiamine 100 mg daily

›Always administer before IV glucose to prevent precipitating Wernicke's

Oral niacin (mild to moderate)

›Nicotinamide (niacinamide) preferred over nicotinic acid

›Dosing

›300–1,000 mg/day PO in divided doses

›Preferred to avoid flushing associated with nicotinic acid

›Alternative if nicotinamide unavailable

›Nicotinic acid 50–500 mg PO three times daily

›Flushing side effect expected; warn patients

›Duration

›Continue until full symptom resolution

›Minimum 3–4 weeks; often longer based on underlying cause

›Multi-B vitamin co-supplementation

›Required cofactors for tryptophan-to-niacin conversion

›Riboflavin (vitamin B2)

›Pyridoxine (vitamin B6)

›Thiamine (vitamin B1)

›Zinc and magnesium supplementation

›Support niacin metabolic pathways

›Replace losses from diarrhea

Supportive care

›Fluid and electrolyte management

›IV crystalloid for dehydration

›Normal saline or lactated Ringer's

›Rate based on severity of dehydration and cardiac status

›Electrolyte replacement

›Potassium, magnesium, and phosphate monitoring and replacement

›Refeeding syndrome prevention in severe malnutrition

›Nutritional support

›High-calorie protein-rich diet

›Niacin-rich foods: meat, fish, poultry, eggs, peanuts, legumes, seeds, bran

›Tryptophan-rich protein sources

›Enteral or parenteral nutrition

›If oral intake inadequate despite treatment

›Ensure parenteral multivitamins include niacin per ASPEN guidelines

Dermatological care

›Skin lesion management

›Sun protection

›Avoid sun exposure during active disease

›Broad-spectrum sunscreen and protective clothing

›Emollients

›Moisturize scaling and hyperkeratotic areas

›Prevent fissuring and secondary infection

›Topical corticosteroids with salicylic acid

›For symptomatic relief of dermatitis

›Short course only; avoid in infected lesions

Addressing underlying cause

›Medication-induced pellagra

›Isoniazid

›Consider pyridoxine co-supplementation 25–50 mg/day during TB therapy

›If pellagra develops, discuss alternative TB prevention regimen with ID

›Rifamycin-based alternatives may be appropriate

›Other causative medications

›Review indication and necessity

›Consult prescribing specialist before discontinuation

›Alcohol use disorder treatment

›Brief intervention and referral to treatment

›Motivational interviewing

›Addiction medicine referral

›Pharmacotherapy for alcohol use disorder

›Naltrexone or acamprosate after detoxification

›Food insecurity intervention

›Social work referral

›Shelter and meal program access

›Government nutritional assistance programs

09Special Populations/sp69

Pregnancy

›Physiologic considerations

›Increased niacin requirements during pregnancy

›Recommended dietary allowance increases from 14 to 18 mg niacin equivalents per day

›Lactation further increases requirements

›Tryptophan metabolism changes

›Estrogen diverts tryptophan toward kynurenine pathway

›Reduces endogenous niacin synthesis

›Medication safety

›Nicotinamide preferred in pregnancy

›Generally considered safe; no teratogenicity established at therapeutic doses

›High-dose nicotinic acid relatively contraindicated

›Isoniazid-associated pellagra in pregnancy

›Pyridoxine supplementation essential during isoniazid therapy in pregnancy

›25–50 mg/day pyridoxine recommended by WHO during TB treatment in pregnancy

›Clinical management modifications

›Lower threshold for admission given fetal risk

›Dehydration from diarrhea can compromise placental perfusion

›IV fluid resuscitation with fetal monitoring

›Dermatitis may worsen with pregnancy-associated sun sensitivity

›Strict sun protection measures

›Sunscreen safe in pregnancy

Geriatric

›Risk profile

›Higher prevalence of dietary restriction

›Fixed income and food insecurity

›Decreased appetite and poor dentition

›Polypharmacy risk

10Background/b85

Epidemiology

›Global burden and distribution

›Dietary deficiency accounts for 85% of cases globally

›93% of cases in humanitarian crisis settings

›Endemic in sub-Saharan Africa, South Asia, and maize-dependent regions

›Contemporary systematic review 2000–2023

›Litaiem et al. 2026 systematic review of modern clinical practice

›Chronic alcoholism represents 9.6–35% of cases by population

›Drug-induced cases

›Isoniazid accounts for 14.3% of cases in systematic review

›Rising incidence with tuberculosis preventive therapy scale-up

›Demographics

›Socioeconomic determinants

›64.5% of patients from low-income groups

›Homelessness a significant independent risk factor

›BMI and nutritional status

›54% of alcoholic pellagra patients have BMI below 18.5

›Mortality

›Fatal if untreated in severe cases with encephalopathy

›Complete symptom resolution on average within 27 days of treatment

›ICD-10 coding

›Pellagra: E52

›Niacin deficiency: included under E52

›Drug-induced pellagra: E52 with external cause code (e.g., Y43 for isoniazid)

Pathophysiology

›Niacin biochemistry

›Niacin (vitamin B3) two active forms

›Nicotinamide adenine dinucleotide (NAD)

›Nicotinamide adenine dinucleotide phosphate (NADP)

›Role in cellular metabolism

›Electron carrier in oxidative phosphorylation

›DNA repair via poly-ADP-ribose polymerase

›Essential for skin, GI epithelium, and neuronal function

›Tryptophan-to-niacin pathway

›Dietary tryptophan conversion

›Approximately 60 mg tryptophan required per 1 mg niacin equivalent

›Requires cofactors: B2, B6, iron

›Pathway disruption by isoniazid

›Inhibits tryptophan-to-niacin conversion via pyridoxine depletion

›Kynurenine pathway enzyme inhibition

›Leucine excess inhibition

›High leucine intake (sorghum-based diets) inhibits tryptophan conversion

›Organ-specific pathophysiology

›Skin

›NAD depletion impairs DNA repair in keratinocytes

›UV light exposure exacerbates oxidative damage in niacin-deficient skin

›Gastrointestinal tract

›Rapid turnover of GI epithelium requires continuous NAD supply

›Mucosal atrophy leads to malabsorption and diarrhea

›Nervous system

›NAD essential for neuronal ATP production and myelin maintenance

›Demyelination and neuronal death in prolonged deficiency

›Corn diet and nixtamalization

›Bound niacin in maize

›Niacin exists as niacytin (indigestible complex) in untreated corn

›Traditional nixtamalization (alkali processing with lime) releases bioavailable niacin

›Modern industrialized corn processing without nixtamalization loses this benefit

Therapeutic Considerations

›Choice of niacin preparation

›Nicotinamide versus nicotinic acid

›Nicotinamide preferred: avoids flushing and hepatotoxicity at standard doses

›Nicotinic acid causes prostaglandin-mediated cutaneous flushing

›Both equally effective for niacin deficiency replacement

›Parenteral bioavailability

›IV route ensures absorption independent of GI mucosal integrity

›Critical in severe encephalopathy with impaired swallowing

›Hepatotoxicity risk with high-dose niacin

›Dose-dependent hepatotoxicity

›Risk increases at doses above 2,000 mg/day

›Baseline and monitoring LFTs with parenteral high-dose therapy

›Contraindications

›Active hepatic disease: use with caution and close monitoring

›Uric acid monitoring in gout-prone patients

›Refeeding syndrome awareness

›Risk in severely malnourished patients

›Initiate caloric supplementation gradually

›Phosphate, potassium, and magnesium monitoring essential

›ASPEN refeeding syndrome guidelines applicable

›Treatment response timeline

›Expected clinical course

›Skin and GI symptoms begin improving within days of niacin

›Complete skin resolution expected within 3–4 weeks

›Mean time to full resolution approximately 27 days

›Neuropsychiatric symptoms may take weeks to fully resolve

›Non-response evaluation

›If no improvement after 48–72 hours, reassess diagnosis

›Consider concurrent deficiencies not yet repleted

›Evaluate for alternative or co-existing diagnosis

11Patient Discharge Instructions/pdi45

copy discharge instructions

›Diagnosis and explanation

›You have been diagnosed with pellagra

›Pellagra is caused by a deficiency of vitamin B3 (niacin) or its building block tryptophan

›It causes a characteristic skin rash on sun-exposed areas, stomach problems, and can affect the brain if untreated

›Medications

›Take nicotinamide (niacinamide) exactly as prescribed

›Do not stop taking this medication early even if you feel better

›Take it in divided doses throughout the day as directed

›Take all prescribed B vitamins

›These include thiamine, riboflavin, and pyridoxine if prescribed

›They are needed for your body to use niacin properly

›Take zinc and magnesium supplements if prescribed

›Diet and nutrition

›Eat foods high in niacin every day

›Meat, poultry, and fish

›Eggs and dairy products

›Peanuts, legumes, seeds, and bran

›Avoid alcohol completely

›Alcohol worsens niacin deficiency and can be fatal in combination

›Drink adequate fluids

›Especially important if you have had diarrhea

›Skin care

›Protect your skin from sun exposure during treatment

›Wear sunscreen with SPF 30 or higher on sun-exposed areas

›Wear long sleeves, wide-brimmed hat, and sun-protective clothing

›Keep skin moisturized with gentle emollient cream

›Avoid harsh soaps or scrubbing the affected areas

12References/r30

Guidelines and key sources

›Litaiem N, Sboui K, Zeglaoui F. Pellagra in Contemporary Clinical Practice 2000–2023: A Systematic Review. International Journal of Dermatology. 2026. PMID 41876960

›Systematic review of modern pellagra epidemiology, causes, and treatment

›Primary grounding source for case distribution, deficiency patterns, and outcomes

›Nabity SA, Mponda K, Gutreuter S, et al. Isoniazid-Associated Pellagra During Mass Scale-Up of Tuberculosis Preventive Therapy: A Case-Control Study. Lancet Global Health. 2022. PMID 35427527

›aOR 42.6 for pellagra risk with isoniazid

›Defines onset timing and prevention strategies

›Prabhu D, Dawe RS, Mponda K. Pellagra: a review exploring causes and mechanisms, including isoniazid-induced pellagra. Photodermatology Photoimmunology Photomedicine. 2021

›Mechanism of drug-induced niacin deficiency

›Covers biochemical pathways and clinical management

›Cao S, Wang X, Cestodio K. Pellagra, an Almost-Forgotten Differential Diagnosis of Chronic Diarrhea. Nutrition in Clinical Practice. 2020. PMID 31599018

›Dosing guidance for oral nicotinamide 300–1,000 mg/day

›Clinical diagnostic approach and nutritional management

›Narasimha VL, Ganesh S, Reddy S, et al. Pellagra and Alcohol Dependence Syndrome. Alcohol and Alcoholism. 2019. PMID 30721993

›Alcoholic pellagra clinical characteristics

›Co-occurrence of Wernicke's and seizure data

›Kertesz SG. Pellagra in 2 Homeless Men. Mayo Clinic Proceedings. 2001. PMID 11243279

›Classic clinical description of pellagra in urban homeless population

›Key diagnostic and management pearls for emergency physicians

›Luthe SK, Sato R. Alcoholic Pellagra as a Cause of Altered Mental Status in the Emergency Department. Journal of Emergency Medicine. 2017. PMID 28736097

›Emergency medicine perspective on diagnosis and empiric treatment

›Emphasizes importance of niacin in undifferentiated altered mental status

›Vanek VW, Borum P, Buchman A, et al. ASPEN Position Paper: Recommendations for Changes in Commercially Available Parenteral Multivitamin Products. Nutrition in Clinical Practice. 2012

›Parenteral nutrition niacin requirements

›Institutional guidance for IV supplementation

›Badawy AA. Pellagra and Alcoholism: A Biochemical Perspective. Alcohol and Alcoholism. 2014. PMID 24627570

›Biochemical mechanisms of alcohol-related niacin depletion

›Tryptophan metabolism and kynurenine pathway

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Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.