Eczema

Eczema is a family of inflammatory skin conditions in which the skin becomes red, dry, itchy, and sometimes blistered or thickened. The word is often used as a general term, but in clinical and public-health usage it most often refers to atopic dermatitis (atopic eczema), a chronic, relapsing disease that is most common in children and is closely linked to allergy and the immune system. Other forms include contact dermatitis, dyshidrotic, seborrheic, and stasis eczema. Eczema is a common reason for dermatology visits and affects a large share of people worldwide, so its causes, classification, and treatment have been studied extensively in medicine and public health.

This entry explains what eczema is, how its main types differ, and why it occurs. It covers the biology of the skin barrier, the Th2-dominant immune response, genetic and environmental contributions, and the links between eczema, asthma, and allergic rhinitis. It then describes how the disease is diagnosed and scored for severity, and how treatment has changed, from emollients and topical anti-inflammatory drugs to systemic immunosuppressants, biologics, and JAK inhibitors. The entry also addresses infections, the psychological and social burden of the disease, prevention, the history of the concept, and questions that remain unresolved.

Definition and terminology

Eczema works less as a single diagnosis than as a descriptive umbrella. Clinicians apply the word to a set of itchy, inflamed skin reactions whose surface appearance and microscopic changes overlap. In clinical dermatology, dermatitis is used to describe a variety of different skin conditions that share the same inflammatory reaction pattern with similar clinical manifestations. Under the microscope, the common finding is a process called spongiosis, in which fluid collects between epidermal cells. Lymphocytes move into the dermis and then the epidermis, causing intercellular epidermal edema (spongiosis), hyperproliferation, thickening, and hyperkeratosis. The dermatopathologic term for this process is spongiotic dermatitis or eczematous dermatitis. The two words are therefore close to interchangeable. Eczema is synonymous with dermatitis but is often used, mainly by non–health care professionals, to mean atopic dermatitis.

Atopic dermatitis is the most frequent form and the one most people have in mind when they say "eczema." It is usually defined by a cluster of features rather than by one test. Atopic dermatitis is characterized by severe pruritus, a chronically relapsing course, a distinctive distribution of eczematous skin lesions, and a personal or family history of atopic diseases. The last criterion depends on atopy, a term that describes a hereditary predisposition to IgE-mediated sensitivity. Atopy is defined as an inherited tendency to produce immunoglobulin E (IgE) antibodies in response to minute amounts of common environmental proteins such as pollen, house dust mites, and food allergens. The word is itself recent. The term was based on the word atopy, coined in 1923 by allergologists Arthur Coca and Robert Cooke, and Fred Wise and Marion Sulzberger renamed the condition atopic dermatitis in 1933. Naming remains unsettled, and the literature gives us expressions such as atopic dermatitis, neurodermatitis, atopic eczema, non-atopic eczema, atopiform dermatitis, intrinsic dermatitis, endogenic dermatitis, extrinsic dermatitis, atopic dermatitis/eczema syndrome and so on.

Older classifications divided eczema by cause, into endogenous (intrinsic) and exogenous (extrinsic) forms. Exogenous eczema is driven by outside agents. Exogenous eczema results from external triggers such as allergens, irritants, or physical injury. Examples include allergic contact dermatitis, caused by sensitivity to substances like nickel or fragrance, and irritant contact dermatitis, which occurs from repeated exposure to soaps, detergents, or solvents. Endogenous eczema is attributed to internal factors, and common types include atopic dermatitis (often associated with asthma and hay fever), seborrheic dermatitis (caused by a reaction to skin yeast), discoid dermatitis (coin-shaped lesions on limbs), and lichen simplex (resulting from chronic scratching). In the early German and Japanese classification, the contact-type group was called "vulgar" eczema, while the atopic complex was summarized as endogenous eczema. The generic term "vulgar eczema" was essentially understood to mean contact eczema, intolerance reactions of the skin caused by direct contact with exogenous substances. The "eczematous" disease complex, which belongs to the group of atopic diseases (Greek atopos = out of place), was summarized as "endogenous eczema". The scheme proved hard to apply, because the clinical classification of eczema is unsatisfactory, because it is based partly on etiology and partly on description. Because there are multiple causes, it is not surprising that there is a good deal of overlap between the various named types, and many cases are unclassifiable.

The Greek root points to the visible appearance of early lesions. The word is generally derived from "ekzein (Greek)," which means "boil over" or "break out", and lesions usually start as vesicles. Sources disagree on when the term entered use. One dictionary dates English use to 1745–55; from New Latin, from Greek ékzema. A review states that eventually, eczema was coined in 1817 to describe a fluid‐filled, blistering rash–like sunburn. A history of atopic dermatitis instead credits the Greek physician Aetius of Amida with first using the term in the sixth century.

Usage also differs by audience. Clinicians and coding systems tend to use dermatitis as the umbrella term. For example, in ICD10 2023, the clinical picture is also coded as "eczema nummulare, nummular eczema" under L30 "other dermatitis". Patients and the general public more often hear eczema, and consumer health sites present the two as the same condition. Eczema is a general term for different types of rashes. A European study of internet searches noted that the terminology used not only affects experts, daily clinical practice, and research but especially patients and the general public in terms of their understanding and access to disease‐related information.

Types and clinical subtypes

Atopic dermatitis

Atopic dermatitis is the most common form of eczema, and its distribution shifts with age. In infants, scaly, crusted patches typically appear on the cheeks, scalp, trunk, thighs, shins, and the outer surfaces of the limbs. The diaper area and groin are usually spared, which helps separate the condition from nappy-related rashes. In toddlers and young children, the disease moves toward the flexures: the antecubital and popliteal fossae, the back of the neck, and the wrists and ankles. Adolescents and adults usually keep flexural lesions but may also develop involvement of the hands, feet, and periorbital skin. A US population study described five lesion patterns in adults, ranging from mild, limited disease to severe, widespread involvement. In people over 60, flexural and facial lesions become less frequent, while buttock and genital lesions become more common.

The disease is also defined in relation to other atopic conditions. The Hanifin–Rajka criteria list a personal or family history of asthma, allergic rhinitis, or atopic dermatitis among the basic features. Clinicians often treat a history of allergic rhinoconjunctivitis or asthma, in the patient or relatives, as a clue to the diagnosis. The shared predisposition is discussed further under atopy and in the sections on allergy, asthma, and allergic rhinitis.

Allergic and irritant contact dermatitis

Contact dermatitis is the eczematous reaction that follows contact with an external agent, and it has two main forms. Irritant contact dermatitis (ICD) is far more common: one review puts it at about 80 percent of contact dermatitis cases, compared with 20 percent for allergic contact dermatitis (ACD). ICD arises when enough exposure directly damages epidermal keratinocytes, and it can affect anyone. ACD, by contrast, is a cell-mediated immune reaction that requires prior sensitization to a specific allergen. Common culprits include nickel, gold, topical corticosteroids, fragrances, and preservatives such as methylisothiazolinones. The hands are the most frequently affected site. The two forms can be hard to tell apart, and the distinction matters because it determines management.

Patch testing is the main tool for separating them. Allergens are applied to the back for 48 hours and the sites are read at 96 hours, since reactions usually take 48 to 96 hours to develop. Patch testing is valuable for identifying ACD but is not useful for irritant dermatitis. No patch test can prove that a particular irritant is responsible, so an ICD diagnosis rests on excluding ACD and on a history of adequate exposure. Skin biopsy adds little, because histological changes are often similar in the two forms at an early stage. ICD may also become chronic and slow to resolve even after the irritant is avoided.

Dyshidrotic, nummular, and seborrheic eczema

Dyshidrotic eczema (pompholyx) is characterized by deep-seated vesicles on the palms, the soles, and the sides of the digits, and it is typically bilateral and symmetrical. The vesicles are small and deep, which gives rise to the classic "tapioca pudding" description. Patients often report intense itching before the vesicles appear, and these then dry and peel over one to two weeks. It accounts for a sizeable share of hand eczema, and flares are more frequent in spring and summer and in warmer climates. The cause is unknown.

Nummular eczema is named for its coin-shaped plaques, which are most often found on the arms, back, buttocks, and lower legs, and which may crust, scale, and itch intensely. It can be less responsive to low-potency topical agents than other forms. Its age pattern is described inconsistently: some patient-facing sources note that it most often appears in older adults, unlike atopic dermatitis.

Seborrheic eczema (seborrheic dermatitis) favors sebum-rich areas, including the scalp, the face around the nose and eyebrows, and the upper central chest. It produces yellowish, greasy scales, and in infants it appears as cradle cap. Itch is not always present. In some cases the condition is thought to involve the yeast malassezia, although its cause is not fully settled.

Stasis eczema and neurodermatitis

Stasis (venous) eczema develops when circulation in the legs is impaired, as in varicose veins and edema. It causes redness, scaling, darkening of the skin, and itching. Chronic venous hypertension is generally understood to be central to its development, and it typically affects the lower legs, particularly around the ankles. Long-standing cases may show brown hemosiderin pigmentation and skin hardening, and they may progress to ulceration, so compression therapy and treatment of the underlying venous disease are central to management.

Neurodermatitis, also called lichen simplex chronicus, is a localized, thickened, lichenified plaque that results from repeated rubbing or scratching. It is commonly found on the nape of the neck, the wrists, the ankles, and the anogenital region. Its persistence depends on the itch–scratch cycle, and psychological stress is often reported as a contributor. It is one of the recognized types of eczema in consumer-facing classifications.

Epidemiology and burden

Estimates of how many people have eczema depend on how the condition is defined and counted. Most large figures refer to atopic dermatitis, the most common form. A systematic review and meta-analysis of 310 studies covering more than 25.5 million people estimated a worldwide point prevalence of 11.1% in children and adolescents and 6.3% in adults.The review included 310 studies with more than 25.5 million individuals, and the pooled figures are 11.1% (95% confidence interval 9.4–13.1) in children and adolescents and 6.3% (95% CI 5.0–7.8) in adults. Other analyses produce lower totals. A broader modelling study of 344 studies put the global prevalence at 2.6% (95% uncertainty interval 1.9–3.5), with prevalence rates of 2.0% in adults and 4.0% in children. Textbook-style summaries give wider ranges, such as approximately 15-25% of children and 3-7% of adults. The gap reflects differences in study populations, age bands, and case definitions, and the review literature itself notes a lack of robust prevalence estimates because of this variation. Severity also differs by age group: prevalence is higher in children and adolescents, while adults have a higher proportion of severe disease.

Most cases begin early in life. In 60% of children, the onset of disease occurs during the first year of life. Early-onset disease, defined as onset from birth to age 2, is the most common subtype, and about 60% of cases resolve by age 12. Onset often falls within the first months: the disease often starts in infants aged between 2 and 6 months. Later onset is less frequent. Symptoms that begin after puberty are classed as late-onset, and onset at 60 or older is uncommon. Although the disease is often described as a childhood condition, newer population-based estimates suggest the prevalence of pediatric and adult disease may be similar. Remission is common in childhood-onset cases: in one German birth cohort, 87% of participants with onset before school age were free of symptoms by age 30.

Prevalence varies by region and over time. In the Global Burden of Disease analysis of children aged 0 to 14, the highest rates were found in Central Asia, high-income Asia Pacific, and Western Europe, and the lowest in Sub-Saharan Africa. National rates ranged from 1.50% in Rwanda to 10.67% in Mongolia. The same analysis found that the highest prevalence occurred in children aged 5 to 9 years, with girls having higher rates than boys across all age groups. Trends have diverged. Pediatric cases rose, reaching 72.4 million in 2021, a 6.2% increase from 2000, yet 48 countries, including the United States and Japan, experienced a marked decrease in prevalence. In industrialized countries, the rise has been steeper: since the 1970s, the incidence of eczema has increased up to threefold. Within countries, the increase has been most visible in cities. A systematic review of urban-rural comparisons found that nineteen of twenty-six studies showed higher risk in urban areas, eleven of them significantly, although the authors concluded that the evidence was only some evidence of a higher risk. Trends in China are mixed: prevalence among 3-12-year-olds showed increasing trends in most specific cities, while national rates among 13-14-year-olds fell between 2001 and 2009.

The socioeconomic picture is less settled. Social deprivation and stress are linked with worse symptoms in people with atopic eczema, and social change in recent decades has led to a "westernized" lifestyle associated with high prevalence in industrialized countries. Evidence on how prevalence varies by income or education is less consistent than the evidence on severity. The economic burden is clearer. Eczema leads to productivity loss and absenteeism among affected individuals and their caregivers, and in infancy the condition causes considerable morbidity, in terms of sleep and feeding disruption, parental stress, economic costs, and later atopic outcomes. Detailed figures on healthcare use and costs in specific health systems are covered in the section on health systems and universal health coverage.

Clinical presentation across the life course

Age-related distribution

Atopic dermatitis usually appears in infancy, as early as 3 months of age. The early lesions follow a characteristic sequence. In some infants the first changes appear in the skin creases, with erythema and exudation. Over the following weeks, the rash more often settles on the cheeks, forehead and scalp, and on the outer surfaces of the lower legs, usually sparing the diaper area and the nose. Facial and extensor involvement is a diagnostic pattern in young children, whereas flexural erythema and/or lichenification is typical at all ages.

In school-age children the rash shifts toward the flexures. Lesions occur on flexural surfaces such as the neck and the antecubital and popliteal fossae. In adolescence and adulthood, the head, neck and flexures are typically involved, with mostly lichenified plaques. Adult disease is more varied. It may continue in the school-age flexural pattern or become diffuse, and discoid and papular patterns can develop. Chronic rubbing can produce madarosis, nodular prurigo, and lichenification. Some people whose childhood disease fully resolved have recurrence confined to the hands, linked to occupational and domestic work.

Itch, scratching and the relapsing course

Pruritus is the central feature. Itch often precedes lesions and worsens with dry air, sweating, local irritation, wearing wool garments, and emotional stress. The itch is usually worse at night, and this nocturnal pattern drives much of the sleep loss. Scratching then creates a feedback loop: it can further compromise the epidermal barrier and result in dry skin, microbial colonization, and secondary infections. In one survey, 36% of patients report that they often or always scratch until their skin bleeds.

Sleep disruption is common and affects families as well as patients. Estimates for sleep disturbance climb substantially in people with AD (47-80% in children and 33-87.1% in adults) in one trial protocol, and parents may lose sleep too: mean reduction in parental sleep time during flare-ups in children with AD ranged from 0.66 to 2.6 hours per night. Scratching is not the whole explanation. One study reported that scratching accounted for only 15% of arousals and awakenings in children with AD, which suggests that itch, scratching and other factors each contribute. Disturbed sleep in turn can worsen quality of life, mental health and daytime functioning.

The disease is relapsing and remitting. Its clinical phenotype is characterised by remission and relapse with acute flares on a background of chronic dermatitis. Symptoms wax and wane, and flares can be triggered by the factors listed under environmental triggers.

Acute, subacute and chronic lesions

Clinicians often describe lesions by their stage. Acute eczema involves the constellation of vesicles and/or bullae, erythematous macules and/or plaques, oozing, and crusting. Subacute lesions are defined by the presence of scaly erythematous papules and/or plaques, along with round erosions and/or round crusts. In chronic disease, there are scaly, lichenified plaques that may be hyper- and/or hypopigmented. Lichenification, meaning thickened skin with accentuated skin markings, occurs secondary to scratching and rubbing.

These stages are better understood as points on a continuum than as fixed sequential phases. The designators acute, subacute, and chronic are somewhat arbitrary because they describe parts of a dynamic spectrum. Acute and chronic lesions are often found in the same individual, often overlap, and clinically are sometimes difficult to distinguish. Lesions may also revert to acute, remain subacute, or may progress to chronic rather than following a fixed order. Appearance varies with skin tone. Lichenification and dyspigmentation are more prominent in darker skin. On darker skin, rashes can appear purple, brown, gray or ashy. On lighter skin, rashes appear red or very white and dry.

Associated features that aid recognition

Several features outside the main plaques help clinicians recognize the disease. Dryness is among the most common, and xerosis, pruritus, and erythematous papules coalescing into plaques form the core picture. Scratching can produce prurigo nodules from repeated picking. Crusting and weeping, although often associated with infection, are features of AD per se, especially in younger children, even in the absence of frank infection.

Minor features in the Hanifin and Rajka criteria point to a broader pattern. These include xerosis, ichthyosis, palmar hyperlinearity, keratosis pilaris, nipple eczema, cheilitis, recurrent conjunctivitis, Dennie-Morgan infraorbital fold, and tendency toward non-specific hand or foot dermatitis. The skin's susceptibility to infection is also recognized, particularly to Staph. aureus and Herpes simplex, which is discussed further in the infections section. Taken together, the distribution, itch, relapsing history and personal or family history of atopy are the features that most often lead clinicians to suspect the diagnosis.

Diagnosis, differential diagnosis, and severity assessment

Clinical diagnosis and criteria sets

Atopic dermatitis is diagnosed on clinical grounds, because the field still lacks a definitive test. The Hanifin and Rajka criteria of 1980 were built to address two gaps at once: the absence of an objective laboratory test and inconsistent nomenclature. Under these criteria, a diagnosis requires at least three of four major criteria and three of 23 minor criteria. The major criteria cover pruritus, a typical morphology and distribution, chronic or relapsing dermatitis, and a personal or family history of atopy. The morphology criterion differs by age: flexural lichenification or linearity in adults, and facial and extensor involvement in infants and children. Many minor criteria are not specific to the disease, such as xerosis, raised serum IgE, and early age of onset. An alternative set, the UK Working Party criteria, was derived from the original Hanifin and Rajka list.

Conditions that mimic eczema

Most differential work concerns a small number of conditions that look similar but require different management. Among common mimics, allergic contact dermatitis, psoriasis and cutaneous T cell lymphoma are the ones most often confused with adult-onset atopic dermatitis in clinical practice. Psoriasis is discussed in the psoriasis entry. Cutaneous T-cell lymphoma is a more serious concern. Early mycosis fungoides may closely resemble atopic dermatitis. Important clues include localization to photo-protected "bathing suit" areas, a predilection for people over 50, and failure to respond to standard eczema therapies. Unlike atopic dermatitis, diagnostic confirmation of mycosis fungoides requires a biopsy. In older children, mycosis fungoides often presents with hypopigmented patches associated with a dermatitis.

Infants with severe, generalized eczema are a second group. Infants with severe itch and generalized dermatitis in the setting of recurrent infections should be investigated for evidence of immunodeficiency. Failure to thrive and repeated infections help distinguish the eruption from atopic dermatitis. In some disorders, bleeding accompanies the rash; in Wiskott-Aldrich syndrome, bleeding may be prominent with the dermatitis, because of the associated thrombocytopenia. Genetic conditions with atopic-dermatitis-like features include Netherton's syndrome, severe dermatitis-allergies-metabolic wasting (SAM) syndrome, and primary immunodeficiencies (Hyper-IgE, DiGeorge, and Wiskott-Aldrich syndrome). Nutritional deficiencies, such as zinc or niacin deficiency, are also listed among high-priority differentials in one review. In adults, lack of atopy, adult onset, and symptoms accompanied by weight loss or malaise are key to differential diagnosis. Infestations and fungal disease are excluded in a different way: microscopic evaluation of a skin scraping can help rule out scabies or fungal infections.

Severity instruments

Severity is measured with scores that combine physician-assessed signs, body surface area, and, in some scales, symptoms. Scoring Atopic Dermatitis (SCORAD), the Investigator Global Assessment (IGA), and the Eczema Area and Severity Index (EASI) are the most commonly used assessments of atopic dermatitis signs. A review of randomized controlled trials from 2016 found that the most commonly used severity measures were SCORAD, Visual Analogue Scale (VAS)-pruritus, IGA, and EASI. Total SCORAD ranges from 0 to 103, with an objective component of 0 to 83. EASI was adapted from the Psoriasis Area and Severity Index, and four signs—erythema, papulation/edema, excoriation, and lichenification—are assessed using a scale of 0 to 3. The two instruments weigh different features. IGA assesses intensity but not extent, whereas EASI assesses both, but heavily weights scores by extent (~50%). Because more than two dozen scales exist, for measurement of disease severity, at least 28 different scales exist. Patient-reported tools such as the Patient-Oriented Eczema Measure and the peak pruritus numerical rating scale are also used. In a pooled dupilumab trial analysis, IGAxBSA correlated better with objective measures (EASI, SCORAD) than with patient- or caregiver-reported subjective measures. Smartphone photographs have also been validated for scoring mild to moderate disease, with perfect agreement between clinical IGA and photograph IGA observed for 62% of cases in one study.

Skin biopsy, patch testing, and blood tests

Laboratory findings support but do not establish the diagnosis. Associated laboratory abnormalities include high levels of immunoglobulin E (IgE) and circulating eosinophils, but pathognomonic biomarkers have not yet been identified, so elevated IgE cannot confirm the disease. Patch testing is recommended in a recent consensus guideline for consideration in all atopic dermatitis patients, and can help detect allergic contact dermatitis, which often occurs along with and mimics atopic dermatitis. Its limit is that a positive patch test result does not rule out a diagnosis of CTCL, particularly if clinical suspicion is high or the presentation of ACD is atypical. Skin biopsy is reserved for atypical or refractory presentations, and immunological blood tests are targeted at patients with suspected immunodeficiency. Routine testing is generally unnecessary for typical cases, since diagnosis is typically based on history and physical exam and, given its prevalence and most often benign course, further diagnostic efforts are generally not required.

Skin barrier dysfunction

The outermost layer of the epidermis, the stratum corneum, is often pictured as a "brick and mortar" structure. The bricks are keratin-filled corneocytes, and the mortar is a lipid matrix of ceramides, free fatty acids and cholesterol arranged in lamellar layers. The "bricks" are terminally differentiated keratinocytes composed mostly of keratin filaments and filaggrin. The "mortar" is composed of intercellular lipids arranged into lamellar layers consisting of ceramides, free fatty acids, and cholesterol. Within that lipid fraction, ceramides are the predominant lipid comprising approximately 50% of the intercellular lipid content by mass.

In atopic dermatitis (AD), the lipid mortar is altered in both quantity and structure. Lesional skin contains less total ceramide, and the carbon chains of several ceramide classes are shorter than in healthy skin, a pattern that shifts the lipid profile toward short-chain species In AD lesions, ceramide levels are reduced (in terms of total ceramides and specific types such as NH and NP ceramides), and the carbon chain lengths of certain ceramide classes become shorter. These lipid measures track with functional readouts: the amount and chain lengths of SC ceramides have been shown to correlate with skin barrier parameters, such as SC hydration and transepidermal water loss. Water loss is measurably raised. In one pediatric study comparing flexural lesions with healthy skin, transepidermal water loss averaged 27.24 versus 13.51 g/h/m² (27.24 g/h/m^2^ vs. 13.51 g/h/m^2^, p < 0.001).

Inflammation itself appears to sustain the defect. Experimental work suggests that IL-4 and IL-13 act on the enzymes that build barrier lipids, so the type 2 response erodes the barrier it is partly triggered by type 2 cytokines, particularly IL-4 and IL-13, directly disrupt lipid metabolism by inhibiting enzymes, thereby establishing a vicious cycle of inflammation and barrier dysfunction. Surface acidity is another marker. Normal skin is slightly acidic, but AD skin measures less acidic, and in adults lesional pH sits at 5.40 against 5.27 in nonlesional skin Lesional areas' pH (5.40 ± 0.13) was higher than nonlesional (5.27 ± 0.14), P = .01. A higher pH is thought to favor serine protease activity, which can inhibit the lipid-processing enzymes needed for ceramide synthesis and degrade the proteins that hold corneocytes together Neutralization of the skin's acidic pH enhances serine proteases activity which inhibits key lipid processing enzymes in the synthesis of ceramide, a major component of the lipid lamellae matrix that cemented corneocytes. In addition, activated serine proteases degrade the adhesion proteins that bind the corneocytes together. Soap use is one external factor that raises surface pH and increases endogenous protease activity Use of soaps can increase skin pH, increasing activity of endogenous proteases and leading to breakdown of epidermal barrier function.

The most important genetic contributor to barrier weakness is the filaggrin gene. The profilaggrin precursor is encoded by the FLG gene on chromosome 1q21, and it is cleaved into filaggrin monomers that help corneocytes mature and form the barrier a large polyprotein that is cleaved into filaggrin monomers with important functions in terminal differentiation of the epidermis and formation of the skin barrier. Loss-of-function variants produce a protein that cannot perform these roles FLG loss-of-function (LoF) mutations, which result in nonfunctional filaggrin protein, are known to contribute to the skin barrier defect observed in many patients with AD. Two such variants, R510X and 2282del4, are carried by approximately 9% of people of European origin. Filaggrin breakdown also contributes to hydration, because filaggrin-derived natural moisturizing factors help keep the stratum corneum hydrated, and reduced expression of the enzymes that generate them can worsen water loss The lower expression of skin barrier proteins and enzymes involved in the generation of natural moisturizing factor could further exacerbate barrier defects and perpetuate water loss from the skin.

Once the barrier is breached, the skin becomes more permeable to external agents. Corneocyte dehiscence and defective extracellular matrix result in the breach of the epidermal barrier leaving the skin vulnerable to irritants, allergens, haptens, and microorganisms. In AD, the initiation of AD is characterized primarily by a defective skin barrier that facilitates allergen entry with resulting inflammation and sensitization. Microbial enzymes add to the damage: the epidermal barrier may be further damaged by exogenous proteases from house-dust mites and S. aureus. Surface pH also shapes the microbial environment, since skin pH of 5.7-6.2 allows the growth of S aureus in atopic dermatitis individuals.

Immune mechanisms

Type 2 inflammation is the best-characterized immune pathway in atopic dermatitis. Interleukin-4 (IL-4), IL-13 and IL-5 are produced mainly by T helper 2 (Th2) cells, and they account for much of the acute lesional picture. IL-4 promotes Th2 cell development, while IL-13 acts on non-hematopoietic cells such as keratinocytes and fibroblasts. Both cytokines suppress filaggrin, loricrin and lipid-related proteins, which weakens the barrier, and they also drive collagen deposition in the dermis, a process linked to lichenification. Their most distinctive immunological effect is on B cells: they promote class switching to IgE, which sensitizes mast cells and basophils to release histamine and recruits eosinophils into the skin. Group 2 innate lymphoid cells (ILC2), which express the transcription factor GATA3, add a further source of IL-5 and IL-13 and are found close to basophils in lesional skin.

Epithelial "alarmins" start this cascade. Stressed keratinocytes release thymic stromal lymphopoietin (TSLP), IL-33 and IL-25 when they encounter allergens, microbes or mechanical injury. TSLP activates dendritic cells, which then attract Th2 cells and prime naive T cells toward a type 2 response. IL-33 and TSLP also expand ILC2 populations, creating a positive feedback loop in which IL-4 supports further ILC2 development. Bacterial components, including lipoproteins from Staphylococcus aureus, have been reported to induce TSLP expression, linking microbial exposure to this initiating step.

Itch is driven largely by IL-31, which is produced mainly by Th2 cells and also by mast cells, macrophages, dendritic cells, eosinophils and basophils. IL-31 acts through a receptor on sensory neurons and also impairs keratinocyte differentiation, and its levels correlate with disease severity. IL-33 can increase IL-31 output, and IL-4 and IL-13 may further sensitize sensory pathways. One proposed explanation for the residual itch seen in some patients treated with the IL-4 receptor antibody dupilumab is that IL-31 can also be produced by M2-type macrophages under TSLP stimulation, with periostin from fibroblasts contributing to the signal.

Type 2 signaling does not account for the whole picture. Acute lesions are dominated by Th2 cells, whereas chronic, lichenified lesions show additional Th1 responses (with interferon-γ), Th17 responses (with IL-17A and IL-17F) and Th22 responses (with IL-22). Th22 activation is thought to link barrier and immune defects, because IL-22 inhibits keratinocyte differentiation and promotes epidermal hyperplasia. Age also matters: pediatric lesions tend to show stronger Th22 and Th17 activity, and Th1 signaling appears mainly in long-standing adult disease. Current models describe the acute-to-chronic transition as a quantitative intensification of several axes rather than a simple switch between Th1 and Th2. Early-life studies have also reported that a higher blood Th2-to-Th1 ratio in newborns is associated with later disease, which has led to suggestions that Th1 responses may be partly protective.

The sequence of events remains debated. The "inside-out" model holds that cytokine-driven immune activity comes first and causes secondary barrier impairment, a view supported by the clinical effect of IL-4 and IL-13 blockade and of anti-IgE therapy. The "outside-in" model holds that a primary barrier defect, such as loss-of-function variants in the filaggrin gene, allows allergens and microbes to penetrate the skin and provoke immune deviation. A third formulation, sometimes described as "outside-inside-outside", proposes a self-reinforcing loop in which barrier defects and immune imbalance amplify each other. Many contemporary reviews treat the two classic models as complementary, and it is possible that they apply to different patient subgroups.

Genetics and epigenetics

Family and twin studies provided the first quantitative evidence that atopic dermatitis (AD) has a strong hereditary component. A parent with any atopic disease is estimated to raise a child's risk about 1.5-fold, while a parent with AD raises it roughly three- to five-fold. Shared households complicate this picture, so twin studies were used to separate genetic from shared-environment effects. In a Danish registry of 19,748 children and adolescents, pairwise concordance was about 0.80 in identical girls and 0.41 in fraternal girls, and about 0.74 and 0.37 in boys. A systematic review estimated heritability at approximately 75%, while other reports give a wider range of roughly 60% to 90%. Most of these estimates come from Scandinavian samples, and the Danish estimate of about 82% has been cited as the highest in that population.

Genome-wide association studies (GWAS) have since expanded the list of implicated loci well beyond FLG. In 2011, a meta-analysis of population cohorts reported three new loci near OVOL1, ACTL9 and KIF3A, with the first two lying near genes involved in epidermal proliferation and differentiation. A childhood-onset study of European patients found four loci that reached genome-wide significance, covering the epidermal differentiation complex, a region near LRRC32, the RAD50/IL13 locus, and the major histocompatibility complex. These findings point to two broad themes: skin-barrier structure and immune regulation, with considerable overlap between AD and psoriasis, and variable coincidence between allergic rhinitis and asthma. The number of reported loci has grown quickly. Earlier GWAS had identified 71 associated loci, and a multi-ancestry analysis later reported 101 genome-wide significant loci, including 15 not previously linked to AD or eczema. Counts differ between reviews of the same work; for the 2015 EAGLE meta-analysis, one source gives 25 loci and another gives 31.

Most of these signals are hard to interpret mechanistically. Most disease-associated variants sit in noncoding regions, which suggests they act on gene regulation rather than on protein structure. Lead variants also often fall within broad haplotype blocks, which makes it difficult to identify the causal gene. Cell-type analyses have pointed to keratinocytes as a key cell population in the disease-relevant GWAS signal.

The question of why no single gene explains most cases is answered in part by the modest size of individual effects. The common variants identified in the 2015 analysis accounted for about 15% of variance. Genetic correlations explain only a small portion of disease variability, and mutations in these genes have also been detected in healthy individuals. Polygenic risk scores, which sum the weighted effects of many variants across the genome, are used to estimate cumulative inherited susceptibility and to test shared risk with asthma and other conditions. Their predictive value for individual patients remains limited.

Epigenetic research addresses why the same genotype can produce different disease expression. Epigenetic modifications are mainly mediated by DNA methylation, histone acetylation, and non-coding RNAs. Reported changes include reduced methylation of the FcεRI and IgE-related genes in peripheral blood mononuclear cells, which increases expression and may alter sensitivity to allergens. In lesional skin, the OAS2 gene in innate immune cells is hypomethylated compared with healthy individuals. Many of these studies are small. One genome-wide profiling study compared 12 patients with 6 healthy volunteers. Another reported that differences in DNA methylation are intra-individual rather than inter-individual, which makes blood a weak surrogate for skin.

Epigenetic marks are also a candidate route for gene–environment interaction. Prenatal benzene exposure, used as a proxy for tobacco smoke, was identified as a possible trigger for NLRP2 promoter hypermethylation and reduced expression. Other exposure studies have linked diesel exhaust and bisphenol compounds to methylation changes in immune and barrier-related genes, though these findings come from limited cohorts. Some authors have proposed that familial inheritance and the rising frequency of AD suggest the disease may be an acquired disorder of epigenetic regulation, but this remains a hypothesis. No targeted therapy aimed specifically at AD epigenetic processes is currently available.

Environmental triggers and the skin microbiome

Climate, heat and sweating

Climate affects eczema mainly as an aggravating factor, and the direction of its effect depends on whether the air is dry or humid. Low humidity (dry air) can cause your skin to become dry and itchy. Clinical guidance also notes that heat may induce perspiration, which is one of the most commonly reported aggravators in children with AD. Itch in general is often worse with dry air, sweating, local irritation, wearing wool garments, and emotional stress.

Population data point in a different direction. Lower eczema prevalence was found in areas with higher relative humidity, higher UV index, higher mean temperatures, lower precipitation and less indoor heating. Patients who already have the disease, however, tolerate higher temperatures poorly, and the mechanisms behind protective effects of warmth are uncertain. The result is that a climate can be protective across a population while still aggravating an individual's skin.

Irritants, soaps and fabrics

Irritants act mainly on skin that is already sensitive. Common examples include strong soaps, detergents, harsh cleaning products, and synthetic fabrics or wool. They can cause mechanical or chemical irritation to already sensitive skin. Excessive washing is also listed among common environmental triggers, alongside harsh soaps and sweating.

Fabric effects are largely a matter of texture and fibre. Cotton is typically recommended for AD patients, since it is soft and breathable. Synthetic fabrics and wool are abrasive and can produce itching and skin irritation. Wool can cause a distinct problem, described as wool intolerance (irritation and itching triggered by skin contact with wool). Tightly woven silk is smooth but closely woven and impedes the flow of air.

Dust mites and other allergens

Airborne allergens matter most for people who are sensitized to them. A house dust mite allergy can also trigger an atopic dermatitis flare-up. In a Brunei cohort, specific IgE levels to house dust mite species were highest in the population and correlated with atopic dermatitis. A Korean study found a sharper pattern: those with atopic dermatitis were sensitized to a broader range of minor allergen components of HDM, whereas respiratory allergy was mostly tied to major components.

Mites may also act without a classic IgE response. HDM itself may trigger atopic flares in patients with AD even without elevated IgE through non allergic mechanisms, and in cultured keratinocytes mite exposure stimulated the expression of IL-22Ra and CCL17/TARC. An older small study found mites on the skin of 8 out of 9 patients, and its authors suggested that mites on the skin could contribute to itching and to sensitization through the skin. Other commonly named allergens include pollens, pet dander, and some foods.

Skin microbiome

Atopic skin differs from healthy skin mainly in its bacterial community. Atopic dermatitis is characterized by a marked dysbiosis, with a sharp decline of microbial diversity. During flares, biofilm-growing Staphylococcus aureus emerges as the major colonizer in the skin lesions, in strict association with disease severity. In a pediatric cohort, Staphylococcus aureus predominance was greater in patients with more severe disease, while Staphylococcus epidermidis predominance was seen in those with less severe disease.

The mechanism is still being studied. One proposal is that the chronic production of inflammatory cytokines in the skin of AD individuals concurs at supporting S. aureus biofilm overgrowth at the expense of other microbial commensals. Colonization is not confined to flares: lesional skin is more frequently colonized by S. aureus than non-lesional skin, with a drastic reduction of microbial diversity, and S. aureus colonization also increases in the skin of AD-susceptible individuals during the remission phase of flare episodes. Measured in absolute numbers, no difference was observed between AD and healthy control skin in the absolute abundances of the common skin bacteria Corynebacterium, Cutibacterium, and Streptococcus in children, which suggests the relative rise in S. aureus reflects its own expansion rather than the loss of other bacteria.

Several further points are relevant. S. aureus produces proteases and toxins that further weaken the already compromised barrier function of the skin. Strains also differ: antibiotic prescribing patterns and within-household transmission between siblings shaped colonizing strains. Fungi show a contrasting pattern, as fungal communities are richer and more diverse on the skin of patients with atopic dermatitis, although distribution of the most common species is similar in patients and controls. Animal work supports a causal role for particular strains, since S. aureus expressing variant virulence factors has been shown to elicit atopic dermatitis-like phenotypes in mice.

Allergy and the atopic march

The atopic march is a descriptive framework for the order in which atopic conditions often appear in one person. The classic sequence starts with eczema in infancy, then moves to IgE-mediated food allergy, and later to asthma and allergic rhinitis. The concept was introduced to describe how allergic disease develops during childhood. Early longitudinal work treated it as a single, fixed trajectory, but later studies showed that the course is more varied, and the sequence is often not clearly visible in individual children. Eosinophilic esophagitis has since been proposed as an additional member of the spectrum.

Food allergy is the link that has received the most attention. Sensitization to foods, meaning the presence of food-specific IgE antibodies, is common in eczema. Estimates range from about 30% to 80% of patients, depending on the population and test used, but clinically relevant food allergy is considerably less frequent, especially in milder disease. In children with eczema, IgE-mediated food allergy has been reported in roughly a third of cases in some series. The leading explanation is the dual-allergen exposure hypothesis. A damaged skin barrier allows food proteins to penetrate and prime IgE production before the infant has developed oral tolerance, which normally results from eating the same foods through the gut. Mouse studies support this route: repeated application of peanut protein to skin induced peanut-specific IgE, whereas feeding the same protein generally induced tolerance. Loss-of-function variants in the filaggrin gene have also been associated with peanut allergy, including in children without eczema, which suggests that a barrier defect can contribute to sensitization through a route that does not depend on visible skin disease.

Links from eczema to respiratory allergy are supported by several large cohorts, though their strength varies. In a cohort of roughly 30,000 children, food allergy was associated with subsequent asthma and allergic rhinitis, with the strongest associations for peanut, milk and egg allergy. In another large retrospective analysis, early-onset eczema was associated with later inhalant sensitization and with asthma, rhinitis and food allergy. Severity appears to matter: one cohort reported asthma in about 70% of children with severe eczema, compared with 20% to 30% of those with mild disease and about 8% of the general population. Allergic rhinitis is often described as preceding asthma and as an independent risk factor for it, and in asthmatic children, treating rhinitis has been associated with fewer asthma-related hospital visits. Mouse experiments in which aeroallergens were applied to the skin have produced airway hyperresponsiveness, lending experimental support to a skin-to-airway route.

Positive test results do not by themselves establish clinical allergy. Sensitization is a prerequisite for IgE-mediated food allergy but is not the same thing. In young patients with eczema who had elevated food-specific IgE, only about 30% to 40% reacted in double-blind, placebo-controlled food challenges. Co-sensitization to several allergens does not in itself indicate clinical allergy, and unnecessary dietary restriction can affect a child's nutrition. For this reason, the oral food challenge is regarded as the reference standard for diagnosing food allergy, and results are interpreted alongside the clinical history.

Whether allergy causes eczema, whether eczema precedes and predisposes to allergy, or whether both reflect a shared predisposition remains debated. The multimorbidity view holds that co-occurrence of eczema, asthma and rhinitis does not by itself imply a progressive or causal sequence. A cohort in which parents reported symptoms found that only about 10% of children followed the traditional pattern, while many had persistent eczema alone or respiratory symptoms without eczema. Some reviewers argue that current evidence favors eczema predisposing to food allergy rather than the reverse, with food allergens acting mainly as triggers of flares. The progression from food allergy to asthma in children without eczema is unresolved: it could be causal, or it could reflect shared environment or genetics. Work on the skin-gut axis suggests that skin inflammation may influence the intestine through circulating signals and microbiome changes, which could account for links to food allergy that go beyond sensitization alone.

Rising prevalence and theories of causation

The hygiene hypothesis is the most frequently cited explanation for the rise in atopic disease. It was first advanced in 1989 and has been revised several times since The hygiene hypothesis, proposed in 1989, has undergone significant revisions and modifications.. David Strachan's original version pointed to infections that children picked up from older siblings as a possible safeguard against immune-related conditions Strachan initially suggested that the exchange of early childhood infections between siblings could protect against immune-related diseases. A later "revised" form moved the focus from particular pathogens to microbial contact in general, arguing that the decline of common childhood infections such as hepatitis and tuberculosis has increased susceptibility to allergic disease the 'revised' hygiene hypothesis states that the decrease in early childhood exposure to prototypical infections (e.g. hepatitis and tuberculosis) and, by extension, in any microbial exposure has increased the susceptibility to allergic disease.

The direct evidence is uneven. In a case-control study of children aged 1 to 5 in Norfolk, UK, one older sibling was associated with substantially lower odds of atopic dermatitis (odds ratio 0.59) Reduced odds of AD were associated with rising birth order (OR for one older sibling 0.59, 95% CI: 0.42, 0.84 and for ≥2 older siblings 0.49, 95% CI: 0.31, 0.77).. A review of the broader literature found a convincing inverse relationship only for helminth (parasitic worm) infections, with no consistent protection from other pathogens There is convincing evidence for an inverse relationship between helminth infections and AD but no other pathogens.. Several associations, including those with day care, endotoxin exposure, and unpasteurised farm milk, are thought to reflect a general increase in exposure to non-pathogenic microbes rather than protection from specific infections The protective effect seen with early day care, endotoxin, unpasteurized farm milk and animal exposure is likely to be due to a general increase in exposure to non-pathogenic microbes.. Antibiotic use is the most consistent counterpoint: it has been linked to higher AD risk, and the reviewers proposed that this reflects microbiota disruption This would also explain the risk increase associated with the use of broad-spectrum antibiotics.. Gut microbiota studies have reported that children who later develop AD differ from their peers in composition and diversity the early gut microbiota of children who develop atopic dermatitis later in life is different from that of children who do not develop atopic dermatitis, both in terms of composition, and diversity.. Mediation analyses in a German high-risk birth cohort suggested that cesarean delivery raised AD risk indirectly through microbial changes, while older siblings were associated with a more favourable microbiota mediation analyses confirmed a statistically significant indirect effect of cesarean section delivery, via microbiota pertubations (increase in Clostridium Cluster I), on atopic dermatitis risk. Moreover, this study demonstrated a "beneficial" influence of older siblings on the microbiota composition subsequently linked to a lower risk of atopic dermatitis..

Urban living has been studied as a proxy for a set of exposures rather than as a cause in itself. A systematic review of 26 studies found Nineteen showed a higher risk for eczema in an urbanized area, of which 11 were significant. The authors judged the evidence as suggestive only, and a pooled relative risk was not calculated A pooled relative risk could have been calculated but was not because of heterogeneity.. Other studies have found no difference: a survey of Aceh, Indonesia, reported almost identical prevalence in urban and rural schoolchildren, and a separate analysis of metropolitan and non-metropolitan areas found no significant variation When stratifying by residency, the prevalence of ES in urban and rural area was 20.93% versus 21.05%.. Candidate explanations for urban excess include family size, outdoor air pollution, tobacco smoke, domestic animals, maternal age, and more indoor lifestyles Potential explanations for the risk implicated in living in urban versus rural areas may include differences in family size; exposure to outside air pollution, tobacco smoke, and domestic animals; maternal age; and indoor versus outdoor lifestyles.

Larger cohorts have begun to separate these factors. In the UK Biobank cohort of more than 300,000 adults, air pollution, noise, traffic load, and urban residence were each associated with incident AD, while green space and private gardens were protective Overall, composite air pollution exposure, noise, urban residential, and traffic load significantly increased AD risk, whereas natural environment coverage and domestic gardens were protective.. The same study stratified participants by polygenic risk score and reported dose-dependent associations Moderate and high air pollution mixtures were significantly associated with a higher AD risk, showing dose-dependent relationships.. Meta-analytic evidence for air pollution is strongest for particulate matter: most studies of PM2.5 found increased medical visits for AD, while ozone results were mixed exposure to particulate matter ≤2.5 μm in diameter (PM_2.5) [(10/11) of studies], particulate matter ≤10 μm in diameter (PM_10) (11/13), nitrogen dioxide (NO_2) (12/14) and sulfur dioxide (SO_2) (10/13) was positively associated with AD visits. Results were equivocal for ozone. An umbrella review ranked antibiotic exposure, smoking, and air pollution as the most robust environmental risk factors across age groups Antibiotic exposure, smoking, and air pollution are the most robust environmental risk factors for AD across age groups, whereas other exposures require further investigation.. Diet and other lifestyle variables, by contrast, have far less consistent data.

Attributing changes in prevalence to any single exposure is difficult for several reasons. Many studies are cross-sectional, and their results on air pollution are not consistent Epidemiologic studies overall report that air pollution is associated with AD among both children and adults, though the results are not consistent among cross-sectional studies.. Designs, exposure measurement, and outcome definitions vary widely across the literature, which makes it hard for clinicians to judge how much a given exposure matters However, considerable variation in study design and heterogeneous results make it difficult for clinical dermatologists to judge the true relevance of air pollution as a risk factor for skin diseases.. Genetic change also cannot account for the speed of the rise: the increase in the second half of the twentieth century happened too quickly to be attributable to changes in allele frequencies, which points to environmental drivers, but that observation does not identify which environmental factor is responsible. Correlations with latitude and birth season have led researchers to examine UV light intensity as well as microbial exposure Various environmental factors, such as lack of childhood exposure to pathogens (the 'Hygiene Hypothesis') and UV light intensity, have been put forward to explain these phenomena..

Evidence for several proposed causes remains inconsistent or contested. Direct tests of the hygiene hypothesis have produced mixed results Direct evidence for the hypothesis to date is inconsistent.. The association between household air pollution from indoor fuels and AD, once thought to be modest, weakened after correction for publication bias; the authors concluded that the earlier signal may be a statistical artifact After rigorous adjustment for publication bias, the available published evidence does not support the conclusion that indoor fuel use is an independent risk factor for atopic dermatitis. The weak association observed in the literature appears to be a statistical artifact, potentially influenced by systemic publication bias.. Hygiene-related behaviour is also unresolved: in the Aceh study, partial ablution was associated with reduced eczema symptoms, a finding that the authors connected to the epidermal barrier hypothesis rather than to microbial exposure Partial ablution was independently associated with a reduced risk of ES (OR = 0.36; 95% CI 0.13–0.96)..

Emollients, skin care, and basic management

Emollients as the foundation of care

Regular emollient use is the base layer of management in most guidelines. The European guideline recommends applying emollients daily and generously, and it suggests applying them right after bathing with gentle patting to dry the skin, the so-called soak-and-seal technique (We recommend daily use of emollients, liberally and... We recommend to apply emollients immediately after bathing or showering and soft pat drying). Its expert-consensus grading places several of these practical points on a consensus basis rather than on trial results. The main effects are on secondary prevention: regular application of moisturizers containing emollients, humectants, and occlusive ingredients has been shown to enhance barrier function and reduce the need for topical corticosteroids, and may prolong the interval between flares.

The evidence on primary prevention is less consistent. In high-risk newborns, daily emollients reduced atopic dermatitis and allergic sensitization in the first year in some trials, but two larger and longer randomized controlled trials with a less stringent intervention did not confirm these effects. Cost is a further consideration, since the relatively high cost of emollient treatment compared with a regular infant skin-care routine argues for more evaluation in unselected populations.

Product choice is driven more by tolerability and preference than by proven superiority. Two systematic reviews concluded that emollients were beneficial in the treatment of atopic dermatitis, but that there was insufficient evidence to recommend one over another. Practical guidance favors hydrophilic formulas in summer and lipid-richer products in winter (We suggest using moisturizers with a hydrophilic formula in the summer and moisturizers with a higher lipid content in the winter), and products containing food proteins are not usually recommended due to concerns related to the risk of allergic sensitisation. Some national recommendations also specify weekly quantities, such as the Polish guidance of 250–500 g per week for adults.

Bathing practices and dilute bleach baths

Guidelines advise against alkaline soaps in patients with atopic eczema, and they favor gentle cleansers without potent irritants or relevant allergens (gentle cleansers that do not contain potent irritants or relevant allergens).

Dilute bleach baths, typically containing sodium hypochlorite at about 0.005%, are the most studied bathing adjunct. Dilute bleach baths have become a common and inexpensive adjunctive therapy for maintaining control in patients with moderate-to-severe atopic dermatitis and were recommended in the 2014 American Academy of Dermatology guidelines. Their rationale rests on reducing Staphylococcus aureus colonization, yet laboratory work found that survival of S. aureus at concentrations between 0% and 0.01% was not significantly different, which suggests the clinical effect may not be antibacterial in the simple sense.

Clinical findings are mixed. An earlier set of reviews narratively synthesized observational data along with 5 randomized controlled trials and were uncertain whether they provided added benefit above usual bathing practices with water only. A later meta-analysis of 307 patients with moderate-to-severe disease reported moderate-quality evidence that dilute bleach baths reduce clinician-reported AD severity by a relative 22%. By contrast, the evidence for bacterial reduction or patient-reported benefit is weaker, with low certainty evidence that bleach baths reduce Staphylococcus aureus colonisation or patient-reported improvement in severity. Side effects are generally modest; some patients report skin dryness, pruritus, and, if used when the skin is highly excoriated or infected, stinging or burning. Long-term data are limited, since only 2 studies have tested the impact of the approximately 10-minute baths beyond 4 to 6 weeks.

Avoiding triggers, clothing, and laundry

Patients are commonly asked to record which situations precede their flares, since common triggers include hot temperatures, sudden changes in temperature, environmental allergens, pet dander, and others. Fragranced personal products are a frequent culprit, as perfumes or scented body lotions, shower gels, shampoos or creams can trigger an eczema flare.

Clothing advice is largely consistent across sources. Dermatologists generally advise loose-fitting 100% cotton clothing and never wearing wool next to the skin. Labels and seams are a practical concern, so clothing without tags is preferred, and seams that irritate can be covered with a soft layer. New garments are usually washed before first wear (wash new clothes before wearing them).

For laundry, the usual recommendation is a fragrance-free and dye-free detergent (use laundry detergent that is fragrance free and dye free). Fabric softeners and dryer sheets are commonly avoided, because they are often formulated with synthetic fragrances that frequently irritate eczema-prone skin. Residue is another issue: detergent residues build up over multiple washes, and to minimize this, half the recommended amount of detergent and an extra rinse cycle can be used. Fragrances, optical brighteners, and softeners are more often implicated than enzymes, although this point rests on sources of mixed quality.

Patient education and recognizing flares

Education centers on helping patients apply moisturizer on a routine schedule and act early. A practical tip is to apply moisturizer immediately after bathing. Patients should also understand that mild disease may be controlled with a thick moisturizer most of the time, while many people with eczema need a topical ointment or cream to help with the itch. When symptoms persist after changes to bathing and laundry routines, clinicians generally recommend review, because some other culprit could be responsible for symptoms. Structured programs for families are discussed separately in this entry.

Topical anti-inflammatory therapy

Topical corticosteroids (TCS) remain the most widely used anti-inflammatory agents for eczema. They are sorted into seven classes, from very low/lowest potency (VII) to very high potency (I), based on vasoconstriction assays, so the ranking reflects how strongly a preparation narrows skin blood vessels rather than a direct clinical benefit. The same molecule can behave differently depending on its vehicle and site: ointments are more potent than creams or lotions, and potency increases when TCS are used under occlusive dressings or in intertriginous areas. Current guidance therefore matches the agent to the body region. For adults, the AAD guideline summary advises selecting the potency by anatomical site, and considers a high- or very-high-potency agent for controlling flares in severe disease.

For acute flares, the principle is to use enough potency to regain control quickly and then step down. During significant acute flares, mid- or higher potency TCS for short courses may be appropriate to gain rapid control of symptoms, even in children. The class I agents are the exception: efficacy and side-effects are greatest with the Class I ultra high potency preparations which should only be used for limited time periods (2–3 weeks). For long-term management, the least potent corticosteroid that is effective should be used to minimize the risk of adverse effects. Medium-potency agents are generally reserved for extended courses because their adverse-effect profile over time is more favourable than that of stronger preparations.

Topical calcineurin inhibitors (TCI) provide a steroid-sparing alternative. Tacrolimus ointment (0.03% or 0.1%) is recommended for adults with AD, while pimecrolimus 1% cream is used for mild-to-moderate disease. In a meta-analysis of 25 randomized trials, tacrolimus 0.1% was as effective as the mid-potency TCS hydrocortisone butyrate 0.1%, and in a comparison of tacrolimus with low- and mid-potency steroids, tacrolimus 0.1% was better than low-potency TCS on the face and neck areas and moderate-potency TCS on the trunk and extremities. Their main clinical role lies in sensitive sites: the face, eyelids, and intertriginous areas may be more sensitive to the adverse effects of corticosteroids. Because long-term TCI use does not carry the risks of skin atrophy, impaired epidermal barrier function or enhanced percutaneous absorption, they are used where thinning of the skin would be most harmful.

Concern about malignancy has shaped their use. In March 2005, the FDA posted a Public Health Advisory regarding the potential cancer risk from the use of tacrolimus and pimecrolimus products, and in January 2006 the US Food and Drug Administration issued a boxed warning requirement based on a theoretical risk of malignancy (including lymphoma) with TCI use. Subsequent analyses have failed to demonstrate a causal relationship between TCI use and malignancy or lymphoma risk, especially for pimecrolimus cream. Nonetheless, the warning has left some clinicians reluctant to prescribe these drugs, which has pushed some patients toward agents with more established adverse-effect profiles.

Proactive (intermittent) therapy addresses relapse after the initial flare is controlled. It is defined as long-term, low-dose intermittent application of anti-inflammatory drugs to previously affected and now clinically healthy-looking skin combined with daily application of emollients to always unaffected areas. In a 2002 randomized, double-blind trial of 348 patients, Hanifin and colleagues found that patients proactively receiving 0.05% fluticasone cream were 7.7 times less likely to have an AD relapse than those receiving placebo. A 2003 trial by Berth-Jones and colleagues reported a median time to relapse from 6 weeks for emollient alone vs >16 weeks for both active preparations. The evidence for TCI is thinner: a pooled analysis of two randomized trials found that sequential therapy with TCS/TCI was comparable to monotherapy or emollients, and the authors noted that only two studies satisfied this criterion and were included in the pooled analysis. Failure to gain control at the outset also matters: across 14 randomized trials, failure to achieve control of AD symptoms with initial therapy was associated with a higher risk of relapse. Uptake outside Europe and North America has been uneven; one review noted that the studies demonstrated 'proactive therapy' efficacy has been done mainly in Caucasian subjects instead of in Chinese population.

Newer non-steroidal topical agents broaden the options for patients who cannot use steroids or calcineurin inhibitors long term. Phosphodiesterase-4 (PDE4) inhibitors, such as crisaborole and roflumilast cream, reduce inflammatory signalling within keratinocytes and immune cells by blocking the breakdown of cyclic AMP. Aryl hydrocarbon receptor (AhR) agonists, such as tapinarof, act on a receptor that regulates skin barrier and inflammatory gene programmes. These agents are generally used on mild-to-moderate disease and as steroid-sparing options, and their role in maintenance therapy continues to be defined by ongoing clinical study.

Systemic and biologic treatment

Systemic therapy is reserved for moderate-to-severe atopic dermatitis that does not respond adequately to topical treatment. Options fall into three groups: older immunosuppressants, targeted biologics, and oral JAK inhibitors. Corticosteroids given by mouth are handled separately because guidelines now advise against them for routine use.

Conventional immunosuppressants

Cyclosporine, methotrexate, azathioprine and mycophenolate were the main systemic drugs before targeted agents appeared. Cyclosporine is the most studied. In a head-to-head trial it outperformed methotrexate for up to 16 weeks, after which the two were similarly effective, and a network meta-analysis placed cyclosporine at 3–5 mg/kg per day above methotrexate and azathioprine. The evidence for all four drugs rests largely on small trials and carries low or very low certainty. Cyclosporine is licensed for atopic dermatitis in several European countries but not by the US FDA, and in the US it is approved only for short-term use in psoriasis. Methotrexate is typically dosed at 10–25 mg weekly, and mycophenolate is generally reserved for refractory cases. All four require baseline and ongoing laboratory monitoring of blood counts, kidney and liver function, and lipids, and comorbidities or interacting drugs can make them unsuitable for some patients. Guideline opinions diverge: the 2023 American guideline gives conditional support to mycophenolate in refractory adults, whereas the 2023 AAAAI/ACAAI joint task force suggests cyclosporine over continued standard care and advises against mycophenolate.

Biologics

Four monoclonal antibodies are approved for moderate-to-severe disease in Europe and the US. Dupilumab binds the IL-4 receptor alpha subunit and so blocks signalling from both IL-4 and IL-13. It was approved for adults in 2017, for adolescents in 2019, and in 2023 in Europe for children from six months of age in severe disease. Tralokinumab and lebrikizumab instead neutralise IL-13, binding it at different sites. Tralokinumab was approved in 2021 for adults, and lebrikizumab in Europe in 2023 for patients aged 12 and older weighing at least 40 kg; the FDA approved lebrikizumab in 2024. Nemolizumab, an antagonist of the IL-31 receptor alpha subunit, targets the itch pathway and was approved in 2024 for adults and adolescents. Its pivotal trials tested it mainly alongside topical agents. Dupilumab has the broadest efficacy data, followed by lebrikizumab, with more modest responses for tralokinumab in network analyses. Dosing usually includes a loading phase, for example dupilumab 600 mg followed by 300 mg every two weeks and lebrikizumab 500 mg at weeks 0 and 2 followed by 250 mg every two weeks. Conjunctivitis and injection-site reactions are among the frequently reported effects of these agents.

Oral JAK inhibitors

Upadacitinib and abrocitinib, both JAK1-selective, were the first oral JAK inhibitors approved for atopic dermatitis; the FDA authorised them in January 2022 for patients aged 12 and older. Baricitinib was approved in Europe and Japan in 2020 for adults, at 2 mg and 4 mg daily, but has not been approved for this indication in the US. Because JAK inhibitors act on several cytokine pathways, their use requires baseline screening for latent tuberculosis, attention to active infection, and caution in patients at risk of thromboembolism. Blood counts, liver enzymes and lipids are monitored routinely. Abrocitinib has been reported to relieve itch more quickly than dupilumab in indirect comparisons, though long-term safety data are still accumulating. Because of the safety warnings attached to this class, JAK inhibitors are often reserved for patients who have not responded adequately to biologics.

Systemic corticosteroids

Current guidelines advise against routine systemic corticosteroids in adults with atopic dermatitis. The 2023 American guideline conditionally recommends against them and limits their use to acute, severe exacerbations as a short bridge to a corticosteroid-sparing systemic therapy. Long-term use is discouraged because of its adverse effects, and the same position was carried into the 2025 American update.

Phototherapy, immunotherapy, and other procedural treatments

Phototherapy

Ultraviolet therapy is used for moderate-to-severe atopic dermatitis (AD) when topical treatment is insufficient. Narrowband UVB (NB-UVB), with its output centred at about 311–313 nm, is the most widely used regimen. Compared with broadband UVB, it causes less erythema and, according to dermatology reviews, has longer-lasting efficacy with less photodamage and carcinogenic concern. Medium-dose UVA1 (MD-UVA1) is the other principal option. In a split-body comparison of 9 patients with chronic AD, NB-UVB and MD-UVA1 both reduced dermal inflammatory infiltrate and clinical severity to a similar degree, although the study used a three-times-weekly UVA1 schedule rather than the preferred five-times-weekly one. Evidence-based reviews therefore regard the two as roughly equivalent in efficacy, with UVA1 often preferred for acute flares and NB-UVB for chronic lichenified disease, especially in adults. For children, NB-UVB is generally placed second-line because of concern about long-term adverse effects.

The mechanisms are only partly understood in AD. In psoriasis, NB-UVB suppresses Th1 and Th17 polarization and reverses epidermal hyperplasia. In a 2010s study of AD patients treated with NB-UVB, Tintle and colleagues reported suppression of Th2, Th22 and Th1 pathways, normalization of epidermal hyperplasia and barrier-protein expression, and clearance of inflammatory leukocytes; every patient achieved at least a 50% reduction in SCORAD. Practical drawbacks include the frequent clinic visits required, cumulative cost, and long-term carcinogenic risk, which is most clearly documented for psoralen plus UVA (PUVA) in children treated for psoriasis. UVA1 may aggravate itch and sweating; in one open study, air-conditioned NB-UVB was used for this reason and produced a 68% fall in severity scores together with an 88% reduction in topical corticosteroid use. Photochemotherapy (PUVA) combines an oral or topical psoralen, a photosensitizer, with UVA exposure; its use in AD has declined as NB-UVB and UVA1 have become preferred.

Allergen-specific immunotherapy

Allergen-specific immunotherapy (AIT) is the only approach that targets the sensitization itself rather than the downstream inflammation. It is given by subcutaneous (SCIT) or sublingual (SLIT) routes and is restricted to patients whose AD is linked to clinically relevant sensitization, most often to house dust mite (HDM), and less often to grass pollen or animal dander. One review estimated that around 80% of adult patients fall into a subgroup with aero- or food-allergen sensitization, which is the population in which AIT has been studied.

The most comprehensive evidence comes from a systematic review and meta-analysis of 23 randomized controlled trials involving 1,957 patients, prepared for the 2022 AAAAI/ACAAI practice parameter. Add-on SCIT and SLIT produced similar improvements in SCORAD, with a 50% reduction achieved by 40% of treated patients compared with 26% of controls, and improved quality of life. Both routes increased adverse events, with 66% of SCIT recipients and 13% of SLIT recipients reporting them, against 41% and 8% in placebo groups. Effects on sleep disturbance and eczema flares were judged very uncertain. Earlier trials had produced mixed results. Immunological studies have linked benefit to a tolerogenic IgG4 response to mite allergens, and a 2024 cohort comparing AIT, dupilumab and their combination described AIT as offering disease-modifying, long-term effect, while dupilumab gave faster symptom control.

Wet wrap therapy and other adjunctive measures

Wet wrap therapy (WWT) applies topical corticosteroids under a layer of wet cotton bandages or garments, which is then covered by dry clothing. The usual method is to soak, pat dry, apply an emollient and/or steroid, add the damp layer, and keep it moist. Because it is labour-intensive and carries a risk of infection, it is used for severe flares, under medical supervision, for short periods, and with the skin observed for signs of infection. Wet cotton can also be abrasive when it stretches and contracts. A less intensive alternative, "soak-and-smear," involves a short soak followed by an occlusive emollient and has also been shown to be effective acutely.

The evidence base is limited. A systematic review and meta-analysis of six trials, with 19 to 51 patients each, found that results on severity and quality of life were incomplete and heterogeneous, and the grade of evidence was low; a non-significant trend toward more mild skin infections was observed. A larger paediatric study of 72 children with moderate-to-severe AD found that WWT lowered SCORAD by about 21 points more than dry medication, with the benefit described as acute. In severe, refractory cases in children, diluted corticosteroids used under wet wraps for up to 14 days were reported as safe, with systemic corticosteroid activity as the main serious adverse effect. The mechanism is presumed to involve restoration of the epidermal barrier, and a study measuring this found increased epidermal water content and reduced transepidermal water loss after treatment.

Structured education programmes

"Eczema schools" are group-based educational courses for patients, particularly children, and their caregivers, run by nurses, dermatologists or allied health staff. Their content typically covers daily skin care, correct emollient and corticosteroid use, avoidance of identified irritants and triggers, and recognition of early flares, with the aim of improving self-management. Their place in clinical care is best understood as a supplement to pharmacological treatment rather than a replacement for it.

Infections and complications

Skin affected by eczema is unusually open to microbes. Inflammation that damages the epidermal barrier makes it easier for microorganisms to colonize the skin, and scratching, detergent contact and other environmental stresses add to this effect. Epidermal barrier damage by an inflammatory process facilitates colonization by microorganisms. Mechanical damage by scratching, environmental factors, and contact with detergents contribute to bacterial colonization as well. Lower ceramide levels and a shift in lipid composition also favour bacterial growth, and elevated pH is observed on the surface of the atopic epidermis, often reaching up to 8.00. The dominant organism is Staphylococcus aureus, with more than 90% of patients being colonized in one review, although a later summary gave a range of 46% to 80%, compared with approximately 10% of nonatopic patients. Carriage is heavier in more severe disease, and the reduction in SCORAD scores correlated with the reduction of S aureus numbers.

Clinical infection is suspected when a flare resists normal therapy, and obtaining a bacterial culture of involved skin before starting antibiotics is helpful. Signs of secondary bacterial infection include honey-yellow crusting or pustules. Antibiotic choice depends on the extent of disease. In cases of atopic dermatitis exacerbation with wide-spread weeping lesions, a systemic antibiotic treatment is warranted, with erythromycin no longer being recommended due to an increased resistance rate. For localized superinfected lesions, the topical application of an antibiotic-glucocorticoid preparation may offer advantages to the mere steroid application. In a 1998 review, based on efficacy and resistance data, fusidic acid is the antibiotic of choice. Oral antibiotics for clinically infected lesions should be guided by culture and sensitivity results, and topical anti-inflammatory treatment should continue alongside them.

Current practice increasingly favours restraint. In a randomized study of sixty patients, an 8-week treatment with topical 0.05% fluticasone propionate or 0.03% tacrolimus, with or without complementary fusidic acid was compared. Treatment with topical tacrolimus resulted in a comparable reduction in SCORAD scores to fluticasone but a slower eradication of S aureus. Complementary fusidic acid had no additional benefit compared with fluticasone or tacrolimus alone. The authors concluded that topical anti-inflammatory therapy alone to improve the allergic skin inflammation of AD can reduce S aureus colonization of the skin. Resistance is a further reason for caution. In a Korean study, S. aureus showed the highest resistance rate to benzylpenicillin followed by fusidic acid. For recurrent infection, decolonization includes treatment with intranasal mupirocin in isolation or in combination with either chlorhexidine or dilute bleach baths. Investigational agents aim to reduce bacterial load while sparing the commensal flora; a phase 2 trial of topical niclosamide reduced Staphylococcus aureus colonization and increased Shannon diversity of the skin microbiome in atopic dermatitis patients.

Eczema herpeticum is the most serious viral complication. Herpes simplex viruses (HSV), particularly HSV-1, is a common cause of eczema herpeticum. The infection can rapidly disseminate in the setting of atopic dermatitis and, rarely, progress to involve multiple organ systems, including the central nervous system. Without antiviral treatment, the mortality rate is 10 to 75%, which is why antiviral therapy should begin as soon as the condition is suspected. Acyclovir (ACV) is the first-line drugs for treatment of HSV infections since the 1980s. The recommended intravenous regimen is five to 10 mg/kg of intravenous ACV, 3 times daily, for 5 to 7 days, and oral valacyclovir is an option. Ocular spread is the main concern: herpetic keratitis can cause corneal scarring and permanent visual loss. The differential diagnosis includes chickenpox, impetigo, eczema vaccinatum, and contact dermatitis. A similar-looking enterovirus rash, eczema coxsackium, is managed supportively, because antivirals are not indicated since the cause is enterovirus rather than HSV.

Molluscum contagiosum is another viral trigger. In a 2018 study of children, fifty children with prior or current MCV infection presenting sequentially to an outpatient pediatric dermatology practice over a 1-month period were evaluated. In a subset, MCV infection appears to aggravate atopic dermatitis (AD) symptoms, and in susceptible children the first onset of AD symptoms can occur during the course of MCV infection. Such flares are sometimes called molluscum dermatitis. Molluscum lesions in children with eczema tend to be more persistent, more extensive, and approximately 10% of affected patients develop eczematous dermatitis around the molluscum contagiosum lesions. Not all studies agree: one report concluded that atopic dermatitis does not exacerbate molluscum morbidity, inflammation markers, treatment outcomes or recurrence rates. Treatment is also debated; taking efficacy, cost, adverse effects, ease of use, and availability into consideration, curettage is the preferred option in pediatric patients.

Fungal superinfection is less often the focus of trials. Yeasts of the genus Malassezia and dermatophytes can colonize or complicate chronically inflamed skin, and a fungal cause should be considered when lesions fail to respond to anti-inflammatory treatment or show a sharply defined, ring-like edge. Antiseptics such as dilute bleach and chlorhexidine are used mainly for decolonization of recurrent infection rather than as routine additions to every flare, and whether they add benefit beyond anti-inflammatory treatment remains debated.

Psychological, social, and quality-of-life impact

Sleep loss and daytime functioning

Disturbed sleep is one of the most consistently documented burdens of childhood eczema. Reviews estimate that up to 60% of affected children have disturbed sleep, a share that rises to 83% during flares. Quality of life is also affected in remission: children whose eczema is quiet still show more sleep disturbance than healthy children. Sleep disturbance affects up to 60% of children with eczema, increasing to 83% during exacerbation. Even when in clinical remission, children with eczema demonstrate more sleep disturbance than healthy children.

Polysomnography has clarified what this disturbance looks like. In one small study of 21 children with eczema and 20 controls, overnight recordings showed more time awake during the night, and neurocognitive testing gave a composite score about 16 points lower than in controls. The authors found that eczema status predicted cognitive performance, whereas measures of sleep fragmentation did not. In a parent-reported study of 77 children with eczema, the association between eczema and hyperactivity and oppositional behaviour appeared to run through poor sleep rather than through the skin disease directly. Family life is affected as well: a study from Uruguay reported that atopic eczema impaired quality of life in children of every age group examined, and in their families.

Mental health and stigma

Several meta-analyses have linked atopic dermatitis with depression, anxiety, and suicidal thoughts. In a 2018 review covering children and adults, AD was also associated with depression in children (pooled OR, 1.27; 95% CI, 1.12-1.45); few data were available for anxiety. The same analysis found a positive association between AD in adults and adolescents and suicidal ideation (pooled OR, 4.32; 95% CI, 1.93-9.66). A later meta-analysis reported that stress, depression, anxiety, and suicidal ideation were considerably more frequent in individuals with AD than in healthy ones. Severity appears to matter: more severe AD disease is linked to higher rates of anxiety and depression, severe pruritus, and decreased sleep.

The evidence is not uniform. A Danish general-population study found associations with anxiety, depression, and suicidal ideation in adults, but there was no increased risk of hospitalization or outpatient contacts due to depression or anxiety, or risk of suicide in AD patients. Researchers also note that the true extent and precise pathogenesis of psychological involvement in AD patients remain unclear.

Stigma is a recurring theme. Visible lesions can attract unwanted attention, and children may get bullied or feel socially isolated because of their skin's appearance.

Economic costs

The costs of eczema fall on patients, families, employers, and health systems. In US adults, annual all-cause total direct health care costs for US adults diagnosed with AD were $10,474 per patient per year from 2016 to 2018. Costs rise with disease severity: patients with severe disease had significantly higher all-cause annual health care costs ($23,242) than patients with clear to mild disease ($8,936).

In European analyses, indirect costs often outweigh medical spending. One study estimated the mean annual total cost per patient ranged from €0 to €29,783, with an average cost of €4,331. Productivity losses were central: absenteeism and presenteeism were the main cost drivers, accounting for 24% and 29% of the total cost of AD. For children, caregiver time is a major component. A Romanian estimate found that productivity costs (inquired by caregivers) had the highest share for pediatric AD patients. Because many patients have milder disease, the overall societal burden is large even though per-patient costs are lower than in severe cases. Estimates differ widely by country, perspective, and currency, so cross-study comparison requires caution.

Measuring quality of life

Clinical research relies on disease-specific, patient-reported instruments. The Children's Dermatology Life Quality Index (CDLQI) was initially validated in 1995 and is widely used for school-aged children. Adult studies more often use the Dermatology Life Quality Index (DLQI). Studies of younger children frequently rely on parents as proxies, and sleep is often assessed with separate questionnaires alongside quality-of-life scales. Systematic reviews of instruments for infants, children, and adolescents with eczema have been undertaken to assess their measurement properties, including self- and proxy-reported tools. Higher DLQI scores have been associated with significantly higher total, direct medical, and indirect costs in adults, which links patient-reported burden to economic outcomes.

Special populations and prevention

Infants: emollients and early allergen introduction

Trial evidence on infant skin care is inconsistent. The BEEP trial enrolled 1394 term infants with a family history of atopic disease. At five years, regular emollients had not prevented atopic dermatitis, food allergy, asthma or allergic rhinitis. The STOP-AD trial, which began a specialised emollient in the first week of life and continued it to two months, instead reported a cumulative incidence of AD at 12 months of 32.8% in the intervention group vs. 46.4% in the control group. A pragmatic trial of 1247 infants not selected for risk found a 16% reduction in overall AD incidence at age 2, with the largest effect in children at low risk. Some trials also recorded more skin infections in emollient-treated infants, a result the authors linked to possible transfer of pathogens or disruption of the skin microbiome, suggesting that application of emollient can also assist inoculation of pathogens on the infant skin.

Allergen introduction has firmer support for food allergy than for eczema itself. The LEAP trial recruited infants aged 4–11 months with severe eczema or egg allergy, and early exposure to peanut reduced peanut allergy risk by 81%, with protective effects sustained beyond early childhood. Population-based data show a weaker effect, possibly because only 24% of infants had eczema in that setting. In the HealthNuts cohort, 23% of peanut allergy cases occurred in infants without early onset eczema or egg allergy. US guidance has responded accordingly: the NIAID addendum recommended preemptive testing before peanut introduction for infants with LEAP risk criteria, a recommendation the AAP supports while noting limits on population-wide screening. Allergy societies such as ACAAI now advise that most infants begin eating peanut-containing foods around 4 to 6 months of age.

Pediatric treatment considerations

Age limits and dosing are set product by product in drug labelling, and approvals differ between countries and between agents. Clinicians therefore check the current label for the specific age group before prescribing. In infants, topical corticosteroids are generally chosen at lower potency and applied to limited areas, while calcineurin inhibitors and systemic agents are used under specialist supervision.

Pregnancy and breastfeeding

Topical therapy has the most reassuring safety data. Topical corticosteroids are regarded as low risk, and TCIs are considered safe during pregnancy and lactation when used intermittently on a limited body surface area. Narrowband UVB is a safe therapeutic option during pregnancy and lactation, particularly when TCS alone are ineffective. Low-dose ciclosporin is regarded as acceptable when topical treatment and phototherapy fail, with infant serum levels monitored during breastfeeding.

Systemic data are thinner. Dupilumab is not licensed for use in pregnancy, yet a retrospective analysis of exposure before or during the first six weeks of pregnancy found no significant drug‐associated risk for adverse pregnancy, congenital, neonatal, or post‐partum outcomes during the first trimester. Because Th2-blocking agents may shift immune balance toward Th1 responses, which have been linked to pre-eclampsia and preterm birth, caution should be taken when choosing a treatment option targeting Th2 inflammation. In an international physician survey, systemic corticosteroids for acute flares were the most frequent choice, and dupilumab was the most commonly preferred biologic.

During breastfeeding, short-term systemic glucocorticoids are considered safe, since only 0.1% of the dose taken by the mother is excreted in breast milk. Methotrexate, azathioprine and JAK inhibitors pass into milk and may suppress the newborn's immune system, so they are generally not recommended for breastfeeding mothers. The German S3 guideline states that JAK inhibitors and mycophenolate should not be used while breastfeeding, and that there is currently insufficient clinical data available to make a recommendation for the use of the biologics dupilumab, lebrikizumab, nemolizumab, and tralokinumab in breastfeeding mothers. Topical agents should be kept away from the nipple and areola, since an infant may ingest drug directly.

Primary and secondary prevention

Primary prevention aims to stop eczema from developing, mainly through infant emollients and early allergen introduction. Secondary prevention, which aims to limit progression and further allergic disease in children already affected, has the same mixed evidence base. The BEEP authors suggested that asthma, allergic rhinitis and wheeze may be best considered co-morbidities rather than sequential development of similar diseases, which would weaken the case for preventing eczema as a route to preventing other allergic conditions. A review concluded that emollient treatment has a good safety profile, but also noted that the relatively high cost of emollient treatment (vs regular infant skin-care routine) would support the necessity for further evaluation of their effectiveness in nonpredisposed populations.

History and development of the concept

Skin eruptions resembling eczema have been described since antiquity. Dermatology historians trace precursors of atopic dermatitis to the first and second centuries CE, but for most of medical history the word itself was used loosely, for almost any itchy, weeping or scaly rash. Robert Willan and Thomas Bateman narrowed the term around 1800 to mean an eruption of minute vesicles. This was a description of appearance, not of cause, and critics at the time faulted the scheme for not distinguishing etiology from pathophysiology. The same ambiguity persisted in clinical practice for another century.

The conceptual basis for "atopic" disease came from allergy research. In 1906 Clemens von Pirquet introduced the word "allergy" to describe altered reactivity to a substance. In 1923 Arthur Coca and Robert Cooke coined "atopy," from the Greek atopos ("out of place"), for an inherited tendency toward immediate hypersensitivity. Their starting observations came from patients with allergic rhinitis and asthma, and a 1916 report by Cooke and van der Veer had already noted a family history in roughly half of such patients. Their classification was later criticized for assuming autosomal dominant transmission and for overstating the role of reaginic antibodies. Even so, the term survived. After immunoglobulin E was identified in the 1960s, most authors used "atopy" to mean an inherited tendency to make IgE antibodies against common allergens, although no precise, universally accepted definition has ever been agreed.

The clinical name "atopic dermatitis" followed in 1933, when Fred Wise and Marion Sulzberger used it for infantile eczema that appeared mainly on the face and in the flexures and occurred in people with a family history of atopic disorders. Their definition linked a skin pattern to a heritable background, and it remained a working description for decades. Because no laboratory test existed, Hanifin and Rajka published diagnostic features in 1980 to address both the lack of an objective test and the inconsistent nomenclature. Their scheme required at least three of four major features (pruritus, typical morphology and distribution, chronic or relapsing course, and a personal or family history of atopy) plus three of 23 minor features. Although national variants, including those from the United Kingdom and Japan, have since appeared, the Hanifin–Rajka criteria are still the most widely used. Rajka and Langeland added a severity score in 1989, which graded body area, course, and itch intensity.

From the 1990s onward, the emphasis shifted toward standardized measurement for clinical research. Investigators developed validated severity indices and tools for assessing itch and sleep, and placebo-controlled randomized trials became the standard way to test new drugs. These methods made it possible to compare treatments across studies, though the outcome measures themselves continued to be refined.

The most consequential change came in the late 2010s with targeted therapy. In December 2016 the US Food and Drug Administration approved crisaborole, a topical phosphodiesterase-4 inhibitor, for mild to moderate disease in patients aged two years and older. On 28 March 2017 the agency approved dupilumab, a monoclonal antibody that blocks signaling by IL-4 and IL-13, as the first biologic for atopic dermatitis, for adults whose disease was not controlled by topical prescription drugs. Approval rested on three phase 3 trials involving 2,119 adults. Later labels extended dupilumab to children, first aged 6 to 11 years in 2020 and then aged 6 months to 5 years in 2022. Subsequent agents, including other interleukin-13 and interleukin-31 antibodies and oral JAK inhibitors, have been developed on the basis of the same mechanistic framework, and their long-term outcomes are discussed elsewhere in this entry.

Unresolved questions and debates

Concern about topical corticosteroids is one of the most persistent problems in eczema care. These drugs remain a first-line treatment, yet a systematic review of 16 cross-sectional studies found that "topical corticosteroid phobia" affected between 21% and 84% of the people surveyed, depending on the study. The studies defined the phobia in different ways, from ordinary worry to irrational fear. In the two studies that compared groups directly, patients who reported the phobia had higher rates of non-adherence to prescribed treatment. Reviewers link these beliefs to misinformation from clinicians, relatives, the media and the internet. The scientific question of long-term safety is also less settled than either side of the debate often implies. A systematic review of long-term adverse effects identified only seven eligible studies, two of them randomised trials, so the evidence base for prolonged use is thin relative to how widely these drugs are prescribed. Clinicians therefore face a gap between reassurance based on short-term data and the lingering uncertainty that patients and carers bring to each prescription.

A second debate concerns whether eczema can be divided into endotypes, meaning subgroups defined by underlying molecular mechanism, that predict which treatment will work. Age, distribution, morphology and comorbidity have long guided choices, and reviews describe that approach as "one-size-fits-all" in practice. Studies in different cohorts have proposed immune profiles such as Th1/Th2/Th17-dominant, Th2/Th22-dominant and Th2/eosinophil-dominant groups, and other work describes a neuroimmune-pruritic endotype and a chronic remodelling endotype driven by IL-22. Ethnic differences add complexity; for example, Japanese patients with atopic dermatitis have been reported to show increased Th17 frequencies in blood and acute lesions. However, candidate biomarkers have not been validated for routine use, and most clinical trials still enrol patients by severity rather than by endotype. Until that changes, the link between a proposed endotype and a predicted response to a specific drug remains largely a research hypothesis.

Long-term outcomes of the newer systemic agents form a third area of uncertainty. Biologics that block IL-4 or IL-13 signalling and oral JAK inhibitors have produced substantial improvements in trials. Yet in one review's account, only about 40% of patients treated with dupilumab reached clear or almost clear skin, and comparative real-world data remain limited. For JAK inhibitors, a network meta-analysis found no increase in cancer risk relative to placebo or other agents, though the risk was higher than with TNF inhibitors, while observational data suggest a modestly raised risk of thromboembolic events compared with dupilumab and methotrexate. A 2026 meta-analysis of observational studies reported that adverse events were common but mostly mild to moderate, with infections, including herpes virus infections, among the most frequent. Its authors also noted higher rates of acne, anaemia and creatine kinase elevation than with anti-IL-4/IL-13 agents. Several trial programmes are still following patients for years, and experts have called for further long-term data and for work to identify subgroups best suited to each class. Cost and access form a parallel gap. Biologics and JAK inhibitors are considerably more expensive than conventional topical and systemic drugs, and reimbursement rules differ between health systems, so patients with identical clinical indications may receive very different treatment.

The causes of the rising prevalence of eczema, and the most effective ways to prevent it, remain open. Attribution is difficult because changes in diagnostic practice, survey methods and population composition can all alter reported rates, and single exposures are hard to isolate from the many factors that vary together across countries and generations. Trial evidence on early emollient use and allergen introduction, discussed in the special-populations section, has not yet given consistent answers. Prevention strategies therefore remain provisional, and each new cohort study or trial tends to refine rather than settle the questions above.

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