Atopic dermatitis

Meet the patient

A 6-year-old boy is brought in by his exhausted mother. For two years he has scratched his antecubital and popliteal fossae until they weep, wakes three times a night, and now refuses short-sleeved shirts at school. His cheeks were a crusted mess as a baby; he wheezes in spring and sneezes around the cat.^[1]

Two exam questions are now live and you must answer both: why does his skin behave this way? (barrier and immunity) and what will actually give him his nights back? (the right rung of the treatment ladder). Everything below exists to answer those two questions at consultant depth.^[1][2]

The three-word handle — red, dry, itchy

Atopic dermatitis is a chronic, relapsing, inflammatory skin disease defined by pruritus, an eczematous morphology, and a typical age-dependent distribution. It is the cutaneous first stop of the atopic march, travelling in company with asthma, allergic rhinitis and food allergy.^[1]

The morphology shifts with time, and each phase asks for a different potency of cream — learn the four faces:^[1]

The mantra: red, dry, itchy. Red is the inflammation, dry is the broken barrier, itchy is the IL-31 driving the scratch that keeps both going. Hold those three words and the disease, the scoring, and the drugs all fall into place.^[1]

How common — and where it walks next (the atopic march)

AD is the most common chronic inflammatory skin disease globally, and it rarely travels alone. It affects up to 20 percent of children and up to 3 percent of adults; prevalence is still increasing, especially in low-income countries. It is the leading cause of the global burden from skin disease, and it is associated with food allergy, asthma, allergic rhinitis and mental-health disorders. First manifestations usually appear early in life and often precede asthma or allergic rhinitis — the atopic march.^[23][2][1]

^{[23] [22] [8] [9]}

The atopic march is the sequence every candidate must recite: AD in infancy, then food allergy, then asthma, then allergic rhinitis — the same barrier leak and Th2 bias expressing themselves up the respiratory tree. The skin is the gateway, which is why controlling childhood eczema is not cosmetic.^[1]

The risk-factor cluster runs on autopilot — group it once and it stays:^[1]

• Genetic: family history of atopy; filaggrin plays an important role in AD and allergic disease — FLG variants impair the barrier.^[6]
• Environmental: urbanisation, low humidity, aeroallergens, tobacco smoke, occupational irritants.
• Barrier defects: filaggrin loss (genetic or Th2-driven downregulation) raises transepidermal water loss and opens the door to allergen and microbe.^[6][7]
• Infection: in children with moderate-to-severe AD and clinical signs of secondary bacterial infection, dilute bleach baths plus intermittent intranasal mupirocin reduced EASI versus water baths (all also received 14 days of oral cephalexin).^[21]

Why the barrier fails — filaggrin and the Th2 fire

AD is one disease with two engines: a leaky barrier and a type 2 inflammatory fire — and each fuels the other. Barrier failure lets allergen and bug in; the immune response then damages the barrier further. Break either loop and the disease improves.^[1]

Filaggrin is the word that scores. It aggregates keratin filaments and is proteolysed into the natural moisturising factors that hold water in the stratum corneum. FLG loss-of-function mutations — or Th2-driven downregulation of filaggrin and the tight junctions — raise transepidermal water loss and open the door to allergen and microbe.^[6][7]

Once the barrier leaks, keratinocytes sound the alarm, releasing TSLP, IL-25 and IL-33, which drive Th2 differentiation. The cytokines that follow each do a distinct job — name them by function, not order:^[1]

• IL-4 and IL-13 — the central drivers: barrier dysfunction, IgE class switching, eosinophil recruitment, fibrosis.
• IL-31 — the itch cytokine, firing on peripheral nerves to drive the scratch you cannot stop.
• IL-5 and IL-9 — eosinophil and mast-cell survival.
• IL-22 and IL-17 — epidermal hyperplasia in chronic, lichenified lesions.^[1]

Etymology for viva gold: filaggrin — "filament-aggregating protein". The name tells you its job; lose it and the keratin scaffolding collapses, the skin dries, and the march begins.^[6]

The itch–scratch cycle — the engine of chronicity

Itch is not a symptom of AD; it is the mechanism that maintains it. Scratching damages the already-fragile barrier, drives S. aureus colonisation, releases more TSLP and IL-31, and lichenifies the skin — which itches more. Break the cycle and chronic eczema improves; feed it and no cream will keep up.^[1]

This is why sedating antihistamines earn their place at night (for sleep, not for the itch per se), why emollients are foundation not afterthought, and why the itch-dominant phenotype is the one that most rewards an IL-31 blocker.^[2]

Meet the patient at each age — distribution by age

Distribution changes with age, and the change is the single most examined fact about the clinical pattern. One line carries the marks: extensors and face in the infant, flexures in the child, hands and head-and-neck in the adult.^[1]

The classic trap: a baby with crusted, weeping cheeks is not "just baby acne" or impetigo — the atopic distribution plus the family history makes AD the leading diagnosis until seborrhoeic dermatitis and impetigo are excluded.^[1]

The secondary changes tell you how long it has gone on: excoriations, lichen simplex chronicus, prurigo nodules, and post-inflammatory hypo- or hyperpigmentation. The pigment change can distress patients more than the itch — name it and reassure.^[1]

How severe? The scoring alphabet

You cannot escalate to a biologic without a number, and the number is EASI. Severity scoring separates "a bit dry" from "biologic-eligible", and every modern AD trial is built on the same handful of instruments.^[1]

^[22]

Know the calculation, not just the name. Examiners ask what goes into each score, and the components are where the marks live:^[1]

The thresholds that unlock a biologic

Three trial-entry numbers gate most modern systemic programmes, and a fellowship candidate names them as a set. Measure Up (upadacitinib) and JADE MONO-1 (abrocitinib) enrolled EASI at least 16, IGA or vIGA-AD at least 3, and at least 10% BSA after inadequate topical control. Treat-to-target in those programmes is EASI-75 or IGA 0/1 by week 16 (week 12 for JADE MONO-1). DLQI/POEM bands and NICE TA814 numeric gates are not reproduced from the abstracts cited here — quote the trial inclusion set rather than an unsourced four-number AAD/NICE composite.^[9][13]

Treat to a target, not to a prescription. Aim for EASI-75 or IGA 0/1 by week 16 (the coprimary window of SOLO, Measure Up, ECZTRA, ADvocate and ARCADIA); if it is not met, escalate or switch rather than drift.^{[8][9][10][11][15]}

The foundation — emollients, triggers, and the bath you did not think of

Every AD patient, however severe, starts and stays on emollients. The AAD topical guideline issues a strong recommendation for moisturizers alongside the anti-inflammatory topicals — they are foundation, not adjunct, applied liberally and frequently.^[3]

The non-drug bundle that actually changes outcomes:^[3]

• Emollients — liberally and frequently, all skin, including as soap substitute and bath additive.
• Trigger avoidance — fragrances, detergents, wool, overheating, aeroallergens, and the stressors that light the flare.
• Infection control — dilute bleach baths plus intranasal mupirocin reduced eczema severity in children with moderate-to-severe AD and clinical signs of secondary bacterial infection in a randomised trial; treat secondary infection promptly.^[21]
• Psychosocial support — sleep, anxiety, depression, school and work impact are part of the disease, not extras.^[3]

The topical ladder — match potency to site

Topical anti-inflammatory therapy is the cornerstone, and the recurring trainee error is using the wrong potency on the wrong skin. The rule is simple and load-bearing: mild for face and flexures, moderate for trunk and limbs, potent only for thick plaques on palms and soles — and never the face with a potent steroid.^[3]

^[3]

The potency ladder, named as a memory device:^[1]

• Face, eyelids, genitals, skin folds: mild (hydrocortisone 1%) — atrophy is irreversible.
• Trunk and limbs: moderate (e.g. betamethasone valerate 0.025%, clobetasone butyrate 0.05%) for moderate disease.
• Thick, lichenified plaques on palms, soles or limbs: potent to very potent (clobetasol propionate 0.05%, mometasone furoate 0.1%) for short courses only.
• Quantify with the fingertip unit — one fingertip covers two adult palms — so you prescribe a quantity, not a tube.^[1]

Everyone forgets: topical calcineurin inhibitors do not cause skin atrophy, which is exactly why they own the face, eyelids and flexures for maintenance. The transient stinging on application is the reason patients stop them in week one — warn, and they stay on.^[3]

Phototherapy — the middle rung

Phototherapy carries an AAD 2024 conditional recommendation for AD refractory to topical therapies. It is commonly combined with topical treatment or used as a bridge while slower systemic agents take effect. Exact session frequency and course length are protocol-dependent — do not quote an unsourced 8-to-12-week recipe.^[12]

Systemic therapy — when topicals and light are not enough

Systemic therapy is for moderate-to-severe disease refractory to optimised topical therapy and phototherapy, or when quality of life has collapsed. The choice is no longer "steroids or nothing" — it is a deliberate ladder from conventional immunosuppressants to targeted biologics and JAK inhibitors.^[1]

The AAD 2024 systemic guideline gives strong recommendations for dupilumab, tralokinumab, abrocitinib, baricitinib and upadacitinib, conditional recommendations for phototherapy, azathioprine, ciclosporin, methotrexate and mycophenolate, and recommends against systemic corticosteroids. The 2025 focused update adds strong recommendations for tapinarof cream, roflumilast cream, lebrikizumab, and nemolizumab with concomitant topical therapy.^[12][5]

The whole spine, as one ladder:^[1]

^{[3] [21] [20] [12] [17] [5] [16] [9]}

The conventional systemics are steroid-sparing workhorses, chosen by speed and safety profile. Ciclosporin is fastest (SCORAD-50 42% vs 8% with methotrexate at week 8) but causes more treatment-related adverse events — monitor blood pressure, renal function and blood counts. Methotrexate 15 mg weekly, increased to 25 mg if needed, was equivalent by week 20 (EASI-50 92% vs 87%). Azathioprine 2.5 mg/kg/day dropped mean SASSAD 26% vs 3% placebo, with leukopenia and deranged liver enzymes on active treatment. Mycophenolate sodium 1440 mg daily matched ciclosporin as maintenance after a 5 mg/kg ciclosporin run-in, with delayed onset over the first 10 weeks. TPMT-guided azathioprine dosing is local-protocol teaching, not in the Berth-Jones abstract.^[17][19][18]

Systemic corticosteroids have no home in chronic AD. The AAD 2024 systemic guideline makes a conditional recommendation against systemic corticosteroids because of rebound flares and adverse effects.^[12]

^{[1] [8] [9] [16] [10] [11]}

The quick-reference table for the viva — drug, target, and the trial that named it:^[5]

^{[2] [5]}

Before the first dose, screen. Hepatitis B surface antigen and core antibody, hepatitis C antibody, HIV, and TB (IGRA or Mantoux) per local guideline; bring inactivated vaccines up to date, because live vaccines are contraindicated once immunosuppression begins; and draw baseline FBC, renal and liver function, creatinine, LFT, lipids for JAK inhibitors, and a pregnancy test.^[1]

The drug doses — named agents at named doses

The protocols below reflect the dosing used in the pivotal randomised trials and the strength of the current AAD 2023-2025 recommendations. Local formularies and product labels may differ — individualise, and prescribe from local product information.^[3][12]

^{[3] [20] [20] [8] [12] [16] [9] [12] [16] [13] [12] [14] [12] [10] [12] [11] [5] [15] [5] [17] [12] [18] [12] [19] [12] [17] [18] [12]}

The trials that changed practice

Four landmark programmes built the modern systemic ladder. Each moved a class from "interesting" to "guideline-strong", and a fellowship candidate names the trial with the drug.^[1]

^{[8] [9] [10] [11]}

The differential — discriminators, not lists

AD mimics hide in four patterns, and the discriminator is what earns the mark. Run the pattern, then the one-line tell.^[1]

^[1]

The one-line discriminator: well-demarcated with silvery scale on extensors is psoriasis; poorly demarcated and itchy in flexures is AD. Everything else refines around those two poles.^[1]

Investigations — clinical first, then exclude

The diagnosis is clinical — investigations exist to exclude mimics, grade severity, and clear the patient for systemic therapy, never to confirm AD. Reach for them with a question already in mind.^[1]

• Skin swab or culture if secondary bacterial (S. aureus) or viral (HSV) infection is suspected.
• KOH preparation to exclude tinea corporis in annular lesions.
• Patch testing if contact dermatitis is plausible — especially adults with hand or refractory disease.
• Total and specific IgE (RAST) may support atopic status but are not diagnostic.
• Biopsy if the diagnosis is uncertain, features are atypical, or treatment is failing.
• Baseline bloods before systemic immunosuppression — FBC, renal and liver function, creatinine, LFT, hepatitis B and C, HIV, TB screening (IGRA or Mantoux), pregnancy test where relevant.^[1]

Histology is rarely needed, but know it: spongiosis (intercellular oedema) with epidermal thickening in chronic lesions, parakeratosis, and a superficial perivascular lymphocytic infiltrate with eosinophils. Unlike psoriasis, there are no regular acanthosis, no Munro microabscesses, no neutrophilic collections.^[1]

Comorbidities — the atopic body and mind

AD is a systemic disease, and the comorbidities are part of the assessment, not a footnote. The AAD 2022 comorbidity guideline catalogues associations across allergic, atopic, immune-mediated, mental-health and bone-health domains, plus skin infections.^[4]

Screen actively for asthma, allergic rhinitis and food allergy (the atopic march), and — just as importantly — for anxiety, depression and the sleep deprivation that chronic itch inflicts. A patient whose eczema is "controlled" but who is still not sleeping is not controlled.^[4]

Special sites and populations

Site and life-stage change the first choice and the monitoring — state them explicitly.^[3]

• Children: emollients and mild-to-moderate topical corticosteroids first-line; topical calcineurin inhibitors for facial and flexural maintenance; avoid potent steroids on face and folds; phototherapy and systemic therapy only under specialist care.
• Pregnancy and breastfeeding: emollients and mild topical corticosteroids are generally safe; avoid most systemic immunosuppressants and biologics unless specialist-directed; ciclosporin may be used in selected cases under specialist care.
• Hand and foot eczema: potent topical steroids under occlusion for thick plaques; patch test if an occupational or contact aetiology is suspected.
• Eyelid eczema: low-potency steroids or topical calcineurin inhibitors; avoid chronic potent steroid use because of glaucoma and cataract risk.^[3]

Eczema herpeticum — the emergency

This is the complication that must never be missed, and there is nothing funny about it. A child or adult with AD who develops widespread, monomorphic, punched-out erosions with haemorrhagic crusting, fever, malaise, or a history of cold-sore contact has eczema herpeticum — a dermatology emergency caused by herpes simplex virus disseminating through broken barrier skin.^[1]

Treat promptly with systemic aciclovir, and consider admission, especially in the young, the extensive, or the systemically unwell. Do not wait for the swab to return in a deteriorating patient — the clinical picture is enough to start.^[1]

Secondary bacterial infection presents with weeping, crusting, pustules and rapid flare — S. aureus is the usual culprit; treat with antiseptics or antibiotics as appropriate. Molluscum contagiosum runs more extensive and persistent courses in AD skin.^[1]

Generalised erythroderma — the whole skin inflamed and scaling — is an admission: the patient loses fluid, electrolytes and temperature control through the broken barrier, and needs inpatient stabilisation.^[1]

^[1]

How AD patients come to harm — the preventable list

• Eczema herpeticum missed as "a flare" — the delayed-antiviral harm.^[1]
• A potent steroid used on the face or eyelids long-term, ending in skin atrophy, striae, glaucoma or cataract.^[1]
• Systemic corticosteroids prescribed for chronic AD, ending in a rebound flare worse than the original.^[1]
• A biologic or JAK inhibitor started without TB, hepatitis and vaccination screening.^[1]
• Ciclosporin continued without blood pressure and creatinine monitoring, ending in nephrotoxicity.^[17]
• Azathioprine continued without blood-count and liver-enzyme monitoring (leukopenia and deranged enzymes occurred on active treatment in the crossover trial).^[19]
• A JAK inhibitor given in pregnancy, or to a patient needing live vaccines.^[1]
• An itchy, sleepless child labelled "just eczema" while depression and school refusal take hold.^[4]

Prognosis and follow-up

AD is chronic and relapsing; the goal is control, not cure. Modern targeted therapies achieve high rates of EASI-75 or IGA 0/1, but relapse is the rule after stopping — so maintenance planning is part of the prescription, not an afterthought.^[1]

Follow-up intervals track the therapy and severity:^[1]

• Topical therapy: review at 4 to 8 weeks.
• Phototherapy: review every 2 to 4 weeks during induction.
• Systemic or biologic therapy: review at 8 to 16 weeks initially, then every 3 to 6 months, with laboratory monitoring as appropriate.^[1]

^{[1] [2]}

Guidelines and regional deltas

• AAD 2023 topical guideline — emollients, topical corticosteroids, calcineurin inhibitors, crisaborole and ruxolitinib.^[3]
• AAD 2024 systemic and phototherapy guideline — strong recommendations for dupilumab, tralokinumab, abrocitinib, baricitinib and upadacitinib; conditional for phototherapy, ciclosporin, methotrexate, azathioprine and mycophenolate; recommends against systemic corticosteroids.^[12]
• AAD 2025 focused update — adds strong recommendations for tapinarof cream, roflumilast cream, lebrikizumab and nemolizumab with topical therapy.^[5]

The mantra, and the mnemonic

^[1]

The mantra: emollients always, steroid the flare by site, calm the Th2 fire when the scores say so — and never miss eczema herpeticum.^[1][2]

^{[1] [1]}

Ward-round test — three stems, thirty seconds each

Stem 1 — the itchy child whose cream is on the wrong skin (answer)ShowHide

A mother has been applying clobetasol propionate 0.05% to her 4-year-old's cheeks and eyelids for three months for "stubborn eczema". The cheeks are now thin and telangiectatic. What went wrong, and what do you do? Model: A potency–site mismatch. Clobetasol is a Class I ultra-potent steroid; the face and eyelids take only mild potency (hydrocortisone 1%) or — better still for maintenance — a topical calcineurin inhibitor such as tacrolimus 0.1% ointment, which is non-atrophogenic and owns the face and flexures. Stop the clobetasol immediately, switch to a calcineurin inhibitor plus emollients, screen for glaucoma and cataract from the periocular exposure, and educate on the potency ladder: mild for face and flexures, moderate for trunk and limbs, potent only for thick plaques on palms and soles.^[1][3]

Stem 2 — punched-out erosions and a fever (answer)ShowHide

A 7-year-old with known AD presents with a rapid flare, widespread monomorphic punched-out erosions with haemorrhagic crusting, fever and malaise. His sibling has a cold sore. What is this, and what is the first action? Model: Eczema herpeticum — herpes simplex virus disseminating through broken barrier skin, a dermatology emergency. Do not wait for the swab in a deteriorating child. Start systemic aciclovir immediately, consider admission (young, extensive, systemically unwell), and screen for and treat any secondary S. aureus infection. This is the complication that must never be missed — the monomorphic punched-out morphology against fever and cold-sore contact is the tell.^[1]

Stem 3 — is this patient biologic-eligible? (answer)ShowHide

A 28-year-old has AD despite optimised topical therapy and phototherapy. Her EASI is 17, IGA 3, BSA 14%. What is the threshold question, and what is first-line? Model: She has moderate-to-severe AD refractory to optimised topical therapy — her numbers (EASI 17, IGA 3, BSA 14%) match the Measure Up / JADE MONO-1 entry set: EASI at least 16, IGA/vIGA-AD at least 3, and at least 10% body surface area. Do not add an unsourced DLQI at-least-11 as a fourth AAD gate. Before immunosuppression, complete pre-treatment screening per local protocol. Dupilumab 300 mg subcutaneously every other week carries a strong AAD recommendation (SOLO IGA 0/1 36–38% vs 8–10% placebo). An anti-IL-13 or a JAK inhibitor is the alternative when the mechanism or speed differs. Treat to EASI-75 or IGA 0/1 by week 16; if not met, switch or escalate.^{[9][8][12][13]}

References23ShowHide

1. [1]Langan SM, Irvine AD, Weidinger S. Atopic dermatitis Lancet, 2020.PMID 32738956
2. [2]Guttman-Yassky E, Renert-Yuval Y, Brunner PM Atopic dermatitis Lancet, 2025.PMID 39955121
3. [3]Sidbury R, Alikhan A, Bercovitch L, et al. Guidelines of care for the management of atopic dermatitis in adults with topical therapies J Am Acad Dermatol, 2023.PMID 36641009
4. [4]Davis DMR, Drucker AM, Alikhan A, et al. American Academy of Dermatology Guidelines: Awareness of comorbidities associated with atopic dermatitis in adults J Am Acad Dermatol, 2022.PMID 35085682
5. [5]Davis DMR, Frazer-Green L, Alikhan A, et al. Focused update: Guidelines of care for the management of atopic dermatitis in adults J Am Acad Dermatol, 2025.PMID 40531067
6. [6]Drislane C, Irvine AD. The role of filaggrin in atopic dermatitis and allergic disease Ann Allergy Asthma Immunol, 2020.PMID 31622670
7. [7]Margolis DJ Atopic dermatitis: filaggrin and skin barrier dysfunction Br J Dermatol, 2022.PMID 35128630
8. [8]Simpson EL, Bieber T, Guttman-Yassky E, et al. Two Phase 3 Trials of Dupilumab versus Placebo in Atopic Dermatitis N Engl J Med, 2016.PMID 27690741
9. [9]Guttman-Yassky E, Teixeira HD, Simpson EL, et al. Once-daily upadacitinib versus placebo in adolescents and adults with moderate-to-severe atopic dermatitis (Measure Up 1 and Measure Up 2): results from two replicate double-blind, randomised controlled phase 3 trials Lancet, 2021.PMID 34023008
10. [10]Wollenberg A, Blauvelt A, Guttman-Yassky E, et al. Tralokinumab for moderate-to-severe atopic dermatitis: results from two 52-week, randomized, double-blind, multicentre, placebo-controlled phase III trials (ECZTRA 1 and ECZTRA 2) Br J Dermatol, 2021.PMID 33000465
11. [11]Silverberg JI, Guttman-Yassky E, Thaçi D, et al. Two Phase 3 Trials of Lebrikizumab for Moderate-to-Severe Atopic Dermatitis N Engl J Med, 2023.PMID 36920778
12. [12]Davis DMR, Drucker AM, Alikhan A, et al. Guidelines of care for the management of atopic dermatitis in adults with phototherapy and systemic therapies J Am Acad Dermatol, 2024.PMID 37943240
13. [13]Simpson EL, Sinclair R, Forman S, et al. Efficacy and safety of abrocitinib in adults and adolescents with moderate-to-severe atopic dermatitis (JADE MONO-1): a multicentre, double-blind, randomised, placebo-controlled, phase 3 trial Lancet, 2020.PMID 32711801
14. [14]Simpson EL, Forman S, Silverberg JI, et al. Baricitinib in patients with moderate-to-severe atopic dermatitis: Results from a randomized monotherapy phase 3 trial in the United States and Canada (BREEZE-AD5) J Am Acad Dermatol, 2021.PMID 33600915
15. [15]Silverberg JI, Wollenberg A, Reich A, et al. Nemolizumab with concomitant topical therapy in adolescents and adults with moderate-to-severe atopic dermatitis (ARCADIA 1 and ARCADIA 2): results from two replicate, double-blind, randomised controlled phase 3 trials Lancet, 2024.PMID 39067461
16. [16]Blauvelt A, Teixeira HD, Simpson EL, et al. Efficacy and Safety of Upadacitinib vs Dupilumab in Adults With Moderate-to-Severe Atopic Dermatitis: A Randomized Clinical Trial JAMA Dermatol, 2021.PMID 34347860
17. [17]Goujon C, Viguier M, Staumont-Sallé D, et al. Methotrexate Versus Cyclosporine in Adults with Moderate-to-Severe Atopic Dermatitis: A Phase III Randomized Noninferiority Trial J Allergy Clin Immunol Pract, 2018.PMID 28967549
18. [18]Haeck IM, Knol MJ, Ten Berge O, et al. Enteric-coated mycophenolate sodium versus cyclosporin A as long-term treatment in adult patients with severe atopic dermatitis: a randomized controlled trial J Am Acad Dermatol, 2011.PMID 21458107
19. [19]Berth-Jones J, Takwale A, Tan E, et al. Azathioprine in severe adult atopic dermatitis: a double-blind, placebo-controlled, crossover trial Br J Dermatol, 2002.PMID 12174106
20. [20]Reitamo S, Ortonne JP, Sand C, et al. A multicentre, randomized, double-blind, controlled study of long-term treatment with 0.1% tacrolimus ointment in adults with moderate to severe atopic dermatitis Br J Dermatol, 2005.PMID 15948994
21. [21]Huang JT, Abrams M, Tlougan B, et al. Treatment of Staphylococcus aureus colonization in atopic dermatitis decreases disease severity Pediatrics, 2009.PMID 19403473
22. [22]Leshem YA, Hajar T, Hanifin JM, Simpson EL What the Eczema Area and Severity Index score tells us about the severity of atopic dermatitis: an interpretability study Br J Dermatol, 2015.PMID 25580670
23. [23]Nutten S Atopic dermatitis: global epidemiology and risk factors Ann Nutr Metab, 2015.PMID 25925336