What Is Eczema (Atopic Dermatitis)?
Atopic dermatitis (AD), popularly known as eczema, is a chronic inflammatory skin disease characterized by intense pruritus, dry skin, and recurrent eczematous lesions. It is the most common chronic skin disease, affecting up to 20% of children and 2-10% of adults in industrialized countries.
AD results from a complex interaction between skin barrier dysfunction, immune dysregulation (Th2 predominance), and environmental factors. It is part of the "atopic march" — the progression from atopic dermatitis to allergic rhinitis and asthma that occurs in many patients.
The disease has an enormous impact on quality of life. Intense pruritus disrupts sleep, daily activities, and psychological well-being. Children with AD lose an average of 1-2 hours of sleep per night during flares, affecting school performance and development.
Defective Skin Barrier
Filaggrin gene mutations and ceramide deficiency compromise the skin barrier, letting allergens in and water out.
Type 2 Inflammation
Exaggerated Th2 immune response with excessive IL4, IL13, IL31, and IgE production.
Chronic Relapsing Disease
Flare-and-remission course. Continuous proactive treatment outperforms reactive treatment given only during flares.
Pathophysiology
The pathophysiology of AD involves two pillars: epidermal barrier defect and type 2 immune dysregulation. Mutations in the FLG (filaggrin) gene are the main genetic risk factor, present in 20-50% of patients. Filaggrin is essential for the formation of the stratum corneum and water retention in the skin.
The compromised barrier lets environmental allergens, irritants, and microorganisms in (especially Staphylococcus aureus, which colonizes 90% of atopic skin). This activates dendritic cells and Th2 lymphocytes, which produce IL-4, IL-13, IL-31, and IL-5. IL-4 and IL-13 further suppress filaggrin and barrier protein production, perpetuating the cycle.
IL-31, produced by Th2 lymphocytes, is the main mediator of pruritus in AD. It acts directly on sensory neurons via the IL-31RA receptor. IL-13 causes epidermal thickening and dermal fibrosis. Understanding these pathways led to the development of highly effective biologic therapies, such as dupilumab and tralokinumab.
Symptoms
Pruritus is the cardinal symptom and an essential criterion for diagnosis. Skin lesions vary by age: in infants, they predominate on the face and extensor surfaces; in older children and adults, on the flexures (folds of the arms and knees). Dry skin (xerosis) is nearly universal.
Manifestations of Atopic Dermatitis
- 01
Intense pruritus
Often unbearable itching, worse at night. The most debilitating symptom and a mandatory diagnostic criterion.
- 02
Dry skin (xerosis)
Rough, dry, scaly skin, even in áreas without active inflammation. A direct result of the skin barrier defect.
- 03
Acute eczematous lesions
Erythema, papules, vesicles, exudation, and crusts during acute phases. Often with secondary S. aureus infection.
- 04
Chronic lichenification
Skin thickening with accentuated skin lines in chronically scratched áreas. Characteristic of long-standing disease.
- 05
Typical age-based distribution
Infants: face and extensors. Children: flexures (antecubital, popliteal). Adults: hands, face, neck, and flexures.
- 06
Sleep disturbance
Children lose 1-2 h of sleep/night during flares. Adults report chronic insomnia. Family quality of life is significantly affected.
SEVERITY CLASSIFICATION (SCORAD / EASI)
| SEVERITY | SCORAD | CHARACTERISTICS |
|---|---|---|
| Mild | <25 | Limited áreas, mild pruritus, minimal sleep impact |
| Moderate | 25-50 | Extensive or flexural áreas, moderate pruritus, sleep disturbance |
| Severe | >50 | Disseminated or erythroderma, unbearable pruritus, severe impact on quality of life |
Diagnosis
The diagnosis is clinical, based on the Hanifin-Rajka criteria or the simplified UK Working Party criteria. There is no confirmatory laboratory test. Serum IgE is elevated in 80% of cases but is neither specific nor necessary for diagnosis.
🏥Diagnostic Criteria (UK Working Party)
Fonte: Williams et al. — simplified criteria
Mandatory Criterion
Mandatory + 3 or more of the following- 1.Skin pruritus (or reported scratching) in the past 12 months
Minor Criteria (minimum 3)
- 1.History of flexural involvement (antecubital, popliteal, cervical)
- 2.Personal history of asthma or allergic rhinitis (or in a 1st-degree relative if <4 years)
- 3.Generalized dry skin in the past year
- 4.Visible flexural dermatitis (or on face/extensors if <4 years)
- 5.Onset before 2 years of age (not applicable if <4 years)
Differential Diagnosis
Atopic dermatitis is often confused with other pruritic dermatoses. Flexural distribution, atopy history, and chronicity are the main differentiating features.
DIFFERENTIAL DIAGNOSIS
Differential Diagnosis
Psoriasis
Read more →- Well-demarcated plaques
- Silvery scale
- Nail involvement
Diagnostic Tests
- Biopsy if needed
Allergic Contact Dermatitis
- Distribution matches contact
- Positive patch test
Diagnostic Tests
- Patch test
Scabies
- Intense nighttime pruritus
- Affected family members
- Burrows between fingers
Diagnostic Tests
- Dermoscopy
- Skin scraping
Tinea Corporis
- Active borders
- Clear center
- Positive KOH
Diagnostic Tests
- KOH
Seborrheic Dermatitis
- Scalp and central face
- Yellowish greasy scale
- No vesicles
Contact Dermatitis: When Distribution Is the Key
Allergic contact dermatitis (ACD) can be clinically indistinguishable from atopic dermatitis in acute phases — both present with erythema, vesicles, and pruritus. The key differentiating feature is lesion distribution: in ACD, lesions are localized to áreas of allergen contact (e.g., neck from nickel costume jewelry, wrists from a bracelet, face from cosmetics). Exposure history is indispensable.
Patch testing is the gold standard for ACD diagnosis and should be performed in patients with atypical eczema patterns, contact-suggestive distribution, or treatment-refractory disease. The acupuncturist physician systematically investigates potential contact allergens, including cosmetics, metals, and frequently used materials.
Scabies: The Great Mimicker of Eczema
Scabies is a diagnosis that must never be missed. Sarcoptes scabiei causes intense pruritus that predominates at night, with characteristic lesions in the interdigital spaces, wrists, umbilical region, glans, and breasts. Involvement of other household members is highly suggestive. In immunosuppressed patients, it can present as crusted (Norwegian) scabies with generalized hyperkeratosis and high parasitic load.
Dermoscopy (delta-wing sign — the mite at the end of the burrow) has 80-90% sensitivity for diagnosis. Treatment with topical 5% permethrin or oral ivermectin should include all household contacts. Refractory eczema across an entire family should always raise suspicion of undiagnosed scabies.
Psoriasis vs. Eczema: Practical Clinical Distinction
Psoriasis and atopic dermatitis are the two most prevalent chronic inflammatory skin diseases and may coexist in the same patient. In psoriasis, lesions are erythematous plaques with silvery, well-demarcated scale on extensor surfaces (elbows, knees) and scalp. The Köbner phenomenon (lesions appearing in áreas of trauma) and nail involvement with onycholysis and pitting are characteristic.
When the diagnosis is in doubt, biopsy distinguishes the two conditions histologically — acanthosis with parakeratosis and neutrophils in psoriasis vs. spongiosis with eosinophilic infiltrate in atopic dermatitis. Treatment diverges importantly: anti-IL-17 and anti-IL-23 biologics are highly effective for psoriasis, whereas anti-IL-4/IL-13 biologics are indicated for atopic dermatitis.
Treatment
Treatment of AD is stepped according to severity. The foundation of all treatment is restoration of the skin barrier with emollients. The advent of biologic therapies (dupilumab) and JAK inhibitors (baricitinib, upadacitinib, abrocitinib) has revolutionized the management of moderate to severe forms.
Foundation: Barrier Care
Continuous — all severitiesEmollients/moisturizers 2-3x daily (ideally with ceramides). Short warm baths (5-10 min). Syndet cleansers (pH 5.5). Avoid irritants (wool, fragrances). Maintain adequate ambient humidity.
Mild to Moderate: Topical Therapy
Proactive + reactiveTopical corticosteroids (potency matched to location and age). Calcineurin inhibitors (tacrolimus, pimecrolimus) for face and sensitive áreas. Crisaborole (topical PDE4 inhibitor). Proactive treatment: 2x/week application to recurrence-prone áreas.
Moderate to Severe: Phototherapy
Narrowband UVB, 2-3x/weekNarrowband UVB phototherapy: effective and safe as a systemic alternative. Immunomodulates, reduces S. aureus colonization, and relieves pruritus.
Severe: Systemic Therapy
Biologics and JAK inhibitorsDupilumab (anti-IL-4Rα): first-line systemic, excellent safety. Tralokinumab (anti-IL-13). JAK inhibitors: baricitinib, upadacitinib, abrocitinib — rapid action, oral. Cyclosporine: rescue option.
Acupuncture as Treatment
Acupuncture has been studied in atopic dermatitis with a focus on its antipruritic, anti-inflammatory, and possible modulation of the Th2 immune response effects. Experimental studies — primarily in animal models and small clinical series — suggest an effect on type 2 inflammation markers (such as IgE, IL-4, and IL-13), observations that have not yet translated into a definitive conclusion about the immunomodulatory mechanism in clinical practice.
The antipruritic effect is particularly relevant. Neuroimaging studies show that acupuncture reduces pruritus-induced brain activation and modulates activity in the anterior cingulate córtex and insula. Endogenous opioid release contributes to the anti-itch effect.
In practice, acupuncture can be combined with conventional dermatologic treatment to help control pruritus and reduce flare frequency. It is particularly considered in patients seeking to reduce corticosteroid use or in cases with a significant stress component.
Prognosis
Childhood AD achieves complete remission in 60-70% of cases by adolescence. The remaining 30-40% carry the disease into adulthood, often as hand eczema or flexural dermatitis. Childhood severity is the main predictor of persistence.
With modern treatments — especially biologics and JAK inhibitors — patients with moderate to severe AD who previously had very compromised quality of life can now achieve clear or almost clear skin. The dupilumab response rate (EASI-75) is 50-70% at 16 weeks.
Myths and Facts
Myth vs. Fact
Eczema is caused by poor hygiene.
AD is a genetic and immunologic disease unrelated to hygiene. Paradoxically, excessive washing can worsen it by stripping protective lipids from the skin barrier.
Myth vs. Fact
Topical corticosteroids are dangerous and should be avoided.
Topical corticosteroids are safe and effective when used correctly (appropriate potency, limited duration, indicated áreas). Corticosteroid phobia is one of the main causes of AD undertreatment.
Myth vs. Fact
Eliminating milk and gluten improves eczema.
Elimination diets are only indicated when food allergy is documented by testing and oral challenge. Indiscriminate dietary restrictions do not improve AD and can cause nutritional deficiencies, especially in children.
When to Seek Help
Frequently Asked Questions
Frequently Asked Questions
Atopic dermatitis has no definitive cure, but 60 to 70% of children achieve complete remission by adolescence. In cases that persist into adulthood, modern treatments — especially biologics such as dupilumab — provide excellent disease control with clear or almost clear skin in most patients.
The most common triggers include dry skin, excessive sweating, temperature changes, wool and synthetic fabrics, harsh soaps and detergents, fragranced cosmetics, inhalant allergens (mites, animal dander), emotional stress, and, in some cases, specific foods in young children with documented allergy.
Topical corticosteroids are safe when used correctly: potency matched to the location (lower potency for face, folds, genitals), limited duration during flares, and transition to calcineurin inhibitors for maintenance. Skin atrophy occurs with prolonged high-potency use on thin-skinned áreas. Proactive treatment (2x/week application to recurrence-prone áreas) is effective and safe long-term.
Dairy restriction is only indicated when food allergy is documented by testing and physician-supervised oral challenge. Indiscriminate elimination does not improve eczema and can cause severe nutritional deficiencies in children. Food-allergy investigation should be done in children under 5 years with moderate to severe AD refractory to optimized topical treatment.
Clinical evidence suggests that acupuncture can reduce SCORAD (severity index), lower pruritus intensity, and improve quality of life as complementary therapy. The antipruritic effect is the best-documented, with neuroimaging studies showing reduced pruritus-induced brain activation. The acupuncturist physician can integrate this approach into conventional treatment.
For moderate to severe eczema in adults, options include dupilumab (anti-IL-4Rα, subcutaneous biologic — first-line systemic), tralokinumab (anti-IL-13), and oral JAK inhibitors (baricitinib, upadacitinib, abrocitinib) for rapid response. Cyclosporine is an option for urgent cases. The dermatologist defines the best strategy based on patient profile.
Proactive treatment applies topical corticosteroid or tacrolimus twice weekly to recurrence-prone áreas, even when the skin appears normal. It cuts flare frequency and severity by up to 50%. International guidelines recommend the approach, and it outperforms treating only during flares. The physician should guide it and indicate the specific áreas.
Short warm baths (5 to 10 minutes) — with syndet (pH 5.5 cleanser) or no soap on unsoiled áreas, followed immediately by moisturizer — are beneficial and part of basic treatment. Long hot baths strip protective lipids from the skin barrier and worsen xerosis. Apply moisturizer within 3 minutes of the bath, while the skin is still damp.
Hand eczema in adults can be a manifestation of atopic dermatitis, but it can also be contact dermatitis (occupational or domestic), dyshidrotic dermatitis, or nummular eczema. Differentiation requires a detailed history (occupation, exposures, progression pattern) and, when needed, patch testing. Correct treatment depends on etiologic diagnosis.
Signs of secondary bacterial infection include honey-colored crusts (S. aureus), sudden increase in inflammation and pruritus, pus, erythema with well-defined borders (impetigo or erysipelas), fever, and malaise. Eczema herpeticum (HSV infection) is an emergency: grouped vesicles with hemorrhagic crusts over eczematous áreas, often with fever, requiring urgent antiviral treatment.
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