아토피 피부염.

01 —What it is

Atopic eczema (also called atopic dermatitis, or just AD) is a chronic, relapsing, inflammatory skin disease. It affects about 20% of children and around 10% of adults globally. For most, it begins before the age of five. Around half resolve by adolescence; the rest carry it into adulthood, sometimes for life.^¹

The hallmark features are itch, dry skin, and red, inflamed, sometimes weeping or scaly patches — typically in the bends of the elbows and knees, the neck, the wrists and ankles, and the face in younger children. On darker skin, the inflammation can appear violet, grey, or darker brown rather than red, which is one reason the condition is sometimes missed or undertreated in skin of colour.^²

02 —The biology, plainly

Two systems fail together in eczema: the skin barrier and the immune response. They feed each other.

Filaggrin and the barrier

The protein filaggrin is what holds the topmost layer of your skin together — it binds the dead cell envelopes into the protective shield that keeps water in and irritants out. About a third of people with eczema have a loss-of-function mutation in the FLG gene.^³ Their barrier is leaky from the start. Water escapes (this is why eczema skin is dry). Allergens get in.

Th2 inflammation

When allergens get through the barrier, a particular immune response dominates — a Th2-skewed response, driven by cytokines called IL-4, IL-13, and IL-31. These cytokines do three things: they cause more inflammation, they tell the immune system to make IgE antibodies (the allergy antibodies), and IL-31 in particular directly causes itch at the nerve level.^⁴

The itch–scratch cycle

Itch leads to scratching. Scratching damages the barrier further. A more damaged barrier lets in more allergens. More allergens drive more inflammation. More inflammation drives more itch. This is the central feedback loop of eczema, and it is why interventions that interrupt scratching behaviour (like habit reversal training, see below) actually reduce inflammation, not just discomfort.

Eczema is not a 'skin problem'. It is a barrier problem and an immune problem, and the skin is where you can see them both.

03 —What works: the evidence-based treatment ladder

Step 1 · Emollients (foundation)

Daily, generous use of a fragrance-free emollient is the foundation. Cochrane evidence supports this clearly.^⁵ Use them like sunscreen: a thick layer, often. The specific product matters less than how much and how often.

Step 2 · Topical corticosteroids (for flares)

Topical steroids are the most-studied class of drugs in dermatology. Used correctly, they are safe and effective. Used insufficiently (because of fear), they fail.

The fingertip unit rule: one fingertip of cream covers two adult palms' worth of skin. Use the appropriate potency for the body site (mild on the face, more potent on the limbs). Use for short bursts during flares, then taper. Used this way, the side effects in adolescents are minimal.

The biggest barrier to topical steroids working is steroid phobia (corticophobia). Studies using the validated TOPICOP score consistently find that 40–70% of caregivers have significant fear of steroids, and this fear directly reduces adherence and worsens outcomes.^⁶ The fear is real and deserves to be taken seriously, but the evidence for safety with proper use is also robust.

Step 3 · Topical calcineurin inhibitors and crisaborole

Tacrolimus, pimecrolimus, and the newer crisaborole. Non-steroid options for sensitive areas (face, skin folds) or for steroid-sparing maintenance. Useful in adolescents on the face where steroid use is more limited.

Step 4 · Phototherapy

Narrowband UVB phototherapy is effective for moderate-severe disease. Requires multiple visits per week to a clinic. Practical limitation for adolescents in school.

Step 5 · Systemic therapy (the modern era)

This is where eczema treatment has changed dramatically in the last decade.

• —Dupilumab (Dupixent). The first biologic for eczema. Blocks IL-4/IL-13 signalling. Approved down to age 6 months in many countries. Game-changing efficacy in moderate-severe disease. Given by injection every 2 weeks.^⁷
• —Tralokinumab and lebrikizumab. IL-13 blockers — another biologic option.
• —JAK inhibitors — oral upadacitinib, abrocitinib, and the topical ruxolitinib. Block intracellular cytokine signalling. Powerful, fast-acting, oral. Adolescent data is mounting. Side-effect profile requires monitoring.

Behavioural · Habit reversal training

This is the under-recognised intervention. Norén et al.'s 2018 BJD RCT in children with AD showed that habit reversal training added to topical steroids produced significantly greater SCORAD reduction than steroids alone (−31.7 vs −19.7 at 11 weeks, p=0.0038).^⁸ The 2024 Cochrane review of educational and psychological interventions in eczema supports the broader behavioural-intervention class.^⁹ Yet very few clinics routinely offer it.

04 —What does not work (or works less than the marketing suggests)

• —Elimination diets without confirmed food allergy. Most adolescents with eczema do not have a relevant food trigger, and unnecessary restriction risks growth and psychological harm. If true food-triggered eczema is suspected, this should be assessed properly by an allergist.
• —'Eczema diets' advertised online. No reliable evidence base.
• —Probiotics for treatment (some evidence for prevention in high-risk infants, weak evidence for treatment in established disease).
• —Most 'natural' remedies. Some are mildly emollient; some are actively irritating. Tea tree oil and lavender oil are common sensitisers.
• —Bleach baths — mixed evidence; not as clearly beneficial as previously taught.

05 —Living with it

The clinical literature consistently understates what living with eczema actually costs. Children and families rate atopic dermatitis QoL impact alongside cerebral palsy and chronic kidney disease in HRQoL studies.^¹⁰ 67.7% of children with AD miss at least one day of school for their condition, with 3.9% chronically absent (≥15 days per year), predominantly those with more severe disease.^¹¹ Italian survey data document bullying and self-isolation in adolescents with AD at elevated rates compared with controls.^¹²

None of this is a failure of toughness. It is a predictable consequence of a chronic, itchy, visible, sleep-disrupting condition during the most socially loaded years of life. The point of Skinfluency is to make this part of the conversation a routine part of care.

06 —What to ask your doctor

• —What potency of topical steroid am I using? How long for? When do I step down?
• —How much emollient should I be using per week (in grams or tubes)? Am I using enough?
• —Could habit reversal training help with my scratching? Where can I learn it?
• —Has my POEM score actually changed over the last three months? What is the trend?
• —If my eczema is still bad despite full topical treatment, am I a candidate for dupilumab, JAK inhibitors, or another systemic option?
• —How is this affecting my sleep, my school, my mood — and should that be part of how we measure whether treatment is working?

1. 01
   Weidinger S, Beck LA, Bieber T, Kabashima K, Irvine AD. Atopic dermatitis. Nat Rev Dis Primers 2018;4(1):1. PMID 29930242
2. 02
   Adelekun A, Onyekaba G, Lipoff JB. Skin color in dermatology textbooks: An updated evaluation and analysis. JAAD 2021;84(1):194-196. PMID 32335181
3. 03
   Palmer CN, Irvine AD, Terron-Kwiatkowski A, et al. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat Genet 2006;38(4):441-446. PMID 16550169
4. 04
   Bieber T. Atopic dermatitis. N Engl J Med 2008;358(14):1483-1494. PMID 18385500
5. 05
   van Zuuren EJ, Fedorowicz Z, Christensen R, Lavrijsen A, Arents BWM. Emollients and moisturisers for eczema. Cochrane Database Syst Rev 2017;2(2):CD012119. PMID 28166390
6. 06
   Stalder JF, Aubert H, Anthoine E, et al. Topical corticosteroid phobia in atopic dermatitis: International feasibility study of the TOPICOP score. Allergy 2017;72(11):1713-1719. PMID 28439896
7. 07
   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;375(24):2335-2348. PMID 27690741
8. 08
   Norén P, Hagströmer L, Alimohammadi M, Melin L. The positive effects of habit reversal treatment of scratching in children with atopic dermatitis. Br J Dermatol 2018;178(3):665-673. PMID 28940213
9. 09
   Singleton H, Hodder A, Almilaji O, et al. Educational and psychological interventions for managing atopic dermatitis (eczema). Cochrane Database Syst Rev 2024;8:CD014932. PMID 39132734
10. 10
    Beattie PE, Lewis-Jones MS. A comparative study of impairment of quality of life in children with skin disease and children with other chronic childhood diseases. Br J Dermatol 2006;155(1):145-151. PMID 16792766
11. 11
    Cheng BT, Silverberg JI. Association of pediatric atopic dermatitis and psoriasis with school absenteeism and parental work absenteeism: A cross-sectional United States population-based study. J Am Acad Dermatol 2021;85(4):885-892. PMID 33667540
12. 12
    Stingeni L, Belloni Fortina A, Baiardini I, Hansel K, Moretti D, Cipriani F. Atopic Dermatitis and Patient Perspectives: Insights of Bullying at School and Career Discrimination at Work. J Asthma Allergy 2021;14:919-928. PMID 34321892