Atopic Dermatitis

The diagnostic criteria most commonly used for atopic dermatitis are the major clinical features proposed by Hanifin and Rajka in 1980. According to these criteria, a diagnosis can be made when at least three of the four major features (pruritus, characteristic morphology and distribution of lesions, chronic or relapsing course, and personal or family history of atopic disease) and at least three of the 23 minor features are present. In response to evolving clinical needs, the Korean Academy of Pediatric Allergy and Respiratory Disease proposed a modified version of the Hanifin and Rajka criteria in their 2008 clinical practice guidelines for pediatric atopic dermatitis.

Essential feature 

• Pruritus
• Eczematous skin lesions
• Characteristic morphology and age-specific distribution of lesions
• Infants and young children: involvement of the face, neck, and extensor surfaces of the limbs
• At any age: involvement of flexural areas
• Sparing of groin and axillary areas
• Chronic or relapsing course

Important features (commonly observed in patients and supportive for diagnosis)

• Early onset
• Atopic features
• Personal or family history of atopic diseases
• IgE reactivity (elevated total IgE or specific IgE sensitization)
• Xerosis (dry skin)

Associated features (presence of three or more suggests a diagnosis of atopic dermatitis)

• Atypical vascular responses (e.g., facial pallor, white dermographism)
• Keratosis pilaris / Prominent palmar creases / Ichthyosis
• Periorbital changes 
• Other localized findings (e.g., perioral changes, lesions around the ears)

Skin prick tests, serum assays, and provocation tests are not used for diagnosis itself, but rather to identify aggravating factors.

Skin prick tests

• Intradermal testing is generally avoided due to its lower specificity and potential to cause serious reactions such as anaphylaxis; instead, skin prick testing is typically used. A negative result rules out the allergen as a trigger, while a positive result does not confirm causality. Results may vary depending on the allergen extract, patient age, tester experience, criteria for positivity, and use of medications at the time of testing.

Serum assays

• Serum-specific IgE can also be measured using assays such as the multiple allergen simultaneous test (MAST) or CAP system. These are particularly useful in patients with dermographism, severe widespread atopic dermatitis, or when discontinuation of antihistamines is not feasible. The CAP-FEIA system allows quantitative analysis of specific IgE levels. 

Food challenge tests

• Food challenge testing is the most accurate method for diagnosing food allergy and involves having the patient consume the suspected food under medical supervision to observe symptom provocation. 

Skin barrier function tests

• These include measurements of skin surface hydration, transepidermal water loss (TEWL), and skin pH.

Several tools are available to assess disease severity, among which the SCORAD (Scoring Atopic Dermatitis) index and EASI (Eczema Area and Severity Index) are the most commonly used. It is important to evaluate disease severity over time rather than relying solely on a single-point assessment. In addition to physician-reported findings, patient-reported outcomes such as symptom intensity and disease-related impact on daily life and quality of life should also be considered in clinical assessment.

SCORAD (Scoring Atopic Dermatitis) index 

• There are several methods to assess the severity of atopic dermatitis, among which the SCORAD (SCORing Atopic Devrmatitis) index, proposed by the European Task Force on Atopic Dermatitis in 1993, is the most widely used. The SCORAD index is calculated using the following formula: SCORAD = A/5 + 7B/2 + C, where A represents the extent of the lesions (assessed using the rule of nines across the scalp, face, anterior and posterior trunk, upper and lower limbs, hands, and genital areas), B is the intensity of six clinical signs (erythema, edema/papulation, oozing/crusts, excoriation, lichenification, and dryness), each scored from 0 to 3, and C reflects subjective symptoms (pruritus and sleep loss over the past three days), each scored from 0 to 10. In some cases, a modified SCORAD (excluding subjective symptoms) is used: objective SCORAD = A/5 + 7B/2.

EASI (Eczema Area and Severity Index) 

• Other clinical severity assessment tools include the Eczema Area and Severity Index (EASI) and the Three-Item Severity Score (TIS). The EASI score evaluates four clinical signs—erythema (E), induration/papulation (I), excoriation (Ex), and lichenification (L)—in four body regions: head/neck (H), upper limbs (U), trunk (T), and lower limbs (L). Each region is scored for severity (0–3) and area (0–6, based on percentage involvement), then multiplied by region-specific weights. For patients ≥8 years of age, the weights are H×0.1, U×0.2, T×0.3, and L×0.4; for patients under 7 years, the weights are H×0.2, U×0.2, T×0.3, and L×0.3. The total EASI score ranges from 0 to 72.

Management of atopic dermatitis consists of a stepwise approach:

Step 1: Non-pharmacological interventions

1-1. Dietary Management

• Elimination of confirmed allergens
• Nutritional supplementation and food group substitution

1-2. Environmental control

• House Dust Mites: Encase mattresses and pillows with allergen-proof covers, wash bedding regularly in hot water above 55°C. Remove carpets, stuffed animals, and clutter; vacuum weekly using a HEPA-filter vacuum, and maintain indoor humidity between 40–50%.
• Pets: Avoid keeping cats or dogs if possible, and remove carpets or upholstered furniture, or use HEPA-equipped air purifiers. Bathe cats weekly if feasible, and wipe floors, walls, and furniture surfaces with a damp cloth.
• Cockroaches: Seal entry points and store food in tightly closed containers. Clean frequently and use insecticides 
• Indoor Environmental Pollution (Fine dust, formaldehyde, bacteria, and mold) Management:  Frequent ventilation, especially after renovations or the addition of new furniture

1-3. Skin care

• Skin Hygiene: Daily bathing with mildly acidic cleansers (pH 5.5–6.0) helps remove debris and allergens while minimizing skin irritation.
• Bathing Practices: Lukewarm baths for about 15 minutes, followed by immediate application of moisturizers, avoid using alkaline soaps and scrubbing the skin
• Moisturization: Restore the skin barrier, relieve dryness, and reduce the need for anti-inflammatory medications. 
• Irritant Management: Room temperature should not be too warm, and lightweight pajamas and bedding, trimmed fingernails
• Clothing: Liquid detergents containing non-ionic surfactants 

1-4. Psychological supports

• Parent education, behavioral therapy, cognitive imagery, psychological and family counseling . 

Step 2: Applied to acute or progressive lesions that do not improve with step 1 management and targets skin inflammation. 

2-1. Topical Corticosteroids

• Early intervention with mild steroids can shorten treatment duration and prevent worsening. 
• To avoid systemic effects, apply long-term steroids in the morning and taper gradually to avoid rebound flares. 
• Low-potency steroids like 1% hydrocortisone are generally safe for infants, but high-potency steroids can cause skin atrophy, striae, or systemic effects if misused. 
• Acute lesions may respond to short-term potent steroids, while chronic conditions often require mild maintenance treatment. 
• Steroids are typically applied twice daily, then reduced to once daily or less as symptoms improve. 

2-2. Topical calcineurin inhibitors (Pimecrolimus (Elidel®), tacrolimus (Protopic®))

• Non-steroidal topical anti-inflammatory agents with immunosuppressive effects used to treat atopic dermatitis. 
• The anti-inflammatory potency of 0.1% tacrolimus is comparable to that of medium-potency topical corticosteroids, whereas pimecrolimus 1% is less potent. 
• The most common side effect is a transient burning sensation at the application site. In pediatric studies, pimecrolimus 1% showed fewer local side effects than tacrolimus 0.03%.

2-3. Antihistamines

• Commonly used, though not always effective since histamine is not the sole mediator. 
• First-generation antihistamines like hydroxyzine and chlorpheniramine cause sedation, while second-generation agents (e.g., cetirizine, fexofenadine) have fewer central side effects and additional antiallergic actions. 
• Sedating antihistamines are often used at night to help reduce nocturnal itching. 

2-4. Antibiotics

• Mupirocin ointment: 7–10 days for localized impetigo
• Systemic antibiotics such as flucloxacillin, penicillin V, or first- and second-generation cephalosporins may be used for 7–10 days in more severe cases. 
• Alternatives like clindamycin or oral fusidic acid are used for penicillin-allergic patients, but prolonged use should be avoided to prevent resistant strains like MRSA.

Step 3: Considered when there is no improvement after steps 1 and 2, and involves systemic medication. 

3-1. Systemic Steroids

• Generally avoided in children due to risks such as growth retardation and high relapse rates after discontinuation. 
• Serious side effects: Osteoporosis, cataracts, and lymphopenia

3-2. Cyclosporine

• Suppresses immune responses by inhibiting the calcineurin-dependent T-cell pathway 
• Initiated at 5 mg/kg/day and tapered to 2.5–3 mg/kg/day over 4–6 weeks based on clinical response.
• Close monitoring is essential due to potential nephrotoxicity and hypertension.

3-3. Methotrexate, Azathioprine, Mycophenolate mofetil: When cyclosporine is ineffective or contraindicated

• Methotrexate: Weekly at 0.2–0.5 mg/kg, with peak efficacy seen at 8–12 weeks, but folic acid supplementation is recommended to reduce risks of rare adverse effects such as infection, gastrointestinal upset, bone marrow suppression, and hepatotoxicity; it is also contraindicated in pregnancy due to teratogenicity. 
• Azathioprine: 1–3 mg/kg/day may be considered, but it requires regular blood monitoring due to risks of severe bone marrow suppression, as well as potential carcinogenic and teratogenic effects. 
• Mycophenolate mofetil: Not approved for atopic dermatitis but may be considered when other systemic immunosuppressants are ineffective or contraindicated.

3-4. Intravenous Immunoglobulin (IVIG)

• By neutralizing allergen-specific antibodies or directly suppressing Th2 immune responses through modulation of T cells. 
• Inconsistent treatment outcomes and high relapse rates after therapy 

3-5. Biologics and JAK inhibitors

• Dupilumab: A drug that blocks both IL-4 and IL-13 signaling, has been proven effective and safe in patients with moderate-to-severe atopic dermatitis that is not well controlled with topical treatments. 
• Lebrikizumab and tralokinumab: Monoclonal antibodies targeting IL-13
• Nemolizumab: Inhibitor of IL-31 (a pruritogenic cytokine produced by activated T-helper type 2 cells)
• JAK1 inhibitors: Upadacitinib, abrocitinib, and baricitinib