Atopic Eczema: A Relapsing Inflammatory Skin Disorder
Reviewed by Dr C. J. Odike, MRCGP
Atopic eczema is a chronic, itchy inflammatory skin disorder that improves and flares over time. It develops through an interaction between skin barrier weakness, immune dysregulation, inherited susceptibility and environmental exposures. Regular emollients protect the barrier, while anti inflammatory treatment controls active eczema and prevents complications.
What atopic eczema is Atopic eczema, also called atopic dermatitis, is a chronic inflammatory condition causing dry, itchy and easily irritated skin. Chronic means that the underlying tendency persists, although the visible rash can clear completely between flares. Relapsing means that symptoms return periodically after improving. Flares can last days, weeks or longer without appropriate treatment. Eczema is not contagious, and you cannot catch it through touch, shared towels, swimming pools or ordinary contact. Eczema is not caused by poor hygiene Atopic eczema does not occur because someone is dirty or has failed to wash properly. Excessive washing, harsh soap and vigorous scrubbing can actually remove protective skin lipids and worsen the condition. Visible scaling, crusting or pigment change can attract unfair comments, particularly when eczema affects exposed areas. Clear explanation helps reduce stigma and prevents families from using damaging cleaning routines in an attempt to cure inflammation. The skin is an active protective organ Your skin limits water loss, protects against physical and chemical injury and helps prevent microorganisms entering the body. It also contains immune cells, sensory nerves, pigment producing cells, sweat glands, hair follicles and blood vessels. Healthy skin adapts continually to heat, moisture, friction, infection and environmental exposures. Atopic eczema develops when barrier protection and immune regulation become persistently disturbed and reinforce each other. The epidermis and stratum corneum The epidermis is the outer cellular layer of skin. Its outermost section is called the stratum corneum. The stratum corneum contains flattened cells called corneocytes surrounded by organised lipids, including ceramides, cholesterol and fatty acids. It is sometimes compared with bricks held together by mortar, although the living structure is more complex. When this layer is intact, it retains water and limits entry of irritants, allergens and infectious organisms. Water loss through the barrier A small amount of water normally moves from deeper tissues through the skin and evaporates. This process is called transepidermal water loss. It increases when the stratum corneum becomes damaged or poorly organised. Greater water loss produces dryness, microscopic cracking and increased sensitivity to ordinary products and environmental conditions. Dryness is therefore part of the disease mechanism rather than merely a cosmetic feature. Filaggrin Filaggrin is an important protein produced within developing epidermal cells. It helps organise keratin fibres and later contributes breakdown products forming part of the skin's natural moisturising system. These products support water retention, skin acidity and several antimicrobial and barrier functions. Reduced filaggrin can therefore leave skin drier, more permeable and more vulnerable to irritants and allergens. Filaggrin gene changes Loss of function changes in the FLG gene are among the strongest recognised genetic risk factors for atopic eczema. They are associated particularly with early, persistent or more severe eczema and with some eczema associated allergic disease. However, many people with atopic eczema have no identified FLG mutation, and many carriers never develop severe eczema. Filaggrin genetics increases susceptibility but does not provide a complete explanation or a routine diagnostic test for most people. Barrier dysfunction is broader than filaggrin Atopic skin can also have altered lipids, junction proteins, antimicrobial peptides, pH and interactions between skin cells and nerves. Inflammatory cytokines can reduce production of filaggrin and other barrier proteins even without a genetic mutation. Scratching physically breaks the stratum corneum and allows further water loss and microbial entry. The barrier abnormality is therefore both an early vulnerability and a consequence of continuing inflammation. Immune dysregulation Atopic eczema involves inappropriate activation of several immune pathways rather than one simple allergy reaction. Type 2 inflammatory signals, including interleukin 4 and interleukin 13, are prominent in many stages of disease. Other immune pathways can become more important according to age, ancestry, body site, infection and disease duration. This complexity explains why one trigger or treatment does not behave identically in every person. Barrier and immunity reinforce each other A weakened barrier allows irritants, allergens and microorganisms to interact more easily with immune cells. Inflammation then weakens barrier protein production, increases itch and changes the local microbial environment. Scratching adds physical injury, while infection can intensify inflammation further. Treatment works best when it addresses both barrier support and active immune inflammation rather than focusing on dryness alone. What atopy means Atopy describes a tendency to develop conditions such as atopic eczema, allergic rhinitis, asthma and some food allergies. These conditions often occur within the same person or family because they share genetic and immune risk factors. Having atopic eczema does not mean that every rash is allergic or that all environmental allergens must be eliminated. It also does not mean that asthma or food allergy will inevitably develop. The atopic march concept The atopic march describes a recognised pattern in which eczema may appear before food allergy, asthma or allergic rhinitis. The pattern is strongest in some children with early and severe eczema, particularly when barrier dysfunction is pronounced. Modern evidence shows that progression is not always orderly, one directional or inevitable. Conditions can appear in different sequences or not appear at all. The concept describes association and shared biology rather than a guaranteed journey from skin disease to respiratory allergy. Food allergy and eczema are different conditions Food allergy causes reproducible immune reactions after exposure to a particular food. Atopic eczema can fluctuate for many reasons and is not usually controlled by broadly excluding common foods. Children with moderate or severe early eczema have a higher probability of food allergy, but positive allergy tests can occur without clinical reactions. Testing and dietary changes should follow an allergy focused history rather than large screening panels or internet intolerance tests. Age affects the appearance Atopic eczema changes its preferred distribution as the body grows and patterns of movement, friction and exposure change. No age distribution is absolute, and the condition can affect almost any area. Recognising common patterns supports diagnosis but should not exclude eczema when the distribution is less typical. The person's skin tone also influences how inflammation, scaling and post inflammatory colour change appear. Atopic eczema in infants Infant eczema often begins on the cheeks, forehead or scalp and may spread to the trunk and limbs. The outer or extensor surfaces of the arms and legs are commonly involved during early life. The nappy area may be relatively spared because moisture and occlusion reduce dryness, although other rashes commonly affect this site. Infants cannot describe itch, so rubbing against bedding, irritability and disturbed sleep can provide important clues. Atopic eczema in children As children grow, eczema often becomes prominent within skin folds. Common sites include the fronts of the elbows, backs of the knees, wrists, ankles and neck. Hands, eyelids, skin around the mouth and areas behind the ears may also be affected. Repeated scratching can create thickened skin with exaggerated lines, called lichenification. Atopic eczema in adolescents and adults Adults commonly develop flexural eczema, hand eczema, eyelid disease or inflammation around the face and neck. Some have widespread dry, thickened and excoriated skin, while others experience localised recurrent patches. Occupational wet work, gloves, detergents and repeated hand washing can add irritant or allergic contact dermatitis. Adult onset or treatment resistant disease may therefore require reassessment rather than automatic continuation of the same diagnosis. Eczema in different skin tones Inflammation may appear pink or red on lighter skin but violet, grey, dark brown or subtly discoloured on darker skin. Redness can be difficult to appreciate, so warmth, swelling, texture, itch and the person's report become especially important. Atopic eczema in darker skin may show follicular bumps, papules or a more extensor distribution. Darkening or lightening can persist after inflammation settles and does not necessarily indicate continuing active eczema. Acute eczema An acute flare can become intensely itchy, swollen, warm and inflamed. Small fluid filled blisters, weeping, superficial erosions and crusting may occur. Scratching can produce linear marks and pinpoint bleeding. These features can arise from inflammation alone, infection or both, so the complete clinical pattern matters. Chronic eczema Longstanding rubbing and scratching thickens the epidermis and makes normal skin markings more prominent. The surface can become dry, scaly, cracked and darker or lighter than surrounding skin. Painful fissures are particularly common on hands and feet. Chronic thickening is evidence of repeated inflammation and itch rather than permanent evidence that treatment cannot work. Itch is the central symptom Itch, also called pruritus, is usually the most disruptive symptom of atopic eczema. Inflammatory signals activate specialised sensory nerves within the skin. Heat, sweat, dry air, wool, stress and attention to the sensation can increase perceived itch. Itch can continue after the visible inflammation appears improved because barrier and nerve recovery take time. The itch scratch cycle Scratching gives brief relief because pain and touch signals temporarily compete with itch signals. The mechanical action then damages the barrier, releases inflammatory mediators and creates further itching. Night time scratching may occur without full awareness and can be difficult to control through willpower. Effective treatment reduces the biological drive to scratch rather than blaming the person for lacking self control. Sleep disruption Itch often becomes more noticeable at night because there are fewer distractions and body temperature changes under bedding. Repeated waking affects concentration, mood, learning, work performance and family functioning. Parents may lose substantial sleep while applying treatments or preventing an infant from scratching. Sleep impact should be included when assessing severity, even when the visible area of eczema appears limited. Psychological and social effects Visible eczema can cause embarrassment, unwanted questions, bullying, social withdrawal and anxiety about appearance. Pain, itch and treatment burden can contribute to low mood and reduced quality of life. People may avoid swimming, exercise, intimacy or particular clothing because of discomfort or stigma. Psychological support is part of eczema care rather than evidence that the skin symptoms are imagined. Flares and remissions A flare is a period when itch, inflammation or skin damage becomes more active than the person's usual state. A remission is a period of minimal or absent active inflammation. Flares may follow an identifiable exposure, but they often occur without one clear cause. Searching endlessly for a single trigger can create anxiety and distract from consistent barrier and anti inflammatory treatment. Irritant triggers Irritants directly damage or disturb the skin barrier without requiring a specific allergy. Common examples include soap, detergent, fragranced products, solvents, chlorine, saliva, urine and repeated wet work. Even water can worsen hand eczema when exposure is frequent and followed by evaporation. Reducing unnecessary exposure and replacing soap with a suitable emollient wash can lower cumulative barrier damage. Heat and sweating Heat increases skin blood flow and can intensify itch. Sweat contains salt and can sting inflamed or cracked skin. Overheated rooms, heavy bedding, tight clothing and vigorous exercise can therefore provoke symptoms. Exercise remains beneficial, and practical adjustments include breathable clothing, cooler environments, showering gently and reapplying emollient afterwards. Clothing and friction Rough fibres, seams, labels and close fitting clothing can increase friction and itch. Many people tolerate soft cotton or smooth breathable fabrics better than coarse wool. There is no universal fabric suitable for everyone, and synthetic sports clothing may work well for some people. The aim is comfortable temperature and minimal friction rather than a rigid clothing rule. Stress Psychological stress can intensify itch perception and alter immune and barrier responses. An eczema flare can then create additional stress through sleep loss, appearance concerns and treatment burden. This relationship is biological and behavioural rather than proof that eczema is caused by worry. Stress management can support treatment but should not replace appropriate skin therapy. Environmental allergens House dust mites, animal dander, pollen and mould can worsen eczema in some sensitised people. However, allergen avoidance measures are burdensome and often produce limited benefit unless there is a convincing clinical relationship. Removing pets, replacing furniture or undertaking extensive household changes should not be routine first line treatment. Targeted allergy assessment is more useful when exposure causes reproducible skin or respiratory symptoms. Contact allergy Allergic contact dermatitis is a delayed immune reaction to a substance touching the skin. Possible triggers include fragrances, preservatives, hair dye, nickel, rubber chemicals and ingredients within topical treatments. It should be considered when eczema changes distribution, affects exposed sites or becomes resistant to appropriate therapy. Patch testing through dermatology can identify relevant contact allergens and distinguish allergy from ordinary irritation. Infection as a trigger and complication Barrier damage and scratching allow microorganisms to attach and enter more easily. Inflammation also changes antimicrobial defence and the balance of organisms living on the skin. Infection can trigger a flare, while a severe flare can resemble infection through weeping and crusting. The distinction affects antibiotic use and requires assessment of local changes, speed of deterioration and systemic illness. Staphylococcus aureus Staphylococcus aureus frequently colonises atopic skin, particularly during active disease. Colonisation means that bacteria are present without necessarily causing invasive infection. A positive swab can therefore occur during an inflammatory flare that does not need antibiotics. Treating inflammation and restoring the barrier can reduce bacterial burden even when no antimicrobial treatment is prescribed. Signs of bacterial superinfection Possible signs include rapidly increasing pain, pustules, spreading redness, warmth, swelling, purulent discharge and golden crusting. Fever, malaise and rapid deterioration make clinically important infection more likely. Redness can be subtle in darker skin, so tenderness, warmth, swelling and systemic symptoms need equal attention. Cellulitis, extensive infection or systemic illness requires prompt medical assessment and usually oral or intravenous antibiotics. Antibiotics are not required for every flare Weeping and crusting can occur in non infected eczema, and antibiotics add little benefit in many people who remain systemically well. Repeated topical antibiotics can cause resistance and allergic contact dermatitis. If antibiotics are prescribed, emollients and appropriate topical corticosteroids should usually continue because the underlying eczema still needs treatment. Swabs are more useful for recurrent, severe or non responsive infection than for every initial presentation. Eczema herpeticum Eczema herpeticum is widespread herpes simplex infection developing within eczema damaged skin. It can spread rapidly and cause serious systemic illness, eye complications and rarely organ involvement. Typical features include a sudden painful deterioration, clusters of similar blisters and punched out erosions with crusting. Fever, lethargy and distress may occur, but early disease can begin before marked systemic symptoms appear. Recognising eczema herpeticum Ordinary eczema is usually dominated by itch, while eczema herpeticum often becomes unusually painful or tender. Lesions tend to look similar to one another rather than showing the mixed scratches and patches of a routine flare. Cold sores in the person or a close contact may provide a clue, but an exposure is not always remembered. Suspected eczema herpeticum requires immediate systemic antiviral treatment and same day specialist assessment. Eczema herpeticum around the eyes Herpes infection near the eyelids or eyes can threaten the cornea and vision. Eye pain, light sensitivity, blurred vision, eyelid swelling or lesions around the eye require urgent ophthalmological assessment. Topical steroid treatment near suspected herpes infection should not delay antiviral treatment or specialist review. Families should be told clearly that this pattern is different from an ordinary infected eczema flare. Diagnosing atopic eczema Atopic eczema is usually diagnosed clinically from itch, typical appearance, distribution, chronicity and personal or family atopy. There is no single blood test, skin swab or allergy result that confirms the diagnosis. The clinician assesses severity using the visible skin, symptoms, sleep, daily function and psychological impact. A small visible patch can represent severe disease when itch, pain or sleep disruption is substantial. When tests are useful Routine allergy testing is not needed for typical, well controlled atopic eczema. Targeted testing may be considered when immediate food reactions, persistent gastrointestinal symptoms, faltering growth or treatment resistant early eczema raises concern. Skin swabs can help when infection recurs, spreads or fails to respond as expected. Patch testing is useful when allergic contact dermatitis is suspected, while skin scrapings can identify fungal infection. Seborrhoeic dermatitis Seborrhoeic dermatitis commonly causes greasy or flaky scale on the scalp, eyebrows, ears and creases beside the nose. In infants, cradle cap can extend into skin folds and the nappy area and is often less itchy than atopic eczema. The two conditions can coexist, particularly during early infancy. Distribution, itch, scale quality and response to treatment help distinguish them. Psoriasis Psoriasis often causes well defined thickened plaques with scale on the scalp, elbows, knees or body folds. Children can have thinner plaques and less obvious scale, making distinction from eczema difficult. Nail pitting, sharply defined borders and a family history support psoriasis. A rash that worsens repeatedly with eczema treatment should be reassessed rather than treated indefinitely with escalating products. Scabies Scabies causes intense itch, often worst at night, through infestation with a microscopic mite. Typical sites include finger webs, wrists, waist, genitals and ankles, although infants can have scalp, palm and sole involvement. Similar itching in household contacts is an important clue. Scabies requires treatment of affected close contacts and environmental measures, not eczema treatment alone. Fungal infection Tinea can produce an enlarging scaly ring with a more active edge and relative central clearing. Topical corticosteroids can alter its appearance and allow wider spread, producing tinea incognito. A skin scraping can identify fungal elements when the diagnosis is uncertain. Fungal infection can coexist with eczema, particularly on feet, hands and within body folds. Immunodeficiency and other serious alternatives Severe eczema beginning very early with recurrent unusual infections, persistent diarrhoea or poor growth can indicate an immune disorder. Nutritional deficiency, cutaneous lymphoma, drug eruption and genetic barrier disorders can also resemble eczema in selected circumstances. Atypical distribution, systemic illness, treatment failure or unusual infections should prompt specialist reassessment. The eczema label should not become a reason to ignore new or discordant findings. The stepped treatment approach Treatment is stepped up or down according to current severity, affected sites and response. Emollients remain the foundation at every stage, including periods when the visible eczema is clear. Active inflammation requires an anti inflammatory treatment such as an appropriate topical corticosteroid. More severe or resistant disease may need topical calcineurin inhibitors, dressings, phototherapy or systemic specialist treatment. Shared treatment planning A useful plan states which product is used, where it is applied, how much is needed and when treatment changes. Practical demonstration is often more effective than another prescription without explanation. Preferences concerning creams, ointments, cultural skin care practices, school routines and work exposures should be discussed. A technically effective product will fail when it is unacceptable, painful or impossible to use consistently. Emollients as foundation therapy Emollients moisturise dry skin and leave a protective film that reduces water loss. They improve flexibility, reduce cracking and support recovery of the stratum corneum. They do not directly suppress all active immune inflammation, so an inflamed flare usually needs additional treatment. Regular use can reduce discomfort and the amount of topical corticosteroid required over time. Types of emollient Ointments contain more oil and usually provide stronger occlusion, making them useful for very dry skin and night time treatment. Creams contain more water and can feel lighter, although preservatives may sting or cause contact allergy in some people. Lotions spread easily over hairy or weeping areas but may provide less lasting protection. The best product is generally an unperfumed preparation that the person can use generously and repeatedly. How much emollient is needed Effective treatment requires substantially more emollient than many small cosmetic moisturiser containers provide. A child with widespread eczema may need approximately 250 to 500 grams weekly, depending on age and body area. An adult treating most of the body may use around 500 grams or more each week. These are practical estimates rather than fixed doses, and requirements rise during dry weather or widespread flares. Applying emollient Apply emollient gently and frequently, including after washing and whenever the skin feels dry or tight. Smooth it along the direction of hair growth rather than repeatedly rubbing hard against the follicles. Use clean hands, and remove products from tubs with a clean spoon or spatula when contamination is a concern. Pump dispensers can reduce repeated contact with the contents and make regular application easier. Washing and bathing Short lukewarm baths or showers are usually better tolerated than prolonged hot bathing. Ordinary soap, bubble bath and fragranced shower products can remove lipids and irritate inflamed skin. A suitable leave on emollient can often be used as a soap substitute, followed by gentle patting dry and reapplication. NICE does not recommend adding separate emollient bath additives for children under 12 because they do not add meaningful benefit to standard care. Emollient fire safety Emollient residue can build up within clothing, bedding and dressings and make fabric burn more rapidly. The risk applies to paraffin containing products and cannot be excluded with paraffin free emollients. Keep treated skin, clothes and bedding away from cigarettes, naked flames, candles and other ignition sources. Washing fabrics can reduce residue but may not remove it completely, so fire precautions remain necessary. Treating an active flare A flare should be treated when itch, roughness, inflammation or other usual warning signs begin. Waiting until skin becomes extensively cracked and bleeding makes control more difficult. Continue emollients and add the prescribed anti inflammatory treatment to active areas. The plan should explain when to stop, reduce or restart treatment and when lack of response needs review. Topical corticosteroids Topical corticosteroids reduce inflammatory gene activity within skin cells and immune cells. They are the standard first line anti inflammatory treatment for most atopic eczema flares. When the correct potency, amount, site and duration are used, benefits greatly outweigh the risk of adverse effects. Undertreated inflammation itself causes skin thickening, infection risk, pigment change, sleep loss and impaired quality of life. The potency ladder UK topical corticosteroids are grouped as mild, moderately potent, potent and very potent. Hydrocortisone preparations are commonly mild, while other products provide progressively stronger anti inflammatory effects. Potency is chosen according to eczema severity, body site, skin thickness, age and previous response. The percentage printed on the tube does not allow safe comparison between different steroid molecules. Choosing potency by site Thin skin on the face, eyelids, neck, genitals and body folds absorbs treatment more readily. Mild preparations are usually preferred for these sites, with carefully supervised short courses of stronger treatment when necessary. Thicker skin on hands, feet or lichenified limbs may require a potent preparation to control inflammation. Very potent treatment and prolonged courses require specialist or experienced clinical supervision. Topical corticosteroids in children Mild treatment is generally used for mild childhood eczema, while moderate or potent treatment may be needed briefly for more severe disease. Potent topical corticosteroids should not be used in children under 12 months without specialist dermatological supervision. Face and neck treatment is usually mild, except for short supervised treatment of a severe flare. The child's age does not justify leaving severe inflammation untreated with a preparation too weak to work. Once daily or twice daily application NICE recommends prescribing topical corticosteroids for application once or twice daily rather than more frequently. Many modern preparations work effectively once daily, which can reduce treatment burden. More frequent application does not necessarily improve control and can increase product use and anxiety. Follow the specific prescription because potency, formulation and treatment site differ. Fingertip units A fingertip unit is the amount squeezed from a standard nozzle along an adult fingertip from the end to the first crease. One fingertip unit is approximately enough to treat an area equal to two adult handprints. Charts adjust expected amounts for different body areas and children's ages. Using a measured amount prevents both ineffective under application and unnecessary excess. Treat the active eczema, not only the worst spot Topical corticosteroid should cover the whole active area showing itch, roughness, thickening or inflammation. Applying a tiny dot to the centre leaves the surrounding inflammatory process untreated. Treatment usually continues until the flare is controlled and sometimes for approximately 48 hours afterwards, according to the plan. Stopping after one application because the surface looks slightly calmer commonly produces early relapse. Proactive treatment Some people flare repeatedly at the same body sites soon after treatment stops. After control is achieved, a clinician may recommend applying anti inflammatory treatment on two days each week to those recurrent sites. This proactive approach can reduce flare frequency while emollients continue every day. It should follow a defined plan rather than indefinite unsupervised use across all skin. Addressing corticophobia Corticophobia means excessive fear of topical corticosteroids and can lead to severe undertreatment. Concerns often arise from confusing appropriate short courses with prolonged misuse of potent products. Clinicians should explain the product name, potency, amount, site and expected duration rather than offering vague reassurance. Questions should be welcomed because shared understanding produces safer use than either avoidance or unrestricted application. Topical corticosteroid adverse effects Prolonged inappropriate use, particularly of potent treatment on thin skin, can cause skin thinning, easy bruising and visible small vessels. Stretch marks, acne like eruptions and suppression of adrenal function are possible with extensive high potency exposure. These complications are uncommon with correctly selected intermittent treatment and clinical review. Sudden severe recurrence after prolonged frequent potent use requires medical assessment, but fear of rare withdrawal reactions should not prevent ordinary evidence based treatment. Separating topical treatments Emollient and topical corticosteroid should be applied as separate layers rather than mixed together in the hand. Allow enough time for one product to absorb before applying the other, following local instructions. The order matters less than ensuring that both reach the intended skin and are not diluted or spread unintentionally. A written daily routine can make treatment manageable around school, work and sleep. Topical calcineurin inhibitors Tacrolimus ointment and pimecrolimus cream reduce T cell inflammatory signalling without causing steroid related skin thinning. They are not routine first line treatments for mild eczema. NICE recommends them as second line options in defined situations when topical corticosteroids have not controlled disease or further steroid exposure risks important harm. They are particularly useful for selected facial, eyelid, neck or flexural disease under an appropriate clinical plan. Using tacrolimus and pimecrolimus These medicines are licensed from age two years in relevant indications and should begin with suitable specialist expertise. Transient burning, warmth or stinging is common during the first days, particularly on very inflamed skin. They should not be applied to clinically infected areas until infection has been assessed and treated appropriately. Sun protection and avoidance of unnecessary ultraviolet exposure are advised during treatment. Wet wrap therapy Wet wrap therapy places a damp layer of tubular dressing or clothing over emollient treated skin, followed by a dry outer layer. It can cool severe itch, improve hydration, reduce scratching and increase penetration of topical treatment. Whole body wet wraps are generally introduced by clinicians or trained eczema teams rather than improvised without guidance. Incorrect use can cause chilling, infection, folliculitis or excessive absorption of topical corticosteroid. Wet wraps with topical corticosteroids When topical corticosteroid is used beneath whole body wet wraps in children, NICE recommends an initial period of seven to fourteen days. Specialist dermatological advice is needed before continuing the combination for longer. The corticosteroid may then stop while wet wraps continue with emollient until control improves. Wet wraps should not cover suspected bacterial or viral infection without clinical assessment. Bandages and paste dressings Specialist bandaging can protect excoriated skin, reduce scratching and improve topical treatment penetration. Paste bandages may contain zinc or other soothing ingredients and are covered with an outer layer. They require correct application to avoid pressure injury or restricted circulation. Bandages are an adjunct to barrier and anti inflammatory treatment rather than a cure for the underlying tendency. Antihistamines Histamine is not the main driver of ordinary atopic eczema itch, so antihistamines are not routinely effective. A non sedating antihistamine may help when urticaria or another histamine mediated allergy coexists. A short supervised course of a sedating antihistamine can occasionally support sleep during a severe childhood flare. Sedation, impaired concentration and accidental overdose are concerns, and antihistamines do not replace eczema treatment. Food exclusion and nutritional safety Routine exclusion of milk, egg, wheat or multiple foods is not a standard eczema treatment. Unsupervised restriction can cause inadequate energy, protein, calcium, vitamins and growth, especially in young children. Food avoidance is justified when a competent allergy assessment identifies a likely or confirmed reaction. A paediatric dietitian should support prolonged exclusion so that nutrition and safe food reintroduction are addressed. Growth faltering Severe uncontrolled eczema can impair feeding and sleep and substantially increase nutritional demands. Restrictive diets, food allergy, chronic infection and systemic disease can add to growth difficulty. Weight loss, crossing growth centiles or poor linear growth requires prompt paediatric assessment. Growth faltering should not be accepted as an unavoidable consequence of eczema or blamed automatically on parental feeding. Phototherapy Phototherapy uses controlled ultraviolet radiation to reduce inflammation in selected moderate or severe eczema. Narrowband ultraviolet B is commonly used through specialist dermatology services. Treatment requires repeated visits and careful dosing to limit burning and cumulative ultraviolet harm. It is unsuitable for some people with photosensitivity, skin cancer risk or medicines that increase light sensitivity. Conventional systemic treatment Severe eczema that remains uncontrolled despite optimised topical therapy may require systemic immune treatment. Options include ciclosporin, methotrexate, azathioprine and mycophenolate mofetil in selected specialist pathways. Each has different monitoring requirements involving blood pressure, blood counts, kidney function, liver function, infection and pregnancy safety. Systemic corticosteroids are generally avoided as routine long term treatment because rebound flares and cumulative adverse effects are substantial. Dupilumab Dupilumab is a biological medicine blocking signalling through the interleukin 4 receptor alpha pathway, affecting interleukin 4 and interleukin 13. It is given by subcutaneous injection for selected moderate or severe atopic dermatitis requiring systemic treatment. It can substantially improve itch, sleep and skin inflammation but does not permanently remove inherited susceptibility. Conjunctivitis, injection reactions and facial symptoms can occur and require specialist review. Other modern systemic options Other biological medicines target type 2 inflammatory cytokines, while oral Janus kinase inhibitors affect intracellular immune signalling. NICE recommends several options for defined ages and disease pathways after inadequate response or intolerance to earlier treatment. Janus kinase inhibitors require assessment of infection, thrombosis, cardiovascular, malignancy, pregnancy and laboratory risks. Choice depends on age, disease pattern, comorbidities, monitoring, speed of action and informed preference. Referral for specialist care Referral is appropriate when diagnosis is uncertain, treatment fails despite correct use or eczema causes major sleep and quality of life impairment. Recurrent infection, suspected contact allergy, severe facial disease, significant psychological distress or need for systemic treatment also justify referral. Children with faltering growth, suspected multiple food allergy or severe early eczema may need paediatric and allergy input. Suspected eczema herpeticum requires same day rather than routine referral. Preventing treatment failure Apparent treatment resistance often results from insufficient product, inadequate potency, incorrect site, short duration or unacceptable formulation. Continuing exposure to irritants, contact allergy, infection or a different diagnosis can also prevent improvement. The clinician should observe treatment technique and review every product actually used, including cosmetics and complementary remedies. Escalating treatment without checking these factors can increase risk while leaving the real problem unresolved. Complementary and herbal treatments Evidence for many herbal creams, supplements and alternative allergy tests is weak or inconsistent. Some unregulated products contain undeclared potent corticosteroids, antimicrobials or contaminants. Natural ingredients can also cause irritant or allergic contact dermatitis. Tell clinicians about complementary treatments so that interactions, steroid exposure and treatment response can be assessed safely. Managing scratching Keep fingernails short and smooth to reduce skin damage, particularly in young children. Cool environments, emollient application, distraction and treatment of inflammation reduce the biological drive to scratch. Cotton gloves or sleep clothing may limit damage for some children but should not become restrictive or unsafe. Punishment and repeated commands to stop scratching usually increase distress without controlling itch. School, nursery and work A written plan can allow emollient application, appropriate clothing and access to prescribed treatment during the day. Staff should understand that eczema is not infectious and should not exclude a child from activities without another reason. Adults with occupational hand eczema may need protective equipment, exposure modification or occupational health assessment. Reasonable adjustments can prevent avoidable flares while preserving education, work and participation. Swimming Many people with eczema can swim, although chlorine or salt water may sting active cracks. Applying emollient before swimming may help some people, provided pool safety rules allow it. Rinse gently afterwards and reapply emollient promptly. Avoid swimming during extensive infection, severe weeping or when a clinician has advised temporary restriction. Vaccination Routine vaccination should continue unless a specific medical contraindication exists. Atopic eczema alone does not weaken the immune system enough to prevent ordinary vaccination. People taking systemic immunosuppressants or selected advanced treatments need specialist advice about live vaccines and timing. Vaccination should not be applied through severely inflamed or infected skin when another suitable site is available. Prognosis in childhood Many children improve substantially as the skin barrier matures, although timing varies. Some continue to have hand, eyelid, flexural or generalised eczema during adolescence and adulthood. Early severe disease, FLG loss of function variants and multiple atopic conditions are associated with greater persistence on average. No individual child's future can be predicted confidently from one flare or one genetic risk factor. Prognosis in adults Adult eczema often follows a relapsing course influenced by occupation, climate, stress, contact allergy and treatment consistency. Long periods of good control are achievable, even when the underlying tendency remains. Repeated severe flares are not inevitable and should prompt review of diagnosis, treatment technique and access to advanced therapy. Management aims for normal sleep, function and participation rather than accepting persistent itch as unavoidable. The central safety message Atopic eczema develops through interacting barrier and immune abnormalities and is not caused by poor hygiene. Daily emollient use supports the barrier, while correctly chosen topical corticosteroids or other anti inflammatory treatments control active disease. Painful rapidly spreading blisters or punched out erosions suggest eczema herpeticum and require same day emergency treatment. Growth faltering, recurrent infection, major sleep disruption or treatment failure requires reassessment rather than increasingly restrictive self treatment.
Atopic eczema is sustained by a two way interaction between a weakened skin barrier and inappropriate inflammation. Consistent emollient use, prompt anti inflammatory treatment, trigger reduction and early recognition of infection can interrupt the itch scratch cycle and prevent avoidable harm.
Medical words made simple
- Atopic eczema
- A chronic relapsing inflammatory disorder causing dry, itchy and easily irritated skin.
- Atopic dermatitis
- Another medical name for atopic eczema.
- Atopy
- A tendency to develop conditions such as eczema, asthma, allergic rhinitis and some food allergies.
- Skin barrier
- The outer protective system that retains water and limits entry of irritants, allergens and microorganisms.
- Epidermis
- The outer cellular layer of the skin.
- Stratum corneum
- The outermost epidermal layer, made from flattened cells surrounded by protective lipids.
- Corneocyte
- A flattened mature cell forming part of the outer skin barrier.
- Ceramide
- A skin lipid helping organise the barrier and reduce water loss.
- Transepidermal water loss
- Water moving through the epidermis and evaporating, which increases when the barrier is impaired.
- Filaggrin
- A skin protein supporting epidermal structure, water retention, acidity and barrier function.
- FLG gene
- The gene encoding filaggrin, with some loss-of-function variants increasing eczema susceptibility.
- Loss-of-function variant
- A genetic change reducing or preventing normal production or function of a protein.
- Immune dysregulation
- Immune activity that is poorly controlled or directed in a way that produces harmful inflammation.
- Cytokine
- A signalling protein used by immune and other cells to coordinate inflammation.
- Interleukin 4
- A type 2 inflammatory cytokine involved in atopic eczema and allergic immune responses.
- Interleukin 13
- A cytokine contributing to inflammation, itch and reduced skin-barrier protein production.
- Atopic march
- A concept describing the association and possible sequence between eczema, food allergy, asthma and allergic rhinitis.
- Pruritus
- The medical term for itch.
- Itch-scratch cycle
- The repeating process in which itch causes scratching, skin damage and further inflammation and itch.
- Flexural eczema
- Eczema affecting skin folds such as the elbow creases and backs of the knees.
- Extensor surface
- The outer surface of a limb, such as the outer elbows or fronts of the knees.
- Lichenification
- Thickened skin with prominent markings caused by repeated rubbing or scratching.
- Excoriation
- A superficial scratch or erosion produced by rubbing or scratching.
- Irritant
- A substance or exposure directly damaging the skin without requiring a specific allergy.
- Allergic contact dermatitis
- A delayed immune skin reaction to a substance touching the skin.
- Patch testing
- Specialist testing using small amounts of contact allergens applied to the back for delayed-reaction assessment.
- Colonisation
- Microorganisms living on a body surface without necessarily causing invasive infection.
- Staphylococcus aureus
- A bacterium frequently found on atopic skin and capable of causing secondary infection.
- Cellulitis
- A spreading bacterial infection involving deeper skin and subcutaneous tissue.
- Eczema herpeticum
- A potentially serious widespread herpes simplex infection occurring within eczema-damaged skin.
- Punched-out erosion
- A small, sharply defined area of superficial skin loss characteristic of eczema herpeticum.
- Emollient
- A moisturising treatment that softens skin, reduces water loss and supports barrier recovery.
- Occlusive
- Forming a surface layer that slows evaporation and increases skin hydration.
- Soap substitute
- A gentle emollient product used for cleansing instead of ordinary soap or fragranced wash.
- Topical corticosteroid
- An anti-inflammatory steroid medicine applied directly to active skin disease.
- Potency
- The anti-inflammatory strength of a topical corticosteroid, classified as mild, moderate, potent or very potent.
- Fingertip unit
- The amount squeezed along an adult fingertip, treating approximately two adult handprint areas.
- Corticophobia
- Excessive fear of topical corticosteroids that can lead to harmful undertreatment.
- Proactive treatment
- Intermittent anti-inflammatory treatment on recurrent problem sites after a flare has been controlled.
- Topical calcineurin inhibitor
- A non-steroid anti-inflammatory skin medicine such as tacrolimus or pimecrolimus.
- Wet wrap therapy
- Treatment using a damp inner dressing and dry outer layer over emollient or prescribed topical therapy.
- Phototherapy
- Specialist treatment using controlled ultraviolet radiation to reduce skin inflammation.
- Biological medicine
- A targeted treatment produced using biological methods and designed to block a specific immune pathway.
- Dupilumab
- An injected biological medicine blocking interleukin 4 and interleukin 13 signalling.
- Janus kinase inhibitor
- A medicine reducing intracellular signalling from several immune pathways.
- Faltering growth
- A pattern in which a child gains weight or grows more slowly than expected and requires assessment.
- Systemic treatment
- Treatment acting throughout the body, usually taken orally or given by injection.
Quick recap
- Atopic eczema is a chronic relapsing inflammatory skin disorder and is not contagious.
- It is not caused by poor hygiene, and harsh washing can worsen barrier damage.
- The stratum corneum retains water and limits entry of irritants, allergens and microorganisms.
- Atopic skin has increased water loss and becomes dry, cracked and sensitive.
- Filaggrin supports skin structure, hydration and acidity.
- FLG loss of function variants increase eczema risk but are neither necessary nor sufficient for disease.
- Barrier dysfunction and immune inflammation reinforce one another.
- The atopic march links eczema statistically with food allergy, asthma and allergic rhinitis but is not inevitable.
- Infant eczema commonly affects the face, scalp and extensor limbs.
- Children and adults often develop flexural, hand, eyelid, face or neck eczema.
- Inflammation may appear violet, grey or brown rather than bright red on darker skin.
- Itch is central, and scratching causes further barrier damage and inflammation.
- Sleep disruption and psychological impact can make a small visible area clinically severe.
- Soap, detergents, heat, sweat, friction, stress and infection can contribute to flares.
- Food allergy and atopic eczema are different conditions, and broad exclusion diets can cause malnutrition.
- Staphylococcus aureus commonly colonises eczema without always requiring antibiotics.
- Fever, increasing pain, pus and spreading warmth increase concern about bacterial infection.
- Eczema herpeticum causes a sudden painful eruption with similar blisters or punched out erosions.
- Suspected eczema herpeticum requires immediate systemic aciclovir and same day specialist assessment.
- Atopic eczema is normally diagnosed clinically rather than through routine allergy testing.
- Scabies, contact dermatitis, fungal infection, psoriasis and immune disorders can mimic eczema.
- Emollients remain the foundation treatment during flares and clear periods.
- Widespread disease needs generous quantities rather than occasional cosmetic moisturising.
- Emollient contaminated fabrics can ignite rapidly and must remain away from flames and cigarettes.
- Topical corticosteroids treat active inflammation and are selected by potency, site, age and severity.
- Correctly used topical corticosteroids are effective and generally safe, while undertreatment causes avoidable harm.
- One fingertip unit treats approximately two adult handprint areas.
- Topical calcineurin inhibitors provide a non steroid second line option for selected sites and ages.
- Wet wraps can reduce severe itch but require correct technique and supervision when corticosteroids are included.
- Severe refractory disease may require phototherapy, systemic immunosuppression, biological treatment or a Janus kinase inhibitor.
- Growth faltering, recurrent infection, treatment failure and severe quality of life impact require reassessment or referral.
- Long periods of good control are achievable even when the underlying eczema tendency persists.