Periorificial face
Scaly, crusted, erosive, or vesiculobullous dermatitis clusters around facial openings.
GI
Zinc Deficiency
Recognize the periorificial-acral pattern, find the absorption or loss problem, and replace without creating copper deficiency.
- Recognize the dermatologic, taste, wound-healing, growth, and immune pattern of zinc deficiency.
- Separate inherited ZIP4 failure from malabsorption, short bowel, parenteral nutrition, alcohol use, and gastrointestinal losses.
- Interpret plasma zinc cautiously and monitor replacement for response and zinc-induced copper deficiency.
- Distinguish zinc deficiency from niacin and biotin deficiency using rash distribution and systemic clues.
Cause and effect
Follow the mechanism step by step
Each step shows how the initiating event produces the final clinical finding.
Quick check
A patient with short bowel syndrome develops diarrhea, poor wound healing, loss of taste, alopecia, and sharply demarcated dermatitis around the mouth and on the distal extremities.
Which deficiency best unifies the findings?
Periorificial plus acral plus taste and wound failure points to zinc.From food to loss
Zinc has limited readily exchangeable stores, so intake, absorption, and gastrointestinal loss matter.
Dietary zinc is more bioavailable from animal proteins; phytates in grains and legumes bind zinc and reduce absorption.
Absorption occurs mainly in the distal duodenum and proximal jejunum through ZIP-family transporters. SLC39A4 encodes ZIP4, and biallelic loss causes acrodermatitis enteropathica.
Short bowel, Crohn disease, celiac disease, pancreatic insufficiency, chronic diarrhea, ostomy output, and intestinal failure reduce delivery or increase gastrointestinal losses.
Parenteral nutrition without adequate trace-element zinc bypasses enteral intake, while burns, dialysis, and persistent diarrhea can raise replacement needs.
Alcohol use raises risk through low intake, malabsorption, liver disease, and urinary or gastrointestinal losses rather than through one isolated mechanism.
Advance from intake to clinical depletion.
Animal-source zinc is readily available; phytate-rich diets reduce the fraction absorbed.
ZIP4 transports luminal zinc into proximal small-intestinal enterocytes.
Albumin and other proteins carry circulating zinc to tissues with high turnover and immune demand.
Diarrhea, short bowel, ostomy output, burns, dialysis, or zinc-free parenteral nutrition can outrun replacement.
Short gut loses the same nutrient that healthy proximal small bowel would absorb.
Dose and exposure numbers worth keeping
Separate daily requirements, the population upper limit, and therapeutic replacement.
The adult recommended dietary allowance is 8 mg daily for women and 11 mg daily for men.
The adult tolerable upper intake level is 40 mg daily from all sources, although supervised therapeutic replacement may exceed it.
Adults with acquired deficiency commonly receive 20 to 40 mg of elemental zinc daily, adjusted to severity, ongoing losses, formulation, response, and specialist guidance.
Acrodermatitis enteropathica commonly requires lifelong elemental zinc around 1 to 2 mg/kg/day with individualized monitoring.
Chronic intake of 50 mg or more daily can inhibit copper absorption, so dose, duration, and copper status matter.
Place each number in the correct clinical category.
Elemental zinc is the number that counts, and copper is the toxicity check.
Three nutritional rashes and one treatment complication
Distribution and the non-skin findings keep lookalike deficiencies apart.
Zinc deficiency causes periorificial, anogenital, and acral or friction-site dermatitis with alopecia, diarrhea, dysgeusia or hyposmia, poor wound healing, growth effects, and impaired immune defense.
Niacin deficiency causes pellagra: symmetric photosensitive dermatitis on exposed surfaces with diarrhea and neuropsychiatric change progressing toward dementia.
Biotin deficiency can also cause periorificial dermatitis and alopecia, but hypotonia, ataxia, seizures, hearing loss, or a biotinidase, raw-egg-white, anticonvulsant, or prolonged parenteral-nutrition context makes it more likely.
Excess zinc can induce copper deficiency, producing anemia, neutropenia, and a sensory ataxic myeloneuropathy rather than recurrence of the original zinc rash.
Match the rash pattern to the systemic tie-breaker.
Periorificial-acral dermatitis, alopecia, diarrhea, dysgeusia, poor healing, and infection susceptibility.
Photosensitive hyperpigmented dermatitis plus diarrhea and cognitive or psychiatric change.
Periorificial dermatitis and alopecia with neurologic abnormalities such as hypotonia, seizures, or ataxia.
Cytopenias and posterior-column or peripheral-nerve dysfunction after chronic high zinc exposure.
The rash starts the differential; distribution and neurologic pattern finish it.
The distribution is the diagnostic image
Zinc deficiency favors orifices, distal sites, friction, hair, nails, and wounds.
Facial lesions cluster around the mouth, nose, and eyes; angular cheilitis can accompany them.
Acral and friction-prone sites include hands, feet, elbows, knees, ankles, knuckles, and pressure areas. Anogenital and perineal involvement is also characteristic.
Hair becomes sparse, brittle, or diffusely lost, while nails can show paronychia, dystrophy, or transverse changes.
Oral clues include dysgeusia and poor appetite. Impaired epithelial repair appears as delayed wound healing, and immune dysfunction appears as recurrent bacterial or fungal infection.
Pellagra instead maps to sun-exposed dorsal hands, forearms, face, and neck; biotin deficiency centers around facial orifices but carries stronger neurologic clues.
Point to the highest-yield examination zones.
Acral and friction sites
Hands, feet, elbows, knees, ankles, and pressure points develop sharply demarcated lesions.
Anogenital and perineal skin
This distribution strongly reinforces an acrodermatitis-like zinc pattern.
Hair and nails
Alopecia, brittle hair, paronychia, and nail dystrophy reveal impaired rapidly dividing tissue.
Mouth and wounds
Dysgeusia, cheilitis, and delayed repair expose zinc-dependent sensory and epithelial functions.
Around openings and at the ends: periorificial plus acral is the zinc map.
Risk states that should trigger the exam
The laboratory result is often late or noisy, so risk plus phenotype should drive suspicion.
Inherited acrodermatitis enteropathica commonly appears after weaning when breast-milk zinc delivery no longer compensates for defective ZIP4-mediated absorption.
Acquired deficiency occurs with chronic diarrhea, short bowel, inflammatory or malabsorptive disease, pancreatic insufficiency, prolonged parenteral nutrition, restrictive intake, and alcohol use disorder.
High-output fistulas or ostomies, burns, dialysis, pregnancy, lactation, and rapid growth increase losses or requirements.
Recurrent infections, delayed wound healing, reduced taste or smell, alopecia, angular cheilitis, paronychia, and growth failure can precede a dramatic full triad.
Choose the patient whose risk and phenotype most strongly support zinc deficiency.
A patient with short bowel, high ostomy output, dysgeusia, and poor wound healingBoth major gastrointestinal loss and characteristic tissue effects are present.
A patient with isolated photosensitive hand dermatitis and progressive confusionThis pattern is more characteristic of niacin deficiency and pellagra.
A patient taking high-dose zinc with anemia and gait ataxiaThis suggests zinc-induced copper deficiency rather than untreated zinc deficiency.
A healthy patient with one brittle nail and no gastrointestinal or dietary riskA nonspecific isolated finding provides little support for systemic zinc deficiency.
Risk plus rash plus taste or healing failure is stronger than any clue alone.
Test carefully, then watch the response
Plasma zinc supports the diagnosis but cannot replace clinical context.
Serum or plasma zinc can be low in true deficiency, but meals, time of day, inflammation, stress, pregnancy, low albumin, hemolysis, and collection contamination can distort the result.
Use a fasting morning sample in trace-element appropriate collection material when possible, interpret it with albumin and inflammatory context, and consider alkaline phosphatase as a supportive zinc-dependent enzyme rather than a definitive test.
Oral elemental zinc is first-line for most acquired deficiency. Treat the underlying malabsorption or loss, and use parenteral zinc when intestinal failure or parenteral nutrition makes enteral replacement inadequate.
Acrodermatitis enteropathica needs lifelong elemental zinc with dose titrated to clinical response and laboratory follow-up.
Monitor long courses or high doses for copper deficiency with symptoms, blood counts, and copper studies; rapid skin, appetite, or taste improvement can provide useful diagnostic confirmation.
Open the step that prevents a testing or treatment error.
Repeat or interpret cautiously because inflammation redistributes zinc and can lower circulating concentration.
Do not diagnose chronic deficiency from one acute-phase sample without phenotype and risk.
Obtain a careful sample and begin appropriate replacement while correcting the cause.
A normal or equivocal value does not fully exclude clinically important deficiency.
Use lifelong elemental zinc and monitor clinical response, zinc, blood counts, and copper.
Stopping therapy permits recurrence because the transporter defect remains.
Screen for anemia, neutropenia, sensory change, and hypocupremia.
Excess zinc can solve one deficiency and manufacture another.
The best zinc test is a careful sample interpreted beside the patient.
Stage 1 of 3: Overview
Overview
Zinc Deficiency
Zinc has limited readily exchangeable stores, so intake, absorption, and gastrointestinal loss matter.
Mechanism check
Choose the controlling mechanism
Pick the causal link that makes the rest of the findings predictable.
Which deficiency best unifies the findings?
- Key finding. A patient with short bowel syndrome develops diarrhea, poor wound healing, loss of taste, alopecia, and sharply demarcated dermatitis around the mouth and on the distal extremities.
- Answer. Zinc deficiency
- Why. Malabsorption plus periorificial-acral dermatitis, alopecia, dysgeusia, and impaired healing is the classic zinc pattern.
- Board rule. Periorificial plus acral plus taste and wound failure points to zinc.
Apply the mechanism clinically
Five patients share dermatitis or alopecia, but only the risk history and distribution identify the missing nutrient and the treatment hazard.
Cross out broken mechanisms and highlight the shared effector. Shuffle the cases to test the causal chain again.
A breastfed 7-month-old develops diarrhea, alopecia, irritability, and sharply demarcated crusted lesions around the mouth, anus, hands, and feet several weeks after weaning.
Which diagnosis and mechanism best fit?
Reason it through
- Which timing clue suggests inherited malabsorption?Symptoms began after weaning removed highly bioavailable breast-milk zinc support.
- Which distribution is most characteristic?The dermatitis is both periorificial and acral, with anogenital involvement.
- Which transporter is defective?SLC39A4 encodes the ZIP4 intestinal zinc uptake transporter.
Which timing clue suggests inherited malabsorption?Which distribution is most characteristic?
- Which timing clue suggests inherited malabsorption?Symptoms began after weaning removed highly bioavailable breast-milk zinc support.
- Which distribution is most characteristic?The dermatitis is both periorificial and acral, with anogenital involvement.
- Which transporter is defective?SLC39A4 encodes the ZIP4 intestinal zinc uptake transporter.
A 52-year-old patient with short bowel syndrome and high ileostomy output receives long-term parenteral nutrition. He develops dysgeusia, poor wound healing, recurrent candidiasis, and acral dermatitis.
Which next step is best?
Reason it through
- Which two processes deplete zinc in this patient?Short bowel impairs absorption and high ostomy output increases gastrointestinal loss.
- Which non-skin clue is especially supportive?Dysgeusia and poor wound healing are characteristic zinc-dependent failures.
- What must be corrected besides prescribing a pill?Parenteral trace-element delivery and ongoing ostomy losses must be assessed and replaced.
Which two processes deplete zinc in this patient?Which non-skin clue is especially supportive?
- Which two processes deplete zinc in this patient?Short bowel impairs absorption and high ostomy output increases gastrointestinal loss.
- Which non-skin clue is especially supportive?Dysgeusia and poor wound healing are characteristic zinc-dependent failures.
- What must be corrected besides prescribing a pill?Parenteral trace-element delivery and ongoing ostomy losses must be assessed and replaced.
A 48-year-old man with alcohol use disorder has low intake, chronic diarrhea, loss of taste, angular cheilitis, sparse hair, and erosive plaques around the mouth and on the feet.
Which deficiency is most likely?
Reason it through
- Why does alcohol increase risk without being a single-pathway cause?It combines poor intake, malabsorption, liver disease, and increased losses.
- Which symptom points beyond a generic nutritional dermatitis?Loss of taste is a high-yield zinc clue.
- Which skin distribution breaks the tie with pellagra?Periorificial and acral lesions favor zinc, while pellagra favors sun-exposed skin.
Why does alcohol increase risk without being a single-pathway cause?Which symptom points beyond a generic nutritional dermatitis?
- Why does alcohol increase risk without being a single-pathway cause?It combines poor intake, malabsorption, liver disease, and increased losses.
- Which symptom points beyond a generic nutritional dermatitis?Loss of taste is a high-yield zinc clue.
- Which skin distribution breaks the tie with pellagra?Periorificial and acral lesions favor zinc, while pellagra favors sun-exposed skin.
A malnourished patient has symmetric hyperpigmented scaly plaques on the dorsal hands and around the neck, chronic diarrhea, and new confusion. There is no dysgeusia or periorificial-acral eruption.
Which deficiency best explains the presentation?
Reason it through
- Which skin exposure pattern is decisive?The dermatitis is symmetric and photosensitive on exposed hands and neck.
- Which two systemic domains complete the classic triad?Diarrhea and neuropsychiatric change accompany the dermatitis.
- What deficiency produces that triad?Niacin deficiency produces pellagra.
Which skin exposure pattern is decisive?Which two systemic domains complete the classic triad?
- Which skin exposure pattern is decisive?The dermatitis is symmetric and photosensitive on exposed hands and neck.
- Which two systemic domains complete the classic triad?Diarrhea and neuropsychiatric change accompany the dermatitis.
- What deficiency produces that triad?Niacin deficiency produces pellagra.
A 61-year-old woman has taken 80 mg of elemental zinc daily for months. Her original dermatitis resolved, but she now has anemia, neutropenia, numb feet, and a wide-based sensory gait.
Which complication is most likely?
Reason it through
- Which exposure exceeds the adult upper intake level?She is taking 80 mg daily, twice the 40 mg adult tolerable upper intake level.
- Which laboratory pattern is the hematologic warning?Anemia plus neutropenia is characteristic of copper deficiency.
- Which neurologic pattern completes the complication?Sensory loss and gait ataxia suggest copper-deficiency myeloneuropathy.
Which exposure exceeds the adult upper intake level?Which laboratory pattern is the hematologic warning?
- Which exposure exceeds the adult upper intake level?She is taking 80 mg daily, twice the 40 mg adult tolerable upper intake level.
- Which laboratory pattern is the hematologic warning?Anemia plus neutropenia is characteristic of copper deficiency.
- Which neurologic pattern completes the complication?Sensory loss and gait ataxia suggest copper-deficiency myeloneuropathy.
Rapid review
Three questions to check
Which deficiency best unifies the findings?
Zinc deficiency. Malabsorption plus periorificial-acral dermatitis, alopecia, dysgeusia, and impaired healing is the classic zinc pattern.
Which timing clue suggests inherited malabsorption?
Symptoms began after weaning removed highly bioavailable breast-milk zinc support.
Which distribution is most characteristic?
The dermatitis is both periorificial and acral, with anogenital involvement.
Medically reviewed
Fatima Ali, DO
PGY-1 Resident Physician in Psychiatry
University Hospitals, Columbia
DO from Kansas City University
Resident physician and founding medical reviewer at Bone Wizardry, focused on clinical accuracy, clear diagnostic reasoning, and practical board-oriented teaching across the curriculum.
Languages: English, Urdu
Primary reviewerFull physician profile
Medically reviewed
Sources
- Zinc: Fact Sheet for Health Professionals2026
- Zinc Deficiency2025
- Acrodermatitis Enteropathica2023
- Niacin Deficiency2023
Bone Wizardry is a study resource for medical students. It is not medical advice.