Atopic dermatitis
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
Atopic eczema, infantile eczema, prurigo Besnier, allergic eczema, neurodermatitis[1]
Family history, living in a city, dry climate[2]
Avoiding things that worsen the condition, daily bathing followed by moisturising cream, steroid creams for flares[3] Humidifier
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]
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 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:
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]
Pathophysiology[edit]
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]
Epidemiology[edit]
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.[106][107] 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[edit]
Conspiracy theories[edit]
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[edit]
Staphylococcus aureus may have a role in producing atopic dermatitis by colonizing on the skin.[118]