Eczema (Atopic Dermatitis)

Eczema, in its most common form, is atopic dermatitis — a chronic, relapsing inflammatory skin disease that makes the skin dry, intensely itchy, and prone to red or discolored, scaly patches. It is not contagious, it tends to flare and settle over time, and for most people it can be well controlled with daily skin care and the right medications.

What is eczema (atopic dermatitis)?

"Eczema" is an umbrella term for several conditions that inflame the skin, but in everyday use it usually means atopic dermatitis (AD) — by far the most common type. Atopic dermatitis is a long-term (chronic) condition driven by a combination of a weakened skin barrier and an overactive immune response. When the barrier leaks moisture and lets in irritants, allergens, and microbes, the immune system reacts with inflammation. That inflammation produces the classic cycle: dryness, itch, scratching, and more barrier damage (the "itch–scratch cycle") (NIH/NIAMS; StatPearls).

Atopic dermatitis is part of a group of related allergic conditions called the atopic triad — eczema, asthma, and allergic rhinitis (hay fever). In children, AD often appears first and may be followed by food allergies, asthma, or hay fever later, a pattern clinicians call the "atopic march" (StatPearls).

The condition is genuinely common. AD affects roughly 1 in 5 children (about 13–20%) and around 7–10% of adults in the United States, making it one of the most frequent chronic skin diseases (AAD; NIH/NIAMS; National Health Interview Survey). It often begins in infancy or early childhood, though it can start at any age. In ICD-10 coding, atopic dermatitis falls under L20 (with L20.9 used for unspecified atopic dermatitis).

What causes eczema and who's at risk?

There is no single cause. Atopic dermatitis results from an interaction of genetics, immune dysregulation, a defective skin barrier, and environmental triggers (StatPearls; NIH).

Skin barrier defects. A major genetic contributor is a mutation in the *filaggrin* (FLG) gene, a protein essential for forming a healthy outer skin barrier. Filaggrin loss-of-function mutations are a well-established risk factor for AD and are associated with earlier, more persistent, and more severe disease (StatPearls). A weak barrier loses water (leading to dryness) and lets in allergens and bacteria.

Immune dysregulation. In AD, the immune system shifts toward a "type 2" inflammatory response involving signaling molecules such as interleukin-4 (IL-4) and interleukin-13 (IL-13). These cytokines drive inflammation and itch and are the direct targets of several modern medications.

Who's at risk. Key risk factors include:

• A personal or family history of eczema, asthma, or hay fever
• Onset in infancy or early childhood (the most common time AD begins)
• Living in urban areas or colder, drier climates
• Exposure to common triggers that provoke flares rather than cause the disease itself

Common flare triggers include dry skin and low humidity, soaps and harsh detergents, fragrances, wool or rough fabrics, heat and sweating, stress, certain skin infections, and, in some people, specific allergens. Triggers vary widely from person to person.

What are the symptoms?

The hallmark symptoms of atopic dermatitis are intense itch (pruritus) and dry, inflamed skin. Itch is often the most distressing feature and can disrupt sleep.

Typical signs include:

• Dry, sensitive, scaly skin
• Red patches on lighter skin; brown, purple, gray, or ashen patches on darker skin (inflammation can look different across skin tones, which sometimes leads to underdiagnosis in people with darker skin)
• Itching that worsens at night
• Oozing, crusting, or weeping during acute flares
• Thickened, leathery skin (lichenification) from chronic scratching
• Cracking, soreness, and sometimes skin-color changes after healing

Location matters and shifts with age:

• Infants: the cheeks, scalp, and outer surfaces of the arms and legs
• Children: the creases of the elbows and knees, wrists, ankles, and neck (flexural areas)
• Adults: the hands, eyelids, neck, and flexural creases; chronic hand eczema is common

The condition is relapsing: periods of flare (worsening) alternate with periods of remission (clearer skin).

How is eczema diagnosed?

There is no single blood test or biopsy that confirms atopic dermatitis. Diagnosis is clinical — a doctor or dermatologist makes it based on the appearance and distribution of the rash, the history of itch, and personal or family history of atopy (StatPearls; AAD).

Diagnostic criteria. Clinicians and researchers often use structured criteria to standardize diagnosis:

• The Hanifin and Rajka criteria (1980) require a combination of major features (such as itch, typical rash appearance and distribution for age, chronic relapsing course, and personal/family history of atopy) plus several minor features. They are detailed and widely used in clinical and research settings (PMID 31611041).
• The UK Working Party criteria are a simplified refinement designed for both clinics and population studies. They require an itchy skin condition plus several of: history of flexural involvement, history of asthma or hay fever, generally dry skin, visible flexural dermatitis, and onset under age 2 (DermNet; PMID 31611041).

Supporting tests are used to rule out other conditions or identify triggers, not to confirm AD itself:

• Patch testing when allergic contact dermatitis is suspected
• Allergy testing (skin prick or specific IgE blood tests) if food or environmental allergies are suspected, though a positive allergy test alone does not diagnose AD
• Skin swabs or cultures if a bacterial (often *Staphylococcus aureus*) or viral infection is suspected
• Skin biopsy occasionally, mainly to exclude conditions that mimic eczema, such as psoriasis or cutaneous T-cell lymphoma

Severity is graded by how much body surface is affected, intensity of signs, itch, and impact on sleep and quality of life. Validated tools such as EASI (Eczema Area and Severity Index) and SCORAD are used in specialist care and clinical trials.

How is eczema treated?

Treatment follows a stepwise approach, matched to severity. The foundation — good daily skin care — applies to everyone, and stronger therapies are added as needed (AAD guidelines).

Lifestyle and skin care first

• Moisturize generously and often. Daily emollients are the cornerstone of AD management. Thick, fragrance-free creams or ointments help repair the barrier and reduce flares. Apply within a few minutes of bathing ("soak and seal").
• Bathe gently. Lukewarm (not hot) baths or showers with a mild, fragrance-free cleanser; pat dry and moisturize immediately.
• Identify and avoid triggers such as harsh soaps, fragrances, wool, overheating, and known allergens.
• Manage the itch and scratching: keep nails short, use cool compresses, and address stress, which can worsen flares.
• Bleach baths (a dilute sodium hypochlorite bath) are sometimes recommended to reduce bacterial load and flares, particularly in people with frequent infections. The 2023 AAAAI/ACAAI Joint Task Force guidelines give a *conditional* recommendation (low-certainty evidence) for dilute bleach baths added to topical therapy in moderate-to-severe AD, while suggesting against them for mild disease. Use only under clinician guidance.

Over-the-counter (OTC) options

• Emollients and barrier creams (the most important OTC tool)
• Low-potency topical corticosteroids such as OTC hydrocortisone 1% for mild flares on appropriate areas, used short-term
• Antihistamines, which do not treat the eczema itself but a sedating antihistamine at night may help sleep when itch is severe

Prescription options

When daily care is not enough, prescription treatments are added in roughly this order:

• Topical corticosteroids (TCS). First-line anti-inflammatory therapy, available in a range of potencies. Lower-potency steroids are used on the face and skin folds; higher-potency for thicker skin and severe flares. Used appropriately, they are effective and safe; prolonged overuse on thin skin can cause thinning (AAD).
• Topical calcineurin inhibitors (TCIs) — tacrolimus ointment and pimecrolimus cream. Steroid-free options useful for sensitive areas (face, eyelids, skin folds) and for long-term maintenance. Topical tacrolimus is roughly comparable to a moderate-potency steroid; pimecrolimus to a mild one.
• Topical PDE-4 inhibitor — crisaborole ointment, a nonsteroidal option for mild-to-moderate AD.
• Topical JAK inhibitor — ruxolitinib cream, for short-term and non-continuous (intermittent) treatment of mild-to-moderate AD in non-immunocompromised patients 2 years and older not controlled by other topicals; it reduces itch and inflammation. Its label carries the JAK-class boxed warning (serious infections, mortality, malignancy, major cardiovascular events, and thrombosis), and use is limited to a small treated body-surface area.
• Phototherapy — narrowband UVB light therapy, an option for moderate-to-severe disease not controlled by topicals.
• Biologics (injectable). For moderate-to-severe AD, dupilumab (an IL-4 receptor alpha antagonist that blocks both IL-4 and IL-13 signaling) is a widely used option, FDA-approved down to 6 months of age. Tralokinumab (approved for ages 12+) and lebrikizumab (FDA-approved September 2024 for ages 12+) both target IL-13. Current AAD guidelines support biologics for moderate-to-severe disease (AAD 2024).
• Oral JAK inhibitors — upadacitinib and abrocitinib are FDA-approved oral options for moderate-to-severe AD (baricitinib is approved for AD in Europe and Japan but not by the FDA for this use). They work quickly on itch but carry a boxed warning regarding serious infections, blood clots, cardiovascular events, and malignancy, so they require careful candidate selection and monitoring (FDA; AAD).
• Traditional systemic immunosuppressants such as cyclosporine, methotrexate, or azathioprine may still be used in select cases, with monitoring.

Antibiotics are reserved for clearly infected eczema, not routine flares.

Can eczema be prevented or managed long-term?

Atopic dermatitis usually cannot be fully prevented, especially when there is a strong genetic or family history. But flares can often be reduced and long-term control is realistic for most people.

Day-to-day prevention of flares rests on consistent barrier care: moisturizing daily even when skin looks clear, avoiding known triggers, gentle bathing, and treating early signs of a flare promptly. Proactive (maintenance) therapy — applying a topical anti-inflammatory (such as a TCI or steroid) a couple of times a week to areas that frequently flare — is an evidence-based strategy to keep skin calm between episodes.

In infants at high risk (strong family history), there has been interest in early, regular emollient use to try to prevent AD, but study results have been mixed and routine emollient prophylaxis is not firmly established as preventive. Discuss individualized prevention with a pediatrician or dermatologist.

Managing the broader picture matters too: sleep, stress, and mental health are all affected by chronic itch, and addressing them is part of comprehensive care.

When should you see a doctor?

See a clinician if eczema is not improving with good skin care and OTC measures, if it is interfering with sleep, school, work, or daily life, or to get an accurate diagnosis and a treatment plan.

Seek prompt medical care for red flags of infection or complications:

• Signs of bacterial infection: increasing redness/warmth, pus, yellow crusting, swelling, pain, or fever
• Eczema herpeticum — a medical emergency: a sudden, painful outbreak of clustered blisters or punched-out sores, often with fever and feeling unwell. This is a herpes virus infection of eczematous skin that spreads rapidly and needs urgent antiviral treatment.
• Widespread, rapidly worsening rash or skin that is weeping and not responding to treatment
• A flare that is severe enough to prevent sleep or cause significant distress

Anyone with signs of a serious or spreading infection should be evaluated the same day or sent for emergency care.

What's the outlook (prognosis)?

For most people, the long-term outlook is good. Atopic dermatitis is a chronic, relapsing condition rather than a steadily progressive one, and it is highly manageable with modern treatment.

In children, AD frequently improves with age; many children see their eczema become milder or clear during childhood or adolescence, though "outgrowing" it completely is not guaranteed. Some people have a persistent or recurring course into adulthood, and a minority experience adult-onset disease. Even when AD persists, today's expanding range of treatments — from improved topicals to targeted biologics and JAK inhibitors — means severe, poorly controlled disease is far less common than in the past (AAD; NIH/NIAMS).

The main burdens are itch, sleep disruption, skin infections, and effects on quality of life and mental health. With consistent skin care, trigger management, and appropriate medication, most people achieve good control and lead full, active lives.

Frequently asked questions

Is eczema contagious? No. Atopic dermatitis cannot be caught from or passed to another person. It is driven by genetics, the immune system, and the skin barrier — not by an infectious organism. (A secondary skin *infection* on top of eczema can be contagious, but the eczema itself is not.)

Will my child grow out of eczema? Often, eczema improves significantly with age, and many children have much milder or clear skin by their teens. However, it can persist or return later in life, so it's best to focus on good control now rather than waiting for it to disappear.

What's the difference between eczema and psoriasis? Both cause red or discolored, scaly patches, but they differ. Eczema is usually intensely itchy, tends to appear in skin creases, and is linked to allergies and asthma. Psoriasis typically causes thicker, well-defined plaques with silvery scale on areas like the elbows, knees, and scalp, and is often less itchy. A dermatologist can distinguish them, occasionally with a biopsy.

Are topical steroids safe for eczema? Used correctly — the right potency for the right body area, for appropriate periods — topical corticosteroids are effective and safe and remain first-line anti-inflammatory therapy. The main risk, skin thinning, comes from prolonged overuse of stronger steroids on thin skin (like the face). Steroid-free options such as topical calcineurin inhibitors and crisaborole are available for sensitive areas and long-term use. Follow your clinician's instructions on amount and duration.

Does diet cause eczema? For most people, diet is not the cause, and broad food avoidance is not recommended and can be harmful, especially in children. Some individuals — more often young children with moderate-to-severe AD — do have food allergies that can trigger flares. Testing and any dietary changes should be guided by a clinician, because positive allergy tests do not by themselves prove a food is worsening the eczema.

---

*This page is for general education and is not medical advice. Atopic dermatitis varies from person to person; talk with a qualified healthcare professional about diagnosis and treatment that's right for you.*