Atopic dermatitis (AD), also known asatopic eczema, is a long-term type of inflammation of the skin.[2] Atopic dermatitis is also often called simplyeczema but the same term is also used to refer todermatitis, the larger group of skin conditions.[2][5] Atopic dermatitis results initchy, red, swollen, and cracked skin.[2] Clear fluid may come from the affected areas, which can thicken over time.[2]
Atopic dermatitis affects about 20% of people at some point in their lives.[2][4] It is more common in younger children.[3] Females are affected slightly more often than males.[6] Many people outgrow the condition.[3]
While the condition may occur at any age, it typically starts in childhood, with changing severity over the years.[2][3] In children under one year of age, the face and limbs and much of the body may be affected.[3] As children get older, the areas on the insides of the knees and folds of the elbows and around the neck are most commonly affected.[3] In adults, the hands and feet are commonly affected.[3] Scratching the affected areas worsens the eczema and increases the risk ofskin infections.[2] Many people with atopic dermatitis develophay fever orasthma.[2]
The cause is unknown but is believed to involvegenetics,immune system dysfunction, environmental exposures, and difficulties with thepermeability of the skin.[2][3] If oneidentical twin is affected, the other has an 85% chance of having the condition.[7] Those who live in cities and dry climates are more commonly affected.[2] Exposure to certain chemicals or frequent hand washing makes symptoms worse.[2] Whileemotional stress may make the symptoms worse, it is not a cause.[2] The disorder is notcontagious.[2] A diagnosis is typically based on the signs, symptoms andfamily history.[3]
Treatment involves avoiding things that make the condition worse, enhancing the skin barrier through skin care and treating the underlying skin inflammation.Moisturising creams are used to make the skin less dry and prevent AD flare-ups. Anti-inflammatorycorticosteroid creams are used to control flare-ups.[3] Creams based oncalcineurin inhibitors (tacrolimus or pimecrolimus) may also be used to control flares if other measures are not effective.[2][8] Certainantihistamine pills might help with itchiness.[3] Things that commonly make it worse includehouse dust mite,stress and seasonal factors.[9]Phototherapy may be useful in some people.[2] Antibiotics (either by mouth or topically) are usually not helpful unless there is secondary bacterial infection or the person is unwell.[10]Dietary exclusion does not benefit most people and it is only needed if food allergies are suspected.[11] More severe AD cases may need systemic medicines such ascyclosporin,methotrexate,dupilumab orbaricitinib.
Other names of the condition include "infantile eczema", "flexural eczema", "prurigo Besnier", "allergic eczema", and "neurodermatitis".[1]
Symptoms refer to the sensations that people with AD feel, whereas signs refers to a description of the visible changes that result from AD.
The pattern of atopic eczema varies with age.
The main symptom of AD isitching which can be intense. Some people experience burning or soreness orpain.[2]
People with AD often have a generally dry skin that can look greyish in people with darker skin tones of colour. Areas of AD are not well defined, and they are typically inflamed (red in a light coloured skin or purple or dark brown in people with dark skin of colour).[12] Surface changes include:
thickening of the skin (lichenification) where the AD has been present for a long time.[2]
Eczema often starts on the cheeks and outer limbs and body in infants and frequently settles in the folds of the skin such as behind the knees, folds of the elbows, around the neck, wrists and under the buttock folds as the child grows.[13] Any part of the body can be affected by AD.[14]
Atopic dermatitis commonly affects the eyelids, where an extra prominent crease can form under the eyelid due to skin swelling known asDennie-Morgan infraorbital folds.[15] Cracks can form under the ears which can be painful (infra-auricular fissure).[16][15]
The inflammation from AD often leaves "footprints" known aspostinflammatory pigmentation that can be lighter than the normal skin or darker. These marks are not scars and eventually go back to normal over a period of months providing the underlying AD is treated effectively.[17]
People with AD often have dry and scaly skin that spans the entire body, except perhaps the diaper area, and intensely itchy red, splotchy, raisedlesions to form in the bends of the arms or legs, face, and neck.[18][19][20][21][22]
Since 1970, the rates of atopic dermatitis in the US and UK have increased 3-6 fold.[25] Even today, people who migrate fromdeveloping nations before the age of 4 years toindustrialized nations experience a dramatic rise in the risk of atopic dermatitis and have an additional risk when living inurbanized areas of the industrial nation.[26] Recent work has shed light on these and other data strongly suggesting that early life industrial exposures may cause atopic dermatitis.[25][27] Chemicals such as(di)isocyanates andxylene prevent the skin bacteria from producingceramide-sphingolipid familylipids.[25][27] Early life deficiency in these lipids predictive which children will go on to develop atopic dermatitis.[28][29][30][31] These chemicals also directly activate an itch receptor in the skin known asTRPA1.[32] The industrial manufacturing and use of both xylene and diisocyanates greatly increased starting in 1970, which greatly expanded the average exposure to these substances. For example, these chemicals are components of several exposures known to increase the risk of atopic dermatitis or worsen symptoms including: wildfires,automobile exhaust,wallpaper adhesives, paints, non-latex foam furniture, cigarette smoke, and are elements of fabrics likepolyester,nylon, andspandex.[26][25][27]
Genes that may contribute to AD are mainly those responsible for immune response (e.g. TH2 cytokine and JAK-STAT pathway genes) and skin barrier (e.g. filaggrin, claudin-1, loricrin).[citation needed]
Immune response: Many people with AD have a family history or a personal history ofatopy. Atopy is a term used to describe individuals who produce substantial amounts ofIgE. Such individuals have an increased tendency to developasthma,hay fever,eczema,urticaria and allergic rhinitis.[18][19] Up to 80% of people with atopic dermatitis have elevated total or allergen-specific IgE levels.[34]
Skin barrier: About 30% of people with AD have mutations in the gene for the production offilaggrin (FLG), which increase the risk for early onset of atopic dermatitis and developing asthma.[35][36] However, expression of filaggrin protein or breakdown products offer no predictive utility in atopic dermatitis risk.[29]
According to thehygiene hypothesis, early childhood exposure to certain microorganisms (such asgut flora andhelminth parasites) protects againstallergic diseases by contributing to the development of theimmune system.[38] This exposure is limited in a modern "sanitary" environment, and the incorrectly developed immune system is prone to develop allergies to harmless substances.[citation needed]
Some support exists for this hypothesis with respect to AD.[39] Those exposed to dogs while growing up have a lower risk of atopic dermatitis.[40] Also, epidemiological studies support a protective role for helminths against AD.[41] Likewise, children with poor hygiene are at a lower risk for developing AD, as are children who drinkunpasteurized milk.[41]
In a small percentage of cases, atopic dermatitis is caused by sensitization to foods[42] such as milk, but there is growing consensus thatfood allergy most likely arises as a result of skin barrier dysfunction resulting from AD, rather than food allergy causing the skin problems.[43] Atopic dermatitis sometimes appears associated withcoeliac disease and non-coeliac gluten sensitivity. Because agluten-free diet (GFD) improves symptoms in these cases,gluten seems to be the cause of AD in these cases.[44][45] A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for heavilyprocessed foods.[41]
Exposure toallergens, either from food or the environment, can exacerbate existing atopic dermatitis.[46] Exposure todust mites, for example, is believed to contribute to the risk of developing AD.[47]
The prevalence of atopic dermatitis in children may be linked to the level ofcalcium carbonate or "hardness" of household drinking water.[48][49] Living in areas with hard water may also play a part in the development of AD in early life. However, when AD is already established, usingwater softeners at home does not reduce the severity of the symptoms.[49][50]
Colonization of the skin by the bacteriumS. aureus is prevalent in those with atopic dermatitis.[51] Abnormalities in the skin barrier of persons with AD are exploited byS. aureus to trigger cytokine expression, thus aggravating the condition.[52]
However, atopic dermatitis isnon-communicable and therefore could not be directly caused by a highlyinfectious organism. Furthermore, there is insufficient evidence for the effectiveness of anti-staphylococcal treatments for treatingS. aureus in infected or uninfected eczema.[53]
The role ofS. aureus in skin irritation occurs via inflammation factors that induceitching, which may damage the skin, further driving inflammation, and facilitating the growth ofS. aureus, thus promoting a chronic cycle.[54]
Disruption of the epidermal barrier is thought to play an integral role in thepathogenesis of AD.[34] Disruptions of the epidermal barrier allows allergens to penetrate the epidermis to deeper layers of the skin. This leads to activation ofepidermal inflammatory dendritic andinnate lymphoid cells which subsequently attractsTh2 CD4+ helper T cells to the skin.[34] This dysregulated Th2 inflammatory response is thought to lead to the eczematous lesions.[34] The Th2 helper T cells become activated, leading to the release of inflammatory cytokines includingIL-4,IL-13 andIL-31 which activate downstreamJanus kinase (Jak) pathways. The active Jak pathways lead to inflammation and downstream activation ofplasma cells andB lymphocytes which release antigen specificIgE contributing to further inflammation.[34] Other CD4+ helper T-cell pathways thought to be involved in atopic dermatitis inflammation include the Th1,Th17, and Th22 pathways.[34] Some specific CD4+ helper T-cell inflammatory pathways are more commonly activated in specific ethnic groups with AD (for example, the Th-2 and Th-17 pathways are commonly activated in Asian people) possibly explaining the differences in phenotypic presentation of atopic dermatitis in specific populations.[34]
Mutations in the filaggrin gene,FLG, also cause impairment in the skin barrier that contributes to the pathogenesis of AD.[34] Filaggrin is produced by epidermal skin cells (keratinocytes) in thehorny layer of the epidermis. Filaggrin stimulates skin cells to release moisturizing factors and lipid matrix material, which cause adhesion of adjacent keratinocytes and contributes to the skin barrier.[34] A loss-of-function mutation of filaggrin causes loss of this lipid matrix and external moisturizing factors, subsequently leading to disruption of the skin barrier. The disrupted skin barrier leads to transdermal water loss (leading to thexerosis or dry skin commonly seen in AD) and antigen and allergen penetration of the epidermal layer.[34] Filaggrin mutations are also associated with a decrease in natural antimicrobial peptides found on the skin; subsequently leading to disruption of skin flora and bacterial overgrowth (commonlyStaphylococcus aureus overgrowth or colonization).[34]
Atopic dermatitis is also associated with the release of pruritogens (molecules that stimulatepruritus or itching) in the skin.[34] Keratinocytes,mast cells,eosinophils andT-cells release pruritogens in the skin; leading to activation ofAδ fibers andGroup C nerve fibers in theepidermis anddermis contributing to sensations of pruritus and pain.[34] The pruritogens include the Th2 cytokines IL-4, IL-13, IL-31, histamine, and various neuropeptides.[34] Mechanical stimulation from scratching lesions can also lead to the release of pruritogens contributing to the itch-scratch cycle whereby there is increased pruritus or itch after scratching a lesion.[34] Chronic scratching of lesions can cause thickening orlichenification of the skin orprurigo nodularis (generalized nodules that are severely itchy).[34]
Another factor in the barrier failure and immunological dysregulation in people with atopic dermatitis may be due to decreases intight junction proteinClaudin-1. Inhibiting Claudin-1 expression in human keratinocytes has been show to both reducetight junction function, as well as increase keratinocyte proliferation in vitro. It has also been discovered that this deteriorates thebioelectric barrier function in the epidermis.[37]
Atopic dermatitis is typicallydiagnosed clinically, meaning it is based on signs and symptoms alone, without special testing.[57] Several different criteria developed for research have also been validated to aid in diagnosis.[58] Of these, the UK Diagnostic Criteria, based on the work of Hanifin andRajka, has been the most widely validated.[58][59]
People must haveitchy skin, or evidence of rubbing or scratching, plus three or more of:
Skin creases are involved – flexural dermatitis of fronts ofankles,antecubital fossae,popliteal fossae, skin around eyes, or neck, (or cheeks for children under 10)
History ofasthma orallergic rhinitis (or family history of these conditions if patient is a child ≤4 years old)
Symptoms began before age 2 (can only be applied to people ≥4 years old)
There are no establishedclinical methods using dietary ortopical strategies to inhibit or prevent atopic dermatitis. Specific dietary plans during pregnancy and in early childhood, such as eating fatty fish (or takingomega-3 supplements), are not effective.[60] Takingprobiotics (for exampleLactobacillus rhamnosus) during pregnancy and feeding probiotics to infants are strategies under research, with only preliminary evidence that they may be preventative.[61][62]
Usingmoisturizers daily in infants during the first year of life does not help to prevent atopic dermatitis, and might even increase the risk of skin infections.[50][63]
No cure for AD is known, although treatments may reduce the severity and frequency of flares.[18] The most commonly used topical treatments for AD are topical corticosteroids (to get control of flare-ups) andmoisturisers (emollients) to help keep control.[64] Clinical trials often measure the efficacy of treatments with a severity scale such as theSCORAD index or theEczema Area and Severity Index.[57][65]
Daily basic care is intended to stabilize the barrier function of the skin to mitigate its sensitivity to irritation and penetration of allergens. Affected persons often report that improvement of skin hydration parallels with improvement in AD symptoms.Moisturisers (or emollients) can improve skin comfort and may reduce disease flares.[66] They can be used as leave-on treatments, bath additives orsoap substitutes. There are many different products but the majority of leave-on treatments (least to most greasy) arelotions,creams,gels orointments. All of the different types of moisturisers are equally effective so people need to choose one or more products based on what suits them, according to their age, body site effected, climate/season and personal preference.[67] Non-medicated prescription moisturisers may also be no more effective thanover-the-counter moisturisers.[68]
The use of emollient bath additives does not provide any additional benefits.[50][69][70]
Creams and ointments containingcorticosteroids applied directly on skin (topical) are effective in managing atopic dermatitis.[68][71] Newer (second generation) corticosteroids, such asfluticasone propionate andmometasone furoate, are more effective and safer than older ones. Strong and moderate corticosteroids work better than weaker ones. They are also generally safe and do not causeskin thinning when used intermittently to treat AD flare-ups. They are also safe when used twice a week for preventing flares (also known as weekend treatment).[72][68][73] Applying once daily is as effective as twice or more daily application.[71]
Allergen immunotherapy may be effective in relieving symptoms of AD, but it also comes with an increased risk ofadverse events.[93] This treatment consists of a series of injections or drops under the tongue of a solution containing the allergen.[94]
The skin of people with AD can easily get infected, most commonly by the bacteriaStaphylococcus aureus. Signs of this include oozing fluid, a yellow crust on the skin, worsening eczema symptoms and fever. Antibiotics are commonly used to target overgrowth ofS. aureus but their benefit is limited, and they increase the risk ofantimicrobial resistance. For these reasons, they are only recommended for people who not only present symptoms on the skin but feel systematically unwell.[50][53][95]
Severalprobiotics seem to have a positive effect, with a roughly 20% reduction in the rate of AD.[101][102][103] Probiotics containing multiplestrains of bacteria seem to work the best.[104]
Use of blood specificIgE orskin prick tests to guide dietary exclusions with the aim of improving disease severity or control is controversial. Clinicians vary in their use of these tests for this purpose, and there are very limited evidence of any benefit.[105]
Health professionals often recommend that people with AD bathe regularly in lukewarm baths, especially in salt water, to moisten their skin.[19][106] Dilutebleach baths may be helpful for people with moderate and severe eczema, but only for people with Staphylococcus aureus.[107]
Avoiding large-diameterwoolen clothing or scratchy fibres is usually recommended for people with AD as they can trigger a flare.[108][109] Safe alternatives are clothes made from fabrics with smaller diameters and smooth fibers. These include super- and ultrafinemerino wool and fabrics with anti-microbial textile finishes. Wearingsilk is also safe but does not improve symptoms of AD.[108][50][110]
Living with AD requires a high level of self-management (for example avoiding triggers) andadherence to treatments (regularly applying medication). Good self-management contributes to better disease outcomes and quality of life.[111][112] However, worries about topical treatments, misconceptions about the condition, unclear information and unsuitable communication from doctors can make living with AD more difficult.[50]
People with AD often do not regard eczema as long-term condition and hope they will outgrow or cure it. This can cause worse adherence to the necessary long-term treatment. Doctors should not imply that it is a short-term condition and should emphasise that even though it cannot be cured it can be controlled effectively.[113][112]
Appropriate communication from doctors can support self-management. Doctors need to address concerns about treatments and provide clear and consistent information about the condition.[113][112] Treatment regimens can be confusing, and written action plans may support people in knowing which treatments to use where and when.[114] A website supporting self-management has been shown to improve AD symptoms for parents, children, adolescents and young adults.[115][116]
Phototherapic treatment involves exposure to broad- or narrow-bandultraviolet (UV) light. UV radiation exposure has been found to have a localized immunomodulatory effect on affected tissues and may be used to decrease the severity and frequency of flares.[117][118] Among the different types of phototherapies only narrowband (NB) ultraviolet B (UVB) exposure might help with the severity of AD and ease itching.[83][119] However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk.[120]UV phototherapy is not indicated in young adults and children due to this risk ofskin cancer with prolonged use or exposure.[34]
While severalChinese herbal medicines are intended for treating atopic eczema, there is no evidence showing that these treatments, taken by mouth or applied topically, reduce the severity of eczema in children or adults.[121]
Atopic dermatitis significantly impairs thequality of life of affected individuals.[122][123] The impact of AD extends beyond physical symptoms, encompassing substantial humanistic andpsychosocial effects. Itsburden is significant, especially given the high indirect costs and psychological impacts on quality of life.[122][124]
According to theGlobal Burden of Disease Study, AD is the skin disease with the highestdisability-adjusted life year burden and ranks in the top 15 of all nonfatal diseases. In comparison with other dermatological conditions like psoriasis and urticaria, AD presents a significantly higher burden.[123]
While AD remains incurable, reducing its severity can significantly alleviate its burden. Understanding the extent of the burden of AD can aid in better resource allocation and prioritization of interventions, benefiting both people with atopic dermatitis and healthcare systems.[125]
Atopic dermatitis significantly decreases the quality of life by affecting various aspects of people's lives. The psychological impact, often resulting in conditions likedepression andanxiety, is a major factor leading to decreasedquality of life. Sleep disturbances, commonly reported in people with AD, further contribute to the humanistic burden, affecting daily productivity and concentration.[122]
Economically, AD imposes a substantial burden on healthcare systems, with the average direct cost per patient estimated at US $4411 and the average indirect cost reaching US $9068 annually.[122] These figures highlight the considerable financial impact of the disease on healthcare systems and people with the condition.[126][127]
Atopic dermatitis also has a marked impact on productivity. The total number of days lost annually due to these factors is about 68.8 days for the general AD population, withpresenteeism accounting for the majority of these days.[122] The impact on productivity varies significantly with the severity of AD, with more severe cases resulting in higher numbers of days lost.[122][128]
Atopic dermatitis leads to the highest loss indisability-adjusted life years compared to other skin diseases in the Middle East and Africa.[129] Patients with AD in these regions lose approximately 0.19quality-adjusted life years (QALYs) annually due to the disease. Egypt experiences the highest QALY loss and Kuwait the lowest.[129]
The average annual healthcare cost per patient varies is highest in the United Arab Emirates, estimated at US $3569, and lowest in Algeria at US $312. These costs are influenced by the economic status of each country and the cost of healthcare. Advanced treatments like targeted therapies and phototherapy are among the main cost drivers.[129]
Indirect costs, primarily due to productivity loss fromabsenteeism and presenteeism average about 67% in these countries. Indirect costs in Saudi Arabia are the highest in the area, estimated at US $364 million.[129] Factors like mental health impact, side effects of treatments, and other indirect costs such as personal care products are not fully accounted for in these estimates, suggesting that the actual burden might be even higher.[129]
To mitigate the burden of AD, experts recommend strategic actions across five key domains: capacity building, guidelines, research, public awareness, and patient support and education. Key measures include increasing the number of dermatologists, establishing evidence-based treatment guidelines, investing in patient education, and enhancing public awareness to reduce stigma.[130] Improving access to effective treatments and conducting further research on AD's impact are also crucial for reducing the disease's clinical, economic, and humanistic burdens in the MEA.[130]
Since the beginning of the 20th century, many inflammatory skin disorders have become more common; AD is a classic example of such a disease. Although AD was previously considered primarily a childhood disease, it is now recognized as highly prevalent in adults, with an estimated adult prevalence of 3–5% globally.[122][123] It now affects 15–30% of children and 2–10% of adults in developed countries, and in the United States has nearly tripled in the past 30–40 years.[19][131] Over 15 million American adults and children have AD.[132]
A number of false and conspiratorial claims about AD have emerged on the internet and have been amplified by social media. Theseconspiracy theories include, among others, claims that AD is caused by5G,formaldehyde in food,vaccines, and topical steroids. Various unproven theories also claim thatvegan diets,apple cider vinegar,calendula, andwitch hazel can cure AD and thatair purifiers reduce the risk of developing AD.[133]
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