Eczema and Dermatitis
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Eczema and Dermatitis UK: A Complete Guide to the Condition
A clinically reviewed guide to eczema and dermatitis — what it is, the six types, what causes it, common triggers, the NHS treatment ladder, secondary infections, and when to seek help. NICE and BAD-aligned throughout.
Eczema is a chronic inflammatory skin condition affecting around 1 in 5 children and 1 in 12 adults in the UK. This page is the condition reference guide — covering all six types, the underlying biology, triggers, the NHS treatment ladder, complications, and when to seek help. Detailed prescription treatment guidance is in the linked sub-guides.
Eczema affects around 1 in 5 children and 1 in 12 adults in the UK, making it one of the most common chronic skin conditions seen in primary care. Despite its prevalence, it is frequently misunderstood — confused with other skin conditions, undertreated, or managed with products that worsen rather than help it. This guide covers the condition itself: what it is, why it happens, how it is diagnosed, and how it is managed in line with NICE guidance. For prescription treatments, see the linked guides below.
What Is Eczema?
Eczema is a chronic inflammatory skin condition characterised by dry, itchy, and inflamed skin. The word “eczema” comes from the Greek for “to boil over” — which captures the hot, weeping, inflamed quality of a severe flare. The most common form is atopic eczema (also called atopic dermatitis), but the term covers a family of related conditions that share the same core feature: an impaired skin barrier combined with immune-mediated inflammation.
Eczema is not contagious. It is not caused by poor hygiene. And it is not simply “dry skin” — it is a systemic inflammatory condition that happens to express itself in the skin, driven by genetics and immune dysregulation. Understanding this distinction matters, because it explains why basic moisturisers alone rarely control it, and why targeted anti-inflammatory treatment is usually needed during flares.
Types of Eczema and Dermatitis
Several distinct conditions fall under the eczema/dermatitis umbrella. Each has a different cause, distribution pattern, and treatment approach:
| Type | Key features | Common sites | Key trigger or cause |
|---|---|---|---|
| Atopic eczema | Chronic, relapsing; associated with asthma and hay fever; begins in childhood in most cases | Flexures (inside elbows, behind knees), face, hands, scalp | Genetic barrier defect; allergens; stress; sweat; infections |
| Contact dermatitis | Divided into irritant (from repeated exposure) and allergic (immune-mediated sensitisation) | Hands most common; wherever contact occurs | Soaps, detergents, metals (nickel), latex, fragrances |
| Discoid eczema | Well-defined, coin-shaped inflammatory plaques; tends to affect adults | Limbs โ particularly lower legs and forearms | Poorly understood; skin injury; dry skin; alcohol |
| Seborrhoeic dermatitis | Flaking, redness in sebaceous gland-rich areas; associated with Malassezia yeast | Scalp (dandruff), face (nasolabial folds, eyebrows), chest | Malassezia overgrowth; stress; immunosuppression |
| Dyshidrotic eczema | Small, intensely itchy blisters; often worsens in summer or with stress | Palms, soles, sides of fingers and toes | Sweating; stress; contact allergens; heat |
| Venous eczema | Associated with poor venous circulation; skin becomes brown, itchy, thickened | Lower legs, particularly around ankles | Chronic venous insufficiency; varicose veins |
This guide focuses primarily on atopic eczema, which accounts for the majority of eczema presentations in UK primary care. For contact dermatitis, patch testing by a dermatologist is often needed to identify the specific allergen.
What Causes Eczema?
Atopic eczema is caused by the interaction of two factors: a genetic skin barrier defect and immune system dysregulation. Neither alone produces eczema — it is the combination that creates the characteristic inflammatory cycle.
Impaired skin barrier
Filaggrin is a protein essential for forming the outer protective skin layer. Loss-of-function mutations in the FLG gene — present in around 30% of people with atopic eczema — produce a leaky, permeable barrier. Irritants, allergens, and microbes that healthy skin would block can penetrate, triggering an immune response.
Immune dysregulation
Eczema involves a Th2-skewed immune response — the same immune pathway that drives asthma and allergic rhinitis. Elevated IgE, IL-4, IL-13, and IL-31 drive inflammation and the intense itch of active eczema. IL-31 is directly responsible for the itch signal.
Microbiome disruption
Staphylococcus aureus colonises the skin of more than 90% of people with atopic eczema during flares (vs ~5% in unaffected skin). S. aureus releases toxins that further damage the barrier and amplify the inflammatory response — creating a cycle of inflammation and infection.
Genetics and family history
Atopic eczema has a strong genetic component. If one parent has atopic eczema, the child's risk is approximately 50%. If both parents are affected, the risk rises to around 80%. The condition clusters with asthma and allergic rhinitis in the same families — the “atopic march”.
Common Triggers
Triggers do not cause eczema — they provoke flares in people who already have the underlying genetic and immune predisposition. Identifying and reducing personal triggers is a core part of long-term eczema management:
- Soap and detergents — the most common irritant trigger. Even “gentle” soaps disrupt the skin barrier. Soap substitutes (emollient washes) should replace soap entirely.
- Sweat — particularly relevant in children; triggers itching and scratching which perpetuates the itch-scratch cycle.
- Synthetic fabrics — nylon, polyester, and wool are common irritants. Cotton and breathable fabrics are better tolerated.
- Stress — psychological stress activates the HPA axis and promotes Th2 immune skewing, directly worsening eczema inflammation.
- Heat and dry air — central heating removes moisture from air and skin; cold weather reduces sebum production. Both worsen barrier function.
- Aeroallergens — house dust mite, pet dander, and pollen. Particularly relevant in adults with sensitisation confirmed by testing.
- Food allergens — in young children, cow’s milk, egg, peanut, wheat, and soy can trigger or worsen eczema. In adults, food allergy as a direct eczema trigger is less common than widely believed.
- Skin infections — Staphylococcus aureus colonisation is both a consequence and a driver of flares. Signs of secondary infection (weeping, honey-coloured crusting, fever) warrant prompt prescriber assessment.
How Eczema Is Diagnosed
Eczema is a clinical diagnosis — there is no blood test or biopsy that confirms it. A prescriber will look for the characteristic pattern of features set out in UK Diagnosis Criteria (the Hanifin and Rajka criteria, as adapted by Williams et al. 1994, widely used in UK primary care):
- Itchy skin condition in the last 12 months (or parental report of scratching or rubbing in a child)
- Plus three or more of: onset before age 2 / history of flexural involvement / visible flexural eczema / history of dry skin / personal history of asthma or allergic rhinitis (or a first-degree relative in children under 4)
Patch testing may be recommended where contact dermatitis is suspected. Skin prick tests or specific IgE blood tests are used when food or aeroallergen sensitisation is suspected as a contributing factor.
The NHS Treatment Ladder for Atopic Eczema
NICE and BAD guidelines recommend a stepwise approach to atopic eczema management, starting with the least potent appropriate treatment and stepping up as needed. The foundation of management at every step is emollient therapy.
| Step | Treatment | When it’s used |
|---|---|---|
| All steps | Emollients (moisturisers) โ applied liberally and frequently to all affected skin | Always, including between flares. The foundation of every eczema management plan. |
| Step 1 | Mild potency topical corticosteroid โ e.g. hydrocortisone 0.5โ1% (Class 1) | Mild eczema; facial eczema; children’s eczema |
| Step 2 | Moderate potency topical corticosteroid โ e.g. clobetasone 0.05% (Eumovate, Class 2) | Moderate eczema not controlled at Step 1 |
| Step 3 | Potent topical corticosteroid โ e.g. betamethasone valerate 0.1% (Betnovate, Class 3) | Moderate-to-severe eczema on body areas |
| Step 4 | Very potent topical corticosteroid โ e.g. clobetasol propionate 0.05% (Dermovate, Class 4) | Severe, resistant, or lichenified eczema; short courses only; prescriber supervision |
| Step 5 | Specialist referral โ phototherapy, immunosuppressants (ciclosporin, methotrexate), dupilumab | Severe eczema not controlled with topical treatment; dermatology input required |
Emollients are the most important part of eczema management and are underused by most patients. Applied at least twice daily to all affected skin — even between flares — they reduce barrier disruption, decrease flare frequency, and reduce the amount of topical steroid needed. For prescription treatment guidance, see the linked sub-guides below.
Eczema in Darker Skin Tones
Eczema is frequently underdiagnosed and undertreated in people with darker skin (Fitzpatrick types IV–VI). The redness that is a cardinal sign of eczema in lighter skin may appear as purple, brown, or grey in darker skin, and can be missed on a brief clinical assessment. Additional features to look for include:
- Post-inflammatory hyperpigmentation (PIH) — dark patches that persist after inflammation resolves
- Follicular prominence — eczema may present as small papules around hair follicles rather than confluent patches
- Lichenification developing earlier — due to the itch-scratch cycle on more reactive skin
PIH is often more distressing to patients than the eczema itself. Treatment of the underlying inflammation is the most effective approach to PIH in this context.
The Itch-Scratch Cycle
The defining symptom of eczema is itch — and itch produces scratching, which worsens the very skin barrier damage that causes itch. This self-perpetuating cycle is central to understanding why eczema is so difficult to control without targeted treatment.
IL-31 is the primary cytokine responsible for the itch of atopic eczema. Scratching releases more inflammatory mediators, further amplifying IL-31 signalling. In chronic eczema, repeated scratching produces lichenification — a visible thickening and leathering of the skin that further impairs barrier function and increases the amount of topical treatment needed to achieve control.
Scratching at night is particularly problematic because cortisol levels are lower during sleep, allowing inflammation to increase. Sedating antihistamines are sometimes used short-term not because they reduce itch directly (antihistamines have limited effect on atopic eczema itch) but because they help reduce nocturnal scratching by inducing sleep.
Secondary Skin Infections
Eczematous skin is highly susceptible to secondary infection due to the damaged barrier and altered microbiome. The most important infections to recognise:
- Staphylococcus aureus — colonises >90% of eczematous skin during flares. Signs of active infection: weeping, honey-coloured crusting, increased warmth and redness, rapid worsening. Treat with topical or oral antibiotics as appropriate.
- Eczema herpeticum — a serious complication caused by the herpes simplex virus spreading across eczematous skin. Presents as a sudden, severe deterioration with punched-out erosions, fever, and malaise. Requires urgent medical assessment and oral or IV aciclovir.
- Molluscum contagiosum — the poxvirus that causes molluscum spreads more readily across eczematous skin. Often self-resolving but can be extensive in severe eczema.
Eczema herpeticum is a medical emergency. If a person with eczema develops a sudden widespread outbreak of small, punched-out blisters or erosions alongside fever and feeling very unwell, seek urgent medical assessment same day. Call 111 or attend A&E. In an emergency, call 999.
When to See a Doctor
- Eczema significantly affecting quality of life, sleep, or daily activities
- OTC treatments not providing adequate control after 4–8 weeks
- Signs of secondary infection (weeping, crusting, fever, rapidly worsening flare)
- Any suspicion of eczema herpeticum (see above)
- Eczema spreading to new areas or changing in character
- A child with eczema not controlled by mild steroids and emollients
- Adult eczema developing for the first time after age 40 — warrants investigation to exclude other diagnoses
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View Eczema Treatments →Eczema & Dermatitis Treatment Guides
Clinically reviewed guides covering all aspects of eczema and dermatitis — from understanding the condition to prescription treatment options. Authored by Dr Abdishakur M Ali, GMC no. 7041056.
Frequently Asked Questions
What is eczema?
Eczema is a chronic inflammatory skin condition that causes patches of skin to become dry, itchy, red, and cracked. The most common form is atopic eczema (atopic dermatitis), which affects around 1 in 5 children and 1 in 12 adults in the UK. Several other types of eczema exist, each with different causes and distribution patterns.
What causes eczema?
Eczema is caused by a combination of genetic and environmental factors. People with eczema have an impaired skin barrier โ the proteins that hold skin cells together and retain moisture do not function normally, allowing irritants and allergens to penetrate and trigger inflammation. Filaggrin gene mutations are the strongest known genetic risk factor. Eczema commonly co-occurs with other atopic conditions โ asthma and hay fever โ suggesting a shared immune pathway.
Is eczema contagious?
No. Eczema is not contagious and cannot be passed from person to person. It is an immune-mediated inflammatory condition with a genetic basis.
What is the difference between eczema and dermatitis?
The terms are often used interchangeably. 'Dermatitis' simply means inflammation of the skin. 'Eczema' is a specific type of dermatitis characterised by dry, itchy, inflamed skin. Atopic eczema, contact dermatitis, and seborrhoeic dermatitis are all forms of dermatitis. In everyday clinical use, 'eczema' usually refers to atopic eczema specifically.
What are the main types of eczema?
The main types are: atopic eczema (most common, linked to family history of allergies), contact dermatitis (caused by contact with irritants or allergens), discoid eczema (coin-shaped patches, typically on limbs), seborrhoeic dermatitis (affects oily skin areas โ scalp, face, chest), dyshidrotic eczema (small blisters on hands and feet), and venous/varicose eczema (associated with poor circulation in the lower legs).
Can eczema be cured?
There is no cure for atopic eczema. The condition is chronic and tends to fluctuate โ flares followed by periods of remission. In children, eczema often improves significantly with age and many children grow out of it entirely. In adults, management focuses on reducing flare frequency and severity through emollients, trigger avoidance, and targeted treatment during flares.
When should I see a doctor about eczema?
See a prescriber if your eczema is significantly affecting your quality of life or sleep, if over-the-counter treatments are not controlling it, if the skin becomes infected (signs include weeping, crusting, increased redness, warmth, or fever), or if you need a prescription-strength treatment such as a potent topical corticosteroid.
References
- NICE. Eczema โ atopic: CKS. Updated 2024. cks.nice.org.uk
- NICE. Atopic eczema in under 12s: diagnosis and management (CG57). 2007, updated 2023. nice.org.uk/guidance/cg57
- British Association of Dermatologists. Guidelines for the management of atopic eczema. 2023.
- Nutten S. Atopic dermatitis: global epidemiology and risk factors. Ann Nutr Metab. 2015;66(Suppl 1):8–16.
- Palmer CN et al. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat Genet. 2006;38(4):441–446.
- NHS. Eczema (atopic). nhs.uk/conditions/atopic-eczema
Medical disclaimer: This article is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional for diagnosis and treatment. The treatments discussed are prescription-only medicines โ a clinical consultation is required before they can be dispensed. In a medical emergency, call 999.


