Quick Answer: Atopic dermatitis (eczema) is a chronic inflammatory disease that begins with a skin barrier defect linked to filaggrin gene mutation and is dominated by a Th2 immune response. Treatment during flares combines topical corticosteroids or calcineurin inhibitors with intensive moisturisation; remission is managed with proactive care and trigger avoidance. In 2025–2026, dupilumab and JAK inhibitors have emerged as highly effective systemic treatment options for moderate-to-severe cases.
What Is Atopic Dermatitis? The True Face of the Disease
Atopic dermatitis (AD), commonly known as eczema, is a chronic inflammatory skin disease. It may begin in childhood and extend into adulthood, persisting lifelong in a significant proportion of patients. While it affects 15–20% of the global population, the estimated prevalence in adults is 5–10% and in children 15–25%.
Atopic dermatitis is more than just "dry skin." It is also associated with chronic itch, sleep disturbance, anxiety and depression. Treatment must therefore address not only the skin, but the patient's overall quality of life.
Disease Pathogenesis: From Filaggrin to Th2 Inflammation
Modern dermatology has established that three core defects underlie atopic dermatitis:
1. Skin Barrier Defect
Filaggrin gene (FLG) mutation is identified in a significant proportion of patients with atopic dermatitis. Filaggrin is a protein that maintains the structural integrity of the epidermal barrier in keratinocytes. Insufficient filaggrin leads to impaired epidermis, increased transepidermal water loss (TEWL), and an open entry point for external allergens.
2. Immune System Dysregulation (Th2 Response)
Allergens entering through the damaged barrier trigger Th2 lymphocyte activation. Th2 cytokines (IL-4, IL-13, IL-31) are produced. IL-4 and IL-13 increase IgE production and lead to the atopic triad (dermatitis + rhinitis + asthma). IL-31 is directly responsible for pruritus.
3. Microbiome Dysbiosis
Patients with atopic dermatitis show excessive Staphylococcus aureus colonisation of the skin microbiome. S. aureus both stimulates the immune response as a superantigen and further impairs barrier function. As a result, S. aureus infection is a common complication during acute flares.
Diagnostic Criteria and Severity Assessment
The diagnosis of atopic dermatitis is based on clinical criteria. The Hanifin-Rajka criteria remain the gold standard. For severity assessment, the EASI (Eczema Area and Severity Index) and SCORAD scores are used.
| Severity | EASI Score | Clinical Picture | Recommended Treatment Step |
|---|---|---|---|
| Mild | 0–7 | Limited lesions, minimal itching | Moisturiser + low-potency topical steroid |
| Moderate | 7–21 | Widespread lesions, sleep disturbance | Topical steroid/TCI + intensive moisturisation + trigger management |
| Severe | 21–50 | Diffuse, weeping lesions, significant sleep loss | Systemic treatment assessment (dupilumab/JAK inhibitor) |
| Very Severe | >50 | Large body surface area affected, severely impaired quality of life | Biological agent or cyclosporine; hospitalisation may be required |
Triggers: Identify and Avoid
| Trigger | Mechanism | Avoidance Strategy |
|---|---|---|
| House dust mite (Dermatophagoides) | Allergen → Th2 activation | Anti-mite mattress covers; weekly washing at 60°C |
| SLS-containing detergents | Barrier disruption, increased inflammation | Use SLS-free cleansers and detergents |
| Wool and synthetic fabrics | Mechanical irritation, excessive sweating | 100% cotton or bamboo; careful clothing selection |
| Sweating and heat | Barrier weakening, S. aureus colonisation | Cool environment, humidity control, shower after exercise |
| Stress | Cortisol → barrier disruption + immune response changes | Stress management, mindfulness, sleep hygiene |
| Fragrance/perfume | Contact sensitisation | Choose fragrance-free products |
| Pet dander | Allergen | Keep pets out of the bedroom |
| Foods (milk, eggs — especially in children) | IgE-mediated or delayed reaction | Eliminate after allergy testing (under physician guidance) |
Care Protocol During Flares
An active flare requires urgent management. The itch-scratch cycle deepens barrier damage; the first 48 hours are therefore critical.
Step-by-step care during a flare
- Lukewarm shower (5–10 min, 32–37°C): Hot showers further damage the barrier — use lukewarm water
- Gentle drying: Pat with a towel rather than rubbing; apply moisturiser while skin retains approximately 10% moisture
- Intensive emollient: Apply 2–3 times daily in generous amounts; ceramide-based products are preferred
- Topical corticosteroid (TCS): Apply only to active lesions at the correct potency; low potency for the face (hydrocortisone 1%), moderate potency for the body
- Wet wrap therapy: For severe flares — apply TCS, cover with a wet bandage and then a dry bandage; rapidly reduces itch
- Antihistamines: Sedating antihistamines may aid sleep but do not directly control itch
- Infection monitoring: Yellow/green discharge, crusting, fever → suspect S. aureus infection → seek dermatology consultation
Proactive Care During Remission
Proactive therapy is the most important paradigm shift in atopic dermatitis management over the past decade. The traditional approach of "treat only when it flares" has given way to the proactive principle of "maintain active barrier therapy even when symptom-free."
- Apply low-potency TCS or a calcineurin inhibitor (pimecrolimus/tacrolimus) 2–3 days per week
- Use generous moisturiser daily (at least 250 g/week)
- Maintain the trigger-avoidance protocol
- Have a rapid-response plan ready at the first signs of early flare
Clinical studies show that proactive therapy can reduce the frequency and intensity of flares by 50–70%.
Topical Treatment Options: Comparison
| Agent | Mechanism of Action | Indication | Limitation |
|---|---|---|---|
| Topical corticosteroid (TCS) | General anti-inflammatory | All age groups, all areas (according to potency) | Prolonged facial use → atrophy, telangiectasia |
| Pimecrolimus (Elidel) | Calcineurin inhibition → T-cell suppression | Face, skin folds, sensitive areas; steroid-phobic patients | Slower onset; burning sensation possible |
| Tacrolimus (Protopic) | Calcineurin inhibition (potent) | Moderate-to-severe, including the face; steroid-resistant cases | Sun sensitivity; burning sensation frequent initially |
| Crisaborole (Eucrisa) | PDE4 inhibition | Mild-to-moderate; steroid alternative | High cost; burning sensation |
| Ruxolitinib cream (Opzelura) | JAK 1/2 inhibition (topical) | Mild-to-moderate atopic dermatitis; available from 2024 | Limited for large surface area application |
New Systemic Treatments of the 2024–2026 Era
The greatest revolution in moderate-to-severe atopic dermatitis treatment in recent years has been biological agents and JAK inhibitors.
Dupilumab (Dupixent)
Dupilumab is a monoclonal antibody that blocks IL-4 and IL-13 receptors. FDA-approved since 2017, it is also prescribed as a biological agent internationally. Administered as a subcutaneous injection every two weeks. In clinical trials, 50–70% of patients achieved a 75% or greater reduction in EASI score (EASI-75). Conjunctivitis (watery, red eyes) is the most common side effect.
JAK Inhibitors
- Upadacitinib (Rinvoq): JAK1-selective; rapid onset (1–2 weeks), very potent. Has shown superiority over dupilumab in comparative studies for severe AD. Requires monitoring for infection and cardiovascular risk.
- Abrocitinib (Cibinqo): JAK1-selective, oral; an alternative for severe AD.
- Baricitinib (Olumiant): JAK1/2; approved in multiple markets, more accessible.
Because JAK inhibitors are taken orally, they offer a significant advantage for patients who prefer not to inject. However, their serious side effect profile makes specialist monitoring mandatory.
Moisturiser Selection: What Actually Works?
There are hundreds of moisturisers on the market. Key ingredients to look for when choosing a moisturiser for atopic dermatitis:
| Ingredient | Function | Priority |
|---|---|---|
| Ceramides (1, 3, 6-II) | Barrier repair — partially compensates for filaggrin deficiency | First choice |
| Cholesterol + free fatty acids | Completes barrier structure together with ceramides | First choice (alongside ceramides) |
| Hyaluronic acid | Deep hydration, water retention | Good complement |
| Glycerin | Humectant — draws in water | Good complement |
| Petrolatum / Vaseline | Occlusive — prevents water evaporation | Very good (in cream form) |
| Fragrance / alcohol | Irritant, allergen | Avoid entirely |
| Propylene glycol | May cause irritation in some patients | Use with caution |
Atopic Dermatitis and Medical Aesthetic Procedures
What should be done when a patient with atopic dermatitis wants a medical aesthetic procedure?
- During active flares: No aesthetic procedures should be performed. Barrier impairment significantly increases the risk of infection, excessive reactions and poor wound healing.
- During remission: Procedures may be performed, but dermatological approval is required. Low-risk procedures (skin boosters, hyaluronic acid fillers) are preferred.
- Laser and peeling: Contraindicated in active or recently affected AD areas; careful assessment is required even in remission.
- Botulinum toxin: Generally well tolerated; the presence of AD is not a direct contraindication.
At Virtuana Clinic, patients with a history of atopic dermatitis are assessed for disease activity at the initial consultation, and the treatment plan is adjusted accordingly.
Atopic Dermatitis in Children: A Guide for Parents
Atopic dermatitis most commonly begins between 6 months and 5 years of age. Management in children differs from that in adults:
- Low-potency TCS (hydrocortisone 1%) is safe; fluorinated steroids are not applied to the face
- Pimecrolimus is approved for children aged 2 years and over
- Tacrolimus can be used in children aged 2 years and over
- Dupilumab is FDA-approved for children aged 6 months and over (as of 2024)
- Probiotic supplementation (lactobacillus) to support the infant skin microbiome is under investigation
This article is for informational purposes only. Please consult a qualified physician for treatment decisions.