What Is Eczema: Causes, Types, Triggers, and Skin Care Strategies

This article is for informational purposes only. Consult a qualified healthcare professional for medical advice, diagnosis, or treatment.

What Is Eczema?

Eczema is a group of inflammatory skin conditions characterized by itchy, dry, red, and inflamed skin. The most common and well-studied form is atopic dermatitis (AD), which is a chronic, relapsing-remitting inflammatory skin disease associated with a personal or family history of allergic conditions (the atopic triad: eczema, asthma, and allergic rhinitis). Eczema is one of the most prevalent chronic skin diseases globally, affecting approximately 10–20% of children and 2–10% of adults, translating to more than 200 million people worldwide. The global prevalence has increased dramatically over the past 30–40 years, particularly in urbanized, industrialized nations, mirroring the rise in other atopic diseases.

In addition to atopic dermatitis, the eczema spectrum includes contact dermatitis, dyshidrotic eczema (pompholyx), nummular eczema, seborrheic dermatitis, and stasis dermatitis — each with distinct mechanisms and distributions.

Types of Eczema

Type	Key Features	Common Locations
Atopic dermatitis	Chronic, itchy, inflammatory; associated with atopic triad; IgE-mediated and barrier dysfunction	Antecubital and popliteal fossae (inner elbows/knees), face, neck, hands in adults
Allergic contact dermatitis	Type IV delayed hypersensitivity to specific contact allergens; diagnosed by patch testing	Site of contact: hands (gloves, metals), earlobes (nickel), hairline (hair dye — PPD)
Irritant contact dermatitis	Non-immunological damage from direct chemical or physical irritation; most common occupational skin disease	Hands (most frequent); any exposed area
Dyshidrotic eczema (pompholyx)	Deep-seated, intensely pruritic vesicles; associated with sweat, heat, stress, and metal sensitivity	Palms, soles, lateral fingers
Nummular eczema	Coin-shaped, often crusted plaques; frequently triggered by dry skin and environmental allergens	Lower legs, back, buttocks
Seborrheic dermatitis	Scaly, greasy patches; driven by Malassezia yeast overgrowth; flares with stress and cold	Scalp (dandruff), nasolabial folds, eyebrows, ears
Stasis dermatitis	Chronic venous insufficiency leads to edema, skin discoloration, and eczematous changes	Lower legs, ankles

Pathophysiology of Atopic Dermatitis

Atopic dermatitis results from a complex interaction between genetic defects in the skin barrier, immune dysregulation, and environmental factors:

Skin Barrier Dysfunction

The stratum corneum (the outermost skin layer) acts as a physical barrier that retains moisture and excludes allergens, irritants, and pathogens. In AD, mutations in the gene encoding filaggrin (FLG) — a protein critical for cornification and skin hydration — are present in approximately 30% of European AD patients. Filaggrin deficiency disrupts the "brick and mortar" structure of the stratum corneum, allowing transepidermal water loss (TEWL) and penetration of allergens and microbes. This is not the only genetic cause — mutations in genes encoding other barrier proteins (loricrin, involucrin, SPINK5) also contribute.

Immune Dysregulation

Barrier disruption allows sensitization to environmental allergens. In the acute phase of AD, a Th2-dominant immune response predominates: IL-4 and IL-13 drive IgE production and suppress barrier gene expression (creating a vicious cycle); IL-31 directly stimulates itch receptors. Chronic AD develops a mixed Th2/Th1 and Th2/Th22 profile, with IL-22 promoting epidermal thickening (lichenification). The cytokine IL-4/IL-13 signaling axis has become the primary drug target in modern AD therapy.

Microbiome Dysbiosis

Staphylococcus aureus colonizes the skin of >90% of AD patients (vs. ~20% of healthy individuals). S. aureus releases exotoxins that act as superantigens, activating T cells and mast cells non-specifically; it also secretes enzymes that degrade barrier proteins and produces IL-1 converting enzyme, further driving inflammation. Reducing S. aureus burden through bleach baths and antimicrobials can improve AD control.

Common Triggers

Environmental allergens: House dust mites, pet dander, pollen, mold — key drivers of flares via IgE-mediated sensitization
Irritants: Soaps, detergents, synthetic fabrics, cigarette smoke, sweat — disrupt barrier without immune sensitization
Temperature and humidity extremes: Cold, dry air increases TEWL; heat and sweating increase itch
Food allergens: In young children, egg, milk, peanut, wheat, and soy can provoke flares; the food-AD relationship is often complex and not always causative
Psychological stress: Stress activates the HPA axis and elevates corticotropin-releasing hormone, which degranulates skin mast cells
Skin infections: S. aureus and, less commonly, herpes simplex virus (eczema herpeticum — a potentially serious complication) trigger flares

Diagnosis

Atopic dermatitis is diagnosed clinically using criteria such as the Hanifin and Rajka or UK Working Party criteria. Key features include: chronic or chronically relapsing itchy rash, typical morphology and distribution (flexural in older children and adults, facial in infants), personal or family history of atopy, and onset in childhood. Patch testing is used when allergic contact dermatitis is suspected. IgE levels and skin-prick tests may be performed to identify sensitizing allergens but do not confirm AD.

Treatment

Skin Care Fundamentals

Moisturization is the foundation of AD management. Applying emollients liberally (at least twice daily, ideally within 3 minutes of bathing — "soak and smear") restores the skin barrier, reduces TEWL, and reduces the frequency of flares. Fragrance-free, preservative-free emollients are preferred. A 2014 randomized controlled trial found that daily full-body emollient use from birth reduced AD incidence at 6 months by 50% in high-risk infants.

Pharmacological Treatments

Treatment	Mechanism	Use
Topical corticosteroids (TCS)	Suppress local inflammation; first-line anti-inflammatory treatment	Short-term flare control; potency matched to body site and severity
Topical calcineurin inhibitors (TCIs): tacrolimus, pimecrolimus	Block T-cell calcineurin-NFAT signaling; steroid-sparing	Face, eyelids, skin folds where TCS risks are higher
Topical PDE4 inhibitor: crisaborole	Reduces cAMP breakdown; anti-inflammatory; non-steroidal	Mild to moderate AD; well-tolerated for chronic use
Dupilumab (biologic)	Anti-IL-4Rα monoclonal antibody; blocks both IL-4 and IL-13 signaling	Moderate-to-severe AD in adults and children ≥6 months; dramatically reduces itch, severity scores, and flares
JAK inhibitors: abrocitinib, upadacitinib, ruxolitinib (topical)	Block JAK-STAT signaling downstream of multiple pro-inflammatory cytokines	Oral: moderate-to-severe AD when dupilumab inadequate; topical ruxolitinib for mild-moderate AD
Phototherapy (NB-UVB, UVA1)	Suppresses T-cell activation and reduces S. aureus colonization	Widespread moderate AD; second-line after topical agents