Medicine:Atopic dermatitis

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Short description: Long-term form of skin inflammation
Atopic dermatitis
Other namesAtopic eczema, infantile eczema, prurigo Besnier, allergic eczema, neurodermatitis[1]
Atopy2010.JPG
Atopic dermatitis of the inside crease of the elbow
SpecialtyDermatology, Clinical Immunology and Allergy
SymptomsItchy, red, swollen, cracked skin[2]
ComplicationsSkin infections, hay fever, asthma[2]
Usual onsetChildhood[2][3]
CausesUnknown[2][3]
Risk factorsFamily history, living in a city, dry climate[2]
Diagnostic methodBased on symptoms after ruling out other possible causes[2][3]
Differential diagnosisContact dermatitis, psoriasis, seborrheic dermatitis[3]
TreatmentAvoiding things that worsen the condition, daily bathing followed by moisturising cream, steroid creams for flares[3] Humidifier
Frequency~20% at some time[2][4]

Atopic dermatitis (AD), also known as atopic eczema, is a long-term type of inflammation of the skin (dermatitis).[2] It results in itchy, red, swollen, and cracked skin.[2] Clear fluid may come from the affected areas, which can thicken over time.[2] AD may also simply be called eczema, a term that generally refers to a larger group of skin conditions.[2][5]

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 slightly more affected 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 of skin infections.[2] Many people with atopic dermatitis develop hay fever or asthma.[2]

The cause is unknown but believed to involve genetics, immune system dysfunction, environmental exposures, and difficulties with the permeability of the skin.[2][3] If one identical 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] While emotional stress may make the symptoms worse, it is not a cause.[2] The disorder is not contagious.[2] A diagnosis is typically based on the signs, symptoms and family 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-inflammatory corticosteroid creams are used to control flares-ups.[3] Creams based on calcineurin inhibitors (tacrolimus or pimecrolimus) may also be used to control flares if other measures are not effective.[2][8] Certain antihistamine pills might help with itchiness.[3] Things that commonly make it worse include house 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 as cyclosporin, methotrexate, dupilumab or baricitinib.

Other names of the condition include "infantile eczema", "flexural eczema", "prurigo Besnier", "allergic eczema", and "neurodermatitis".[1]

Signs and symptoms

Child with atopic dermatitis

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 is itching which can be intense. Some people experience burning or soreness or pain.[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:

  • scaling cracking (fissures)
  • swelling (oedema)
  • scratch marks (excoriation)
  • bumpiness (papulation)
  • oozing of clear fluid
  • 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]

AD commonly affects the eyelids, where an extra prominent crease can form under the eyelid due to skin swelling known as Dennie-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 as postinflammatory 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, raised lesions to form in the bends of the arms or legs, face, and neck.[18][19][20][21][22]

Causes

The cause of AD is not known, although some evidence indicates environmental, immunologic, and potential genetic factors.[23]

Pollution

Since 1970, the rates of atopic dermatitis in the US and UK have increased 3-6 fold.[24] Even today, people who migrate from developing nations before the age of 4 years to industrialized nations experience a dramatic rise in the risk of atopic dermatitis and have an additional risk when living in urbanized areas of the industrial nation.[25] Recent work has shed light on these and other data strongly suggesting that early life industrial exposures may cause atopic dermatitis.[24][26] Chemicals such as (di)isocyanates and xylene prevent the skin bacteria from producing ceramide-sphingolipid family lipids.[24][26] Early life deficiency in these lipids predictive which children will go on to develop atopic dermatitis.[27][28][29][30] These chemicals also directly activate an itch receptor in the skin known as TRPA1.[31] 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 like polyester, nylon, and spandex.[25][24][26]

Climate

Low humidity, and low temperature increase the prevalence and risk of flares in patients with atopic dermatitis.[32]

Genetics

Many people with AD have a family history or a personal history of atopy. Atopy is a term used to describe individuals who produce substantial amounts of IgE. Such individuals have an increased tendency to develop asthma, 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.[33]

About 30% of people with atopic dermatitis have mutations in the gene for the production of filaggrin (FLG), which increase the risk for early onset of atopic dermatitis and developing asthma.[34][35] However, expression of filaggrin protein or breakdown products offer no predictive utility in atopic dermatitis risk.[28]

Hygiene hypothesis

According to the hygiene hypothesis, early childhood exposure to certain microorganisms (such as gut flora and helminth parasites) protects against allergic diseases by contributing to the development of the immune system.[36] This exposure is limited in a modern "sanitary" environment, and the incorrectly developed immune system is prone to develop allergies to harmless substances.

Some support exists for this hypothesis with respect to AD.[37] Those exposed to dogs while growing up have a lower risk of atopic dermatitis.[38] Also, epidemiological studies support a protective role for helminths against AD.[39] Likewise, children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurized milk.[39]

Allergens

In a small percentage of cases, atopic dermatitis is caused by sensitization to foods[40] such as milk, but there is growing consensus that food allergy most likely arises as a result of skin barrier dysfunction resulting from AD, rather than food allergy causing the skin problems.[41] Atopic dermatitis sometimes appears associated with coeliac disease and non-coeliac gluten sensitivity. Because a gluten-free diet (GFD) improves symptoms in these cases, gluten seems to be the cause of AD in these cases.[42][43] A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for heavily processed foods.[39]

Exposure to allergens, either from food or the environment, can exacerbate existing atopic dermatitis.[44] Exposure to dust mites, for example, is believed to contribute to the risk of developing AD.[45]

Role of Staphylococcus aureus

Colonization of the skin by the bacterium S. aureus is extremely prevalent in those with atopic dermatitis.[46] Abnormalities in the skin barrier of persons with AD are exploited by S. aureus to trigger cytokine expression, thus aggravating the condition.[47] However, atopic dermatitis is non-communicable and therefore could not be directly caused by a highly infectious organism. Furthermore, there is insufficient evidence for the effectiveness of anti-staphylococcal treatments for treating S. aureus in infected or uninfected eczema.[48]

Hard water

The prevalence of atopic dermatitis in children may be linked to the level of calcium carbonate or "hardness" of household drinking water.[49][50] 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, using water softeners at home does not reduce the severity of the symptoms.[50]

Pathophysiology

Excessive type 2 inflammation underlies the pathophysiology of atopic dermatitis.[51][52]

Disruption of the epidermal barrier is thought to play an integral role in the pathogenesis of AD.[33] Disruptions of the epidermal barrier allows allergens to penetrate the epidermis to deeper layers of the skin. This leads to activation of epidermal inflammatory dendritic and innate lymphoid cells which subsequently attracts Th2 CD4+ helper T cells to the skin.[33] This dysregulated Th2 inflammatory response is thought to lead to the eczematous lesions.[33] The Th2 helper T cells become activated, leading to the release of inflammatory cytokines including IL-4, IL-13 and IL-31 which activate downstream Janus kinase (Jak) pathways. The active Jak pathways lead to inflammation and downstream activation of plasma cells and B lymphocytes which release antigen specific IgE contributing to further inflammation.[33] Other CD4+ helper T-cell pathways thought to be involved in atopic dermatitis inflammation include the Th1, Th17, and Th22 pathways.[33] 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.[33]

Mutations in the filaggrin gene, FLG, also cause impairment in the skin barrier that contributes to the pathogenesis of AD.[33] Filaggrin is produced by epidermal skin cells (keratinocytes) in the horny 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.[33] 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 the xerosis or dry skin commonly seen in AD) and antigen and allergen penetration of the epidermal layer.[33] 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 (commonly Staphylococcus aureus overgrowth or colonization).[33]

Atopic dermatitis is also associated with the release of pruritogens (molecules that stimulate pruritus or itching) in the skin.[33] Keratinocytes, mast cells, eosinophils and T-cells release pruritogens in the skin; leading to activation of Aδ fibers and Group C nerve fibers in the epidermis and dermis contributing to sensations of pruritus and pain.[33] The pruritogens include the Th2 cytokines IL-4, IL-13, IL-31, histamine, and various neuropeptides.[33] 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.[33] Chronic scratching of lesions can cause thickening or lichenification of the skin or prurigo nodularis (generalized nodules that are severely itchy).[33]

Diagnosis

AD is typically diagnosed clinically, meaning it is based on signs and symptoms alone, without special testing.[53] Several different criteria developed for research have also been validated to aid in diagnosis.[54] Of these, the UK Diagnostic Criteria, based on the work of Hanifin and Rajka, has been the most widely validated.[54][55]

UK diagnostic criteria[55]
People must have itchy skin, or evidence of rubbing or scratching, plus three or more of:
Skin creases are involved - flexural dermatitis of fronts of ankles, antecubital fossae, popliteal fossae, skin around eyes, or neck, (or cheeks for children under 10)
History of asthma or allergic 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 patients ≥4 years old)
History of dry skin (within the past year)
Dermatitis is visible on flexural surfaces (patients ≥age 4) or on the cheeks, forehead, and extensor surfaces (patients<age 4)

Other diseases that must be excluded before making a diagnosis include contact dermatitis, psoriasis, and seborrheic dermatitis.[3]

Treatments

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) and moisturisers (emollients) to help keep control.[56] Clinical trials often measure the efficacy of treatments with a severity scale such as the SCORAD index or the Eczema Area and Severity Index.[53][57]

Moisturisers

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.[58] They can be used as leave-on treatments, bath additives or soap substitutes. There are many different products but the majority of leave-on treatments (least to most greasy) are lotions, creams, gels or ointments. None of the different types of moisturisers are more effective than the others so people need to choose one or more products that suit them, according to their age, body site effected, climate/season and personal preference.[59] Non-medicated prescription moisturisers may also be no more effective than over-the-counter moisturisers.[60]

There is no evidence that the additional use of emollient bath additives is beneficial.[61]

Medication

Topical

Corticosteroids applied directly on skin (topical) have proven effective in managing atopic dermatitis.[18][19][60][62] Newer (second generation) corticosteroids, such as fluticasone propionate and mometasone furoate, are more effective and safer than older ones. Strong and moderate corticosteroids work better than weaker ones. They are also generally safe when used in intermittent bursts to treat AD flare-ups. Applying once daily is as effective as twice or more daily application.[60][62]

In addition to topical corticosteroids, topical calcineurin inhibitors such as tacrolimus or pimecrolimus are also recommended as first-line therapies for managing atopic dermatitis.[60][63] Both tacrolimus and pimecrolimus are effective and safe to use in AD.[64][65] Crisaborole, an inhibitor of PDE-4, is also effective and safe as a topical treatment for mild-to-moderate AD.[66][67] Ruxolitinib, a Janus kinase inhibitor, has uncertain efficacy and safety.[60][63]

Systemic

Oral medications used for AD include systemic immunosuppressants such as ciclosporin, methotrexate, interferon gamma-1b, mycophenolate mofetil, and azathioprine.[18][68] Antidepressants and naltrexone may be used to control pruritus (itchiness).[69] Leukotriene inhibitors such as montelukast are of unclear benefit as of 2018.[70][71]

In 2017, the monoclonal antibody(mAb) dupilumab under the trade name Dupixent was approved to treat moderate-to-severe eczema.[72] In 2021, an additional monoclonal antibody, tralokinumab, was approved in the EU & UK with the trade name Adtralza then later in the US as Adbry for similarly severe cases.[73][74] As of 2023, another monoclonal antibody treatment, lebrikizumab, is awaiting approval in the US and Europe.[75][76] These monoclonal antibodies are highly effective for managing atopic dermatitis, but modestly increase the risk of conjunctivitis.[63][77]

Some JAK inhibitors such as abrocitinib, trade name Cibinqo,[78] and upadacitinib, trade name Rinvoq,[79] have been approved in the US for the treatment of moderate-to-severe eczema as of January 2022. These treatments are among the most effective systemic treatments, but have uncertain serious harms.[63][77]

Allergen immunotherapy may be effective in relieving symptoms of AD but it also comes with an increased risk of adverse events.[80] This treatment consists of a series of injections or drops under the tongue of a solution containing the allergen.[81]

Antibiotics, either by mouth or applied topically, are commonly used to target overgrowth of S. aureus in the skin of people with AD, but there is insufficient evidence for the effectiveness of anti-staphylococcal treatments for treating S. aureus in infected or uninfected eczema.[48]

Diet

The role of vitamin D on atopic dermatitis is not clear, but vitamin D supplementation may improve its symptoms.[82][83][84]

There is no clear benefit for pregnant mothers taking omega 3 long-chain polyunsaturated fatty acid (LCPUFA) in preventing the development of AD in their child.[85][86]

Several probiotics seem to have a positive effect, with a roughly 20% reduction in the rate of AD.[87][88][89] Probiotics containing multiple strains of bacteria seem to work the best.[90]

In people with celiac disease or nonceliac gluten sensitivity, a gluten-free diet improves their symptoms and prevents the occurrence of new outbreaks.[42][43]

Use of blood specific IgE or skin 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.[91]

Lifestyle

Health professionals often recommend that people with AD bathe regularly in lukewarm baths, especially in salt water, to moisten their skin.[19][92] Dilute bleach baths may be helpful for people with moderate and severe eczema, but only for patients with Staphylococcus aureus.[93]

Avoiding woolen clothing or scratchy fibres is usually recommended for people with AD as they can trigger a flare.[94][95]

Self-management

Treatment regimens can be confusing and written action plans may support people to know what treatments to use where and when.[96]

A website supporting self-management has been shown to improve AD symptoms for parents, children, adolescents and young adults.[97][98]

Light

Phototherapic treatment involves exposure to broad- or narrow-band ultraviolet (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.[99][100] Among the different types of phototherapies only narrowband (NB) ultraviolet B (UVB) exposure might help with the severity of AD and ease itching.[77][101] However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk.[102] UV phototherapy is not indicated in young adults and children due to this risk of skin cancer with prolonged use or exposure.[33]

Alternative medicine

While several Chinese herbal medicines are intended for treating atopic eczema, no conclusive evidence shows that these treatments, taken by mouth or applied topically, reduce the severity of eczema in children or adults.[103]

Burden of Disease

Atopic Dermatitis (AD), commonly known as atopic eczema, is a chronic skin condition that significantly impairs the quality of life (QoL) of affected individuals. 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.[104][105]

The impact of AD extends beyond physical symptoms, encompassing substantial humanistic and psychosocial effects. Its burden is significant, especially given the high indirect costs and psychological impacts on quality of life.[104][106]

According to the Global Burden of Disease study, AD is the skin disease with the highest disability-adjusted life-year (DALY) 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.[105]

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 patients and healthcare systems.[107]

Clinical and Economic Burden

AD is associated with various symptoms, including pruritis, depression, and anxiety. The prevalence of itching in AD patients ranges from 21% to 100%,[104] with the median severity of itch averaging around 6 on a 0-10 numerical rating scale.[104][108]

Economically, AD imposes a substantial burden, with the average direct cost per patient estimated at 4411 USD and the average indirect cost reaching 9068 USD annually.[104] These figures highlight the considerable financial impact of the disease on healthcare systems and patients.[109][110]

Humanistic Burden

AD significantly decreases the quality of life by affecting various aspects of patients' lives. The psychological impact, often resulting in conditions like depression and anxiety, is a major factor leading to decreased quality of life. Sleep disturbances, commonly reported in AD patients, further contribute to the humanistic burden, affecting daily productivity and concentration.[104][111]

The average utility value for the general AD population is approximately 0.779, with a gradual decrease in health-related quality of life (HRQoL) correlating with increasing severity of the disease.[104][112]

Productivity Loss

AD 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 unstratified AD population, with presenteeism accounting for the majority of these days.[104] The impact on productivity varies significantly with the severity of AD, with more severe cases resulting in higher numbers of days lost.[104][113]

Burden of Disease in the Middle East and Africa

Atopic Dermatitis leads to the highest loss in disability-adjusted life years (DALYs) compared to other skin diseases in the Middle East and Africa.[114] Patients with AD in these regions lose approximately 0.19 quality-adjusted life years (QALYs) annually due to the disease. Egypt experiences the highest QALY loss and Kuwait the lowest. The estimated utility value for an average patient with AD ranges from 0.54 to 0.77.[114]

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.[114]

Indirect costs, primarily due to productivity loss from absenteeism and presenteeism average about 67% in these countries. Indirect costs in Saudi Arabia are the highest in the area, estimated at US $364 million.[114] 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.[114]

Epidemiology

Since the beginning of the 20th century, many inflammatory skin disorders have become more common; AD is a classic example of such a disease. 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][115] Over 15 million American adults and children have AD.[116]

Society and culture

Conspiracy theories

A number of false and conspiratorial claims about AD have emerged on the internet and have been amplified by social media. These conspiracy theories include, among others, claims that AD is caused by 5G, formaldehyde in food, vaccines, and topical steroids. Various unproven theories also claim that vegan diets, apple cider vinegar, calendula, and witch hazel can cure AD and that air purifiers reduce the risk of developing AD.[117]

Research

Staphylococcus aureus may have a role in producing atopic dermatitis by colonizing on the skin.[118]

See also

References

  1. ↑ 1.0 1.1 "Epidemiology of atopic dermatitis". Clinical and Experimental Dermatology (Cambridge University Press) 25 (7): 522–529. October 2000. doi:10.1046/j.1365-2230.2000.00698.x. ISBN 9780521570756. PMID 11122223. https://books.google.com/books?id=q8OZ4O_gjQUC&pg=PA10. 
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 "Handout on Health: Atopic Dermatitis (A type of eczema)". May 2013. http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp. 
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 "Atopic dermatitis: skin-directed management". Pediatrics 134 (6): e1735–e1744. December 2014. doi:10.1542/peds.2014-2812. PMID 25422009. 
  4. ↑ 4.0 4.1 "Atopic dermatitis: natural history, diagnosis, and treatment". ISRN Allergy 2014: 354250. 2014. doi:10.1155/2014/354250. PMID 25006501. 
  5. ↑ "Revised nomenclature for allergy for global use: Report of the Nomenclature Review Committee of the World Allergy Organization, October 2003". The Journal of Allergy and Clinical Immunology 113 (5): 832–836. May 2004. doi:10.1016/j.jaci.2003.12.591. PMID 15131563. 
  6. ↑ "Atopic Dermatitis" (in en). September 2019. https://www.niams.nih.gov/health-topics/atopic-dermatitis. 
  7. ↑ Evidence-Based Dermatology. John Wiley & Sons. 2009. pp. 128. ISBN 9781444300178. https://books.google.com/books?id=SbsQij5xkfYC&pg=PA128. 
  8. ↑ "Topical calcineurin inhibitors for atopic dermatitis: review and treatment recommendations". Paediatric Drugs 15 (4): 303–310. August 2013. doi:10.1007/s40272-013-0013-9. PMID 23549982. 
  9. ↑ "What causes worsening of eczema? A systematic review". The British Journal of Dermatology 155 (3): 504–514. September 2006. doi:10.1111/j.1365-2133.2006.07381.x. PMID 16911274. 
  10. ↑ "Skin Antiseptics for Atopic Dermatitis: Dissecting Facts From Fiction" (in English). The Journal of Allergy and Clinical Immunology. In Practice 11 (5): 1385–1390. January 2023. doi:10.1016/j.jaip.2023.01.012. PMID 36702247. 
  11. ↑ "Dietary Elimination for the Treatment of Atopic Dermatitis: A Systematic Review and Meta-Analysis" (in English). The Journal of Allergy and Clinical Immunology. In Practice 10 (10): 2657–2666.e8. October 2022. doi:10.1016/j.jaip.2022.06.044. PMID 35987995. 
  12. ↑ "Atopic dermatitis in diverse racial and ethnic groups-Variations in epidemiology, genetics, clinical presentation and treatment". Experimental Dermatology 27 (4): 340–357. April 2018. doi:10.1111/exd.13514. PMID 29457272. 
  13. ↑ "Atopic dermatitis". Rook's Textbook of Dermatology (8th ed.). Chichester, UK: Wiley-Blackwell. 2010. ISBN 978-1-4443-1764-0. OCLC 605909001. https://www.worldcat.org/oclc/605909001. 
  14. ↑ "Atopic Dermatitis" (in en). Rook's Textbook of Dermatology. Malden, Massachusetts, USA: Blackwell Publishing, Inc.. January 2004. pp. 755–786. doi:10.1002/9780470750520.ch18. ISBN 978-0-470-75052-0. 
  15. ↑ 15.0 15.1 "The infra-auricular fissure: a bedside marker of disease severity in patients with atopic dermatitis". Journal of the American Academy of Dermatology 66 (6): 1009–1010. June 2012. doi:10.1016/j.jaad.2011.10.031. PMID 22583715. 
  16. ↑ "Atopic dermatitis". Lancet 396 (10247): 345–360. August 2020. doi:10.1016/S0140-6736(20)31286-1. PMID 32738956. 
  17. ↑ "Skin pigmentation and eczema" (in en). 2021-02-09. https://eczema.org/information-and-advice/living-with-eczema/skin-pigmentation/. 
  18. ↑ 18.0 18.1 18.2 18.3 18.4 "Atopic dermatitis: an overview". American Family Physician 86 (1): 35–42. July 2012. PMID 22962911. http://www.aafp.org/afp/2012/0701/p35.pdf. 
  19. ↑ 19.0 19.1 19.2 19.3 19.4 "Atopic Dermatitis". Medscape Reference. WebMD. 21 January 2014. http://emedicine.medscape.com/article/1049085-overview#showall. 
  20. ↑ "Atopic Dermatitis". Encyclopedia of molecular mechanisms of diseases. Berlin: Springer. 2009. ISBN 978-3-540-67136-7. 
  21. ↑ "Guidance on the diagnosis and clinical management of atopic eczema". Clinical and Experimental Dermatology 37 (Suppl 1): 7–12. May 2012. doi:10.1111/j.1365-2230.2012.04336.x. PMID 22486763. 
  22. ↑ "Assessment of clinical signs of atopic dermatitis: a systematic review and recommendation". The Journal of Allergy and Clinical Immunology 132 (6): 1337–1347. December 2013. doi:10.1016/j.jaci.2013.07.008. PMID 24035157. 
  23. ↑ "Atopic Dermatitis: Update for Pediatricians". Pediatric Annals 45 (8): e280–e286. August 2016. doi:10.3928/19382359-20160720-05. PMID 27517355. 
  24. ↑ 24.0 24.1 24.2 24.3 "NIAID Researchers Identify Link Between Common Chemicals and Eczema | NIH: National Institute of Allergy and Infectious Diseases" (in en). 2023-01-23. https://www.niaid.nih.gov/news-events/researchers-identify-link-between-common-chemicals-and-eczema. 
  25. ↑ 25.0 25.1 Zeldin, Jordan; Chaudhary, Prem Prashant; Spathies, Jacquelyn; Yadav, Manoj; D'Souza, Brandon N.; Alishahedani, Mohammadali E.; Gough, Portia; Matriz, Jobel et al. (2023-01-06). "Exposure to isocyanates predicts atopic dermatitis prevalence and disrupts therapeutic pathways in commensal bacteria". Science Advances 9 (1): eade8898. doi:10.1126/sciadv.ade8898. ISSN 2375-2548. PMID 36608129. Bibcode: 2023SciA....9E8898Z. 
  26. ↑ 26.0 26.1 26.2 "Eczema's cause could be in the air we breathe" (in en). 2023-03-26. https://www.nbcnews.com/health/health-news/causes-eczema-air-breathe-new-science-suggests-rcna76427. 
  27. ↑ Chaudhary, Prem Prashant; Myles, Ian A.; Zeldin, Jordan; Dabdoub, Shareef; Deopujari, Varsha; Baveja, Rajiv; Baker, Robin; Bengtson, Sarah et al. (October 2023). "Shotgun metagenomic sequencing on skin microbiome indicates dysbiosis exists prior to the onset of atopic dermatitis". Allergy 78 (10): 2724–2731. doi:10.1111/all.15806. ISSN 1398-9995. PMID 37422700. 
  28. ↑ 28.0 28.1 Berdyshev, Evgeny; Kim, Jihyun; Kim, Byung Eui; Goleva, Elena; Lyubchenko, Taras; Bronova, Irina; Bronoff, Anna Sofia; Xiao, Olivia et al. (May 2023). "Stratum corneum lipid and cytokine biomarkers at age 2 months predict the future onset of atopic dermatitis". The Journal of Allergy and Clinical Immunology 151 (5): 1307–1316. doi:10.1016/j.jaci.2023.02.013. ISSN 1097-6825. PMID 36828081. 
  29. ↑ Rinnov, Maria Rasmussen; Halling, Anne-Sofie; Gerner, Trine; Ravn, Nina Haarup; Knudgaard, Mette Hjorslev; Trautner, Simon; Goorden, Susan M. I.; Ghauharali-van der Vlugt, Karen J. M. et al. (March 2023). "Skin biomarkers predict development of atopic dermatitis in infancy". Allergy 78 (3): 791–802. doi:10.1111/all.15518. ISSN 1398-9995. PMID 36112082. 
  30. ↑ Yamamoto-Hanada, Kiwako; Saito-Abe, Mayako; Shima, Kyoko; Fukagawa, Satoko; Uehara, Yuya; Ueda, Yui; Iwamura, Maeko; Murase, Takatoshi et al. (July 2023). "mRNAs in skin surface lipids unveiled atopic dermatitis at 1 month". Journal of the European Academy of Dermatology and Venereology: JEADV 37 (7): 1385–1395. doi:10.1111/jdv.19017. ISSN 1468-3083. PMID 36897437. 
  31. ↑ Yadav, Manoj; Chaudhary, Prem Prashant; D'Souza, Brandon N.; Ratley, Grace; Spathies, Jacquelyn; Ganesan, Sundar; Zeldin, Jordan; Myles, Ian A. (2023). "Diisocyanates influence models of atopic dermatitis through direct activation of TRPA1". PLOS ONE 18 (3): e0282569. doi:10.1371/journal.pone.0282569. ISSN 1932-6203. PMID 36877675. Bibcode: 2023PLoSO..1882569Y. 
  32. ↑ "The effect of environmental humidity and temperature on skin barrier function and dermatitis". Journal of the European Academy of Dermatology and Venereology 30 (2): 223–249. February 2016. doi:10.1111/jdv.13301. PMID 26449379. 
  33. ↑ 33.00 33.01 33.02 33.03 33.04 33.05 33.06 33.07 33.08 33.09 33.10 33.11 33.12 33.13 33.14 33.15 33.16 "Atopic Dermatitis". The New England Journal of Medicine 384 (12): 1136–1143. March 2021. doi:10.1056/NEJMra2023911. PMID 33761208. 
  34. ↑ "The Pathogenetic Effect of Natural and Bacterial Toxins on Atopic Dermatitis". Toxins 9 (1): 3. December 2016. doi:10.3390/toxins9010003. PMID 28025545. 
  35. ↑ "Filaggrin mutations associated with skin and allergic diseases". The New England Journal of Medicine 365 (14): 1315–1327. October 2011. doi:10.1056/NEJMra1011040. PMID 21991953. 
  36. ↑ "News Feature: Cleaning up the hygiene hypothesis". Proceedings of the National Academy of Sciences of the United States of America 114 (7): 1433–1436. February 2017. doi:10.1073/pnas.1700688114. PMID 28196925. Bibcode: 2017PNAS..114.1433S. 
  37. ↑ "Atopic dermatitis". The New England Journal of Medicine 358 (14): 1483–1494. April 2008. doi:10.1056/NEJMra074081. PMID 18385500. 
  38. ↑ "Pet exposure and risk of atopic dermatitis at the pediatric age: a meta-analysis of birth cohort studies". The Journal of Allergy and Clinical Immunology 132 (3): 616–622.e7. September 2013. doi:10.1016/j.jaci.2013.04.009. PMID 23711545. 
  39. ↑ 39.0 39.1 39.2 "New insights into the epidemiology of childhood atopic dermatitis". Allergy 69 (1): 3–16. January 2014. doi:10.1111/all.12270. PMID 24417229. 
  40. ↑ "Prevention of food and airway allergy: consensus of the Italian Society of Preventive and Social Paediatrics, the Italian Society of Paediatric Allergy and Immunology, and Italian Society of Pediatrics". The World Allergy Organization Journal 9: 28. 2016. doi:10.1186/s40413-016-0111-6. PMID 27583103. 
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  42. ↑ 42.0 42.1 "Nonceliac gluten sensitivity". Gastroenterology 148 (6): 1195–1204. May 2015. doi:10.1053/j.gastro.2014.12.049. PMID 25583468. "Many patients with celiac disease also have atopic disorders. About 30% of patients' allergies with gastrointestinal (GI) symptoms and mucosal lesions, but negative results from serologic (TG2 antibodies) or genetic tests (DQ2 or DQ8 genotype) for celiac disease, had reduced GI and atopic symptoms when they were placed on GFDs. These findings indicated that their symptoms were related to gluten ingestion.". 
  43. ↑ 43.0 43.1 "Non-celiac gluten sensitivity: literature review". Journal of the American College of Nutrition 33 (1): 39–54. 2014. doi:10.1080/07315724.2014.869996. PMID 24533607. 
  44. ↑ "How epidemiology has challenged 3 prevailing concepts about atopic dermatitis". The Journal of Allergy and Clinical Immunology 118 (1): 209–213. July 2006. doi:10.1016/j.jaci.2006.04.043. PMID 16815157. http://eprints.nottingham.ac.uk/861/2/revised_final_rostrum.pdf. Retrieved 2019-02-05. 
  45. ↑ "Dissecting the causes of atopic dermatitis in children: less foods, more mites". Allergology International 61 (2): 231–243. June 2012. doi:10.2332/allergolint.11-RA-0371. PMID 22361514. 
  46. ↑ "Skin colonization of Staphylococcus aureus in atopic dermatitis patients seen at the National Skin Centre, Singapore". International Journal of Dermatology 36 (9): 653–657. September 1997. doi:10.1046/j.1365-4362.1997.00290.x. PMID 9352404. 
  47. ↑ "Staphylococcus aureus Exploits Epidermal Barrier Defects in Atopic Dermatitis to Trigger Cytokine Expression". The Journal of Investigative Dermatology 136 (11): 2192–2200. November 2016. doi:10.1016/j.jid.2016.05.127. PMID 27381887. 
  48. ↑ 48.0 48.1 "Interventions to reduce Staphylococcus aureus in the management of eczema". The Cochrane Database of Systematic Reviews 2019 (10). October 2019. doi:10.1002/14651858.CD003871.pub3. PMID 31684694. 
  49. ↑ "Potential health impacts of hard water". International Journal of Preventive Medicine 4 (8): 866–875. August 2013. PMID 24049611. 
  50. ↑ 50.0 50.1 "The effect of water hardness on atopic eczema, skin barrier function: A systematic review, meta-analysis". Clinical and Experimental Allergy 51 (3): 430–451. March 2021. doi:10.1111/cea.13797. PMID 33259122. 
  51. ↑ "Targeting key proximal drivers of type 2 inflammation in disease". Nature Reviews. Drug Discovery 15 (1): 35–50. January 2016. doi:10.1038/nrd4624. PMID 26471366. 
  52. ↑ "Type 2 immunity in the skin and lungs". Allergy 75 (7): 1582–1605. July 2020. doi:10.1111/all.14318. PMID 32319104. 
  53. ↑ 53.0 53.1 "Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis". Journal of the American Academy of Dermatology 70 (2): 338–351. February 2014. doi:10.1016/j.jaad.2013.10.010. PMID 24290431. 
  54. ↑ 54.0 54.1 "Diagnostic criteria for atopic dermatitis: a systematic review". The British Journal of Dermatology 158 (4): 754–765. April 2008. doi:10.1111/j.1365-2133.2007.08412.x. PMID 18241277. 
  55. ↑ 55.0 55.1 "The U.K. Working Party's Diagnostic Criteria for Atopic Dermatitis. III. Independent hospital validation". The British Journal of Dermatology 131 (3): 406–416. September 1994. doi:10.1111/j.1365-2133.1994.tb08532.x. PMID 7918017. 
  56. ↑ "What are Topical Treatments for Eczema and How Should They Be Used?" (in en-US). https://nationaleczema.org/eczema/treatment/topicals/. 
  57. ↑ Chopra, Rishi; Silverberg, Jonathan I. (2018). "Assessing the severity of atopic dermatitis in clinical trials and practice". Clinics in Dermatology. Atopic Dermatits: Part II 36 (5): 606–615. doi:10.1016/j.clindermatol.2018.05.012. ISSN 0738-081X. PMID 30217273. https://www.sciencedirect.com/science/article/pii/S0738081X1830141X. 
  58. ↑ "Which emollients are effective and acceptable for eczema in children?". BMJ 367: l5882. October 2019. doi:10.1136/bmj.l5882. PMID 31649114. https://research-information.bris.ac.uk/ws/files/219950607/bmj.l5882.full.pdf. 
  59. ↑ "Effectiveness and safety of lotion, cream, gel, and ointment emollients for childhood eczema: a pragmatic, randomised, phase 4, superiority trial". The Lancet. Child & Adolescent Health 6 (8): 522–532. August 2022. doi:10.1016/S2352-4642(22)00146-8. PMID 35617974. 
  60. ↑ 60.0 60.1 60.2 60.3 60.4 Chu, Derek K.; Chu, Alexandro W. L.; Rayner, Daniel G.; Guyatt, Gordon H.; Yepes-Nuñez, Juan José (2023). "Topical treatments for atopic dermatitis (eczema): Systematic review and network meta-analysis of randomized trials". The Journal of Allergy and Clinical Immunology 152 (6): 1493–1519. doi:10.1016/j.jaci.2023.08.030. ISSN 1097-6825. PMID 37678572. https://www.jacionline.org/article/S0091-6749(23)01113-2/fulltext. 
  61. ↑ "Emollient bath additives for the treatment of childhood eczema (BATHE): multicentre pragmatic parallel group randomised controlled trial of clinical and cost effectiveness". BMJ 361: k1332. May 2018. doi:10.1136/bmj.k1332. PMID 29724749. 
  62. ↑ 62.0 62.1 "Strategies for using topical corticosteroids in children and adults with eczema". The Cochrane Database of Systematic Reviews 2022 (3): CD013356. March 2022. doi:10.1002/14651858.CD013356.pub2. PMID 35275399. 
  63. ↑ 63.0 63.1 63.2 63.3 AAAAI/ACAAI JTF Atopic Dermatitis Guideline Panel; Chu, Derek K.; Schneider, Lynda; Asiniwasis, Rachel Netahe; Boguniewicz, Mark (2023). "Atopic dermatitis (eczema) guidelines: 2023 American Academy of Allergy, Asthma and Immunology/American College of Allergy, Asthma and Immunology Joint Task Force on Practice Parameters GRADE- and Institute of Medicine-based recommendations". Annals of Allergy, Asthma & Immunology: S1081–1206(23)01455–2. doi:10.1016/j.anai.2023.11.009. ISSN 1534-4436. PMID 38108679. 
  64. ↑ "Topical tacrolimus for atopic dermatitis". The Cochrane Database of Systematic Reviews 2015 (7): CD009864. July 2015. doi:10.1002/14651858.CD009864.pub2. PMID 26132597. 
  65. ↑ "Cancer risk with topical calcineurin inhibitors, pimecrolimus and tacrolimus, for atopic dermatitis: a systematic review and meta-analysis". The Lancet. Child & Adolescent Health 7 (1): 13–25. January 2023. doi:10.1016/S2352-4642(22)00283-8. PMID 36370744. 
  66. ↑ "Crisaborole: A Novel Nonsteroidal Topical Treatment for Atopic Dermatitis". The Journal of Pharmacy Technology 35 (4): 172–178. August 2019. doi:10.1177/8755122519844507. PMID 34861031. 
  67. ↑ "Topical Administration of Crisaborole in Mild to Moderate Atopic Dermatitis: A Systematic Review and Meta-Analysis" (in en). Dermatologic Therapy 2023: 1–9. 2023-02-06. doi:10.1155/2023/1869934. ISSN 1529-8019. 
  68. ↑ "The effects of treatment on itch in atopic dermatitis". Dermatologic Therapy 26 (2): 110–119. March–April 2013. doi:10.1111/dth.12032. PMID 23551368. 
  69. ↑ "Neuroimmunological mechanism of pruritus in atopic dermatitis focused on the role of serotonin". Biomolecules & Therapeutics 20 (6): 506–512. November 2012. doi:10.4062/biomolther.2012.20.6.506. PMID 24009842. 
  70. ↑ "A systematic review on the off-label use of montelukast in atopic dermatitis treatment". International Journal of Clinical Pharmacy 40 (5): 963–976. October 2018. doi:10.1007/s11096-018-0655-3. PMID 29777328. 
  71. ↑ "Leukotriene receptor antagonists for eczema". The Cochrane Database of Systematic Reviews 2018 (10): CD011224. October 2018. doi:10.1002/14651858.cd011224.pub2. PMID 30343498. 
  72. ↑ "FDA approves new eczema drug Dupixent". US Food & Drug Administration. 28 March 2017. https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm549078.htm. 
  73. ↑ "Adtralza EPAR". 20 April 2021. https://www.ema.europa.eu/en/medicines/human/EPAR/adtralza.  Text was copied from this source which is © European Medicines Agency. Reproduction is authorized provided the source is acknowledged.
  74. ↑ "Drug Approval Package: ADBRY". US Food & Drug Administration. December 27, 2021. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2022/761180Orig1s000TOC.cfm. 
  75. ↑ "Almirall granted EMA approval for lebrikizumab in atopic dermatitis" (in en). 2022-10-28. https://www.pmlive.com/pharma_news/almirall_granted_ema_approval_for_lebrikizumab_in_atopic_dermatitis_1479922. 
  76. ↑ "Eli Lilly Submits BLA for Lebrikizumab AD Treatment" (in en). 9 November 2022. https://www.dermatologytimes.com/view/eli-lilly-submits-bla-for-lebrikizumab-ad-treatment. 
  77. ↑ 77.0 77.1 77.2 Chu, Alexandro W. L.; Wong, Melanie M.; Rayner, Daniel G.; Guyatt, Gordon H.; Díaz Martinez, Juan Pablo (2023). "Systemic treatments for atopic dermatitis (eczema): Systematic review and network meta-analysis of randomized trials". The Journal of Allergy and Clinical Immunology 152 (6): 1470–1492. doi:10.1016/j.jaci.2023.08.029. ISSN 1097-6825. PMID 37678577. 
  78. ↑ "U.S. FDA Approves Pfizer's Cibinqo (abrocitinib) for Adults with Moderate-to-Severe Atopic Dermatitis". Pfizer Inc. (Press release). 14 January 2022. Retrieved 16 January 2022.
  79. ↑ "U.S. FDA Approves RINVOQ® (upadacitinib) to Treat Adults and Children 12 Years and Older with Refractory, Moderate to Severe Atopic Dermatitis". AbbeVie (Press release). Retrieved March 6, 2022.
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  81. ↑ "Specific allergen immunotherapy for the treatment of atopic eczema". The Cochrane Database of Systematic Reviews 2016 (2): CD008774. February 2016. doi:10.1002/14651858.CD008774.pub2. PMID 26871981. 
  82. ↑ "The role of vitamin D in atopic dermatitis". Dermatitis 26 (4): 155–161. 2015. doi:10.1097/DER.0000000000000128. PMID 26172483. 
  83. ↑ "Vitamin D and atopic dermatitis: A systematic review and meta-analysis". Nutrition 32 (9): 913–920. September 2016. doi:10.1016/j.nut.2016.01.023. PMID 27061361. 
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  87. ↑ "Probiotics for treating eczema". The Cochrane Database of Systematic Reviews 2018 (11): CD006135. November 2018. doi:10.1002/14651858.CD006135.pub3. PMID 30480774. 
  88. ↑ "Prebiotics and probiotics in atopic dermatitis". Experimental and Therapeutic Medicine 18 (2): 926–931. August 2019. doi:10.3892/etm.2019.7678. PMID 31384325. 
  89. ↑ "The role of probiotics in the treatment of adult atopic dermatitis: a meta-analysis of randomized controlled trials". Journal of Health, Population, and Nutrition 41 (1): 37. August 2022. doi:10.1186/s41043-022-00318-6. PMID 35978397. 
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  93. ↑ "Bleach baths for atopic dermatitis: A systematic review and meta-analysis including unpublished data, Bayesian interpretation, and GRADE". Annals of Allergy, Asthma & Immunology 128 (6): 660–668.e9. June 2022. doi:10.1016/j.anai.2022.03.024. PMID 35367346. 
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  116. ↑ "Atopic Dermatitis". www.uchospitals.edu. 1 January 2015. http://www.uchospitals.edu/online-library/content=P01675. 
  117. ↑ "Scratching the surface: a review of online misinformation and conspiracy theories in atopic dermatitis". Clinical and Experimental Dermatology 46 (8): 1545–1547. December 2021. doi:10.1111/ced.14679. PMID 33864398. 
  118. ↑ "Prevalence and odds of Staphylococcus aureus carriage in atopic dermatitis: a systematic review and meta-analysis". The British Journal of Dermatology 175 (4): 687–695. October 2016. doi:10.1111/bjd.14566. PMID 26994362. 

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