Atopic dermatitis

Symptoms refer to the sensations that people with AD feel, whereas signs refer 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, soreness, or pain. Surface changes include: • scaling cracking (skin 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. Any part of the body can be affected by AD. Atopic dermatitis commonly affects the eyelids, where an extra prominent crease can form under the eyelid due to skin swelling known as Dennie-Morgan infraorbital folds. Cracks can form under the ears, which can be painful (infra-auricular fissure). 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 that form in the bends of the arms or legs, face, and neck. == Causes ==

The cause of AD is not known, although evidence indicates environmental, immunologic, bacterial, and potential genetic factors. Pollution Since 1970 the rates of atopic dermatitis in the US and UK have increased three- to sixfold. Even today, people who migrate from developing nations before the age of 4 years old 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. Recent work has shed light on these and other data, strongly suggesting that early life industrial exposures may cause atopic dermatitis. Chemicals such as (di)isocyanates and xylene prevent the skin bacteria from producing ceramide-sphingolipid family lipids. These chemicals also directly activate an itch receptor in the skin known as TRPA1. 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. Genetics Genes that may contribute to AD are mainly those responsible for immune response (e.g., TH2 cytokine and JAK-STAT pathway genes) and the skin barrier (e.g., filaggrin, claudin-1, loricrin). Immune response: 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. However, expression of filaggrin protein or breakdown products offers no predictive utility in atopic dermatitis risk. 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. 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. Those exposed to dogs while growing up have a lower risk of atopic dermatitis. Also, epidemiological studies support a protective role for helminths against AD. Likewise, children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurized milk. 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. 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. A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for heavily processed foods. Exposure to dust mites, for example, is believed to contribute to the risk of developing AD. Hard water The prevalence of atopic dermatitis in children may be linked to the level of calcium carbonate or "hardness" of household drinking water. 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. ==Role of Staphylococcus aureus==

Colonization of the skin by the bacterium S. aureus is prevalent in those with atopic dermatitis. Abnormalities in the skin barrier of persons with AD are exploited by S. aureus to trigger cytokine expression, thus aggravating the condition. 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. The role of S. aureus in skin irritation occurs via inflammation factors that induce itching, which may damage the skin, further driving inflammation, and facilitating the growth of S. aureus, thus promoting a chronic cycle. ==Pathophysiology==

Excessive type 2 inflammation underlies the pathophysiology of atopic dermatitis. Disruption of the epidermal barrier is thought to play an integral role in the pathogenesis of AD. 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 attract Th2 CD4+ helper T cells to the skin. This dysregulated Th2 inflammatory response is thought to lead to the eczematous lesions. 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. Other CD4+ helper T-cell pathways thought to be involved in atopic dermatitis inflammation include the Th1, Th17, and Th22 pathways. 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. Mutations in the filaggrin gene, FLG, also cause impairment in the skin barrier that contributes to the pathogenesis of AD. 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 contribute to the skin barrier. 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. 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). Atopic dermatitis is also associated with the release of pruritogens (molecules that stimulate pruritus or itching) in the skin. 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. The pruritogens include the Th2 cytokines IL-4, IL-13, IL-31, histamine, and various neuropeptides. 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. Chronic scratching of lesions can cause thickening or lichenification of the skin or prurigo nodularis (generalized nodules that are severely itchy). Another factor in the barrier failure and immunological dysregulation in people with atopic dermatitis may be due to decreases in tight junction protein Claudin-1. Inhibiting Claudin-1 expression in human keratinocytes has been shown to both reduce tight junction function, as well as increase keratinocyte proliferation in vitro. It has also been discovered that this deteriorates the bioelectric barrier function in the epidermis. == Diagnosis ==

Atopic dermatitis is typically diagnosed clinically, meaning it is based on signs and symptoms alone, without special testing. Several different criteria developed for research have also been validated to aid in diagnosis. Of these, the UK Diagnostic Criteria, based on the work of Hanifin and Rajka, has been the most widely validated. Other diseases that must be excluded before making a diagnosis include contact dermatitis, psoriasis, and seborrheic dermatitis. == Prevention ==

There are no established clinical methods using dietary or topical strategies to inhibit or prevent atopic dermatitis. Specific dietary plans during pregnancy and in early childhood, such as eating fatty fish (or taking omega-3 supplements), are not effective. Taking probiotics (for example Lactobacillus rhamnosus) during pregnancy and feeding probiotics to infants are strategies under research, with only preliminary evidence that they may be preventative. Using moisturizers 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. == Treatments ==

No cure for AD is known, although treatments may reduce the severity and frequency of flares. Clinical trials often measure the efficacy of treatments with a severity scale such as the SCORAD index or the Eczema Area and Severity Index. Moisturisers Daily basic care stabilizes the barrier function of the skin to mitigate its sensitivity to irritation and penetration of allergens. Affected persons often report that improvement in skin hydration parallels improvement in AD symptoms. Moisturisers (or emollients) can improve skin comfort and may reduce disease flares. 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. 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 affected, climate/season, and personal preference. Non-medicated prescription moisturisers may also be no more effective than over-the-counter moisturisers. The use of emollient bath additives does not provide any additional benefits. Medication Topical Creams and ointments containing corticosteroids applied directly on skin (topical) are effective in managing atopic dermatitis. Newer (second generation) corticosteroids, such as fluticasone propionate and mometasone furoate, are more effective and safer than older ones. Strong and moderate corticosteroids are more effective than weaker ones. They are also generally safe and do not cause skin 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). Applying once daily is as effective as twice or more daily application. Both tacrolimus and pimecrolimus are effective and safe to use in AD. Crisaborole, an inhibitor of PDE-4, is also effective and safe as a topical treatment for mild-to-moderate AD. Ruxolitinib, a Janus kinase inhibitor, has uncertain efficacy and safety. and in the United States in February 2026. Systemic When topical (on skin) treatments fail to control severe AD flares, medications taken by mouth (systemic treatment) can be used. Newer medications, such as monoclonal antibodies and JAK inhibitors, are highly effective for managing atopic dermatitis, but modestly increase the risk of conjunctivitis. These include dupilumab (Dupixent), tralokinumab (Adtralza, Adbry), abrocitinib (Cibinqo), baricitinib (Olumiant) and upadacitinib (Rinvoq). Among monoclonal antibodies, dupilumab and tralokinumab are approved to treat moderate-to-severe eczema in the US and the EU. Lebrikizumab is also approved in the EU for treating moderate-to-severe AD but in the US its approval was declined due to manufacturing issues. Abrocitinib and upadacitinib have also been approved in the US for the treatment of moderate-to-severe eczema. Nemolizumab (Nemluvio) was approved to treat atopic dermatitis in December 2024. Allergen immunotherapy may be effective in relieving symptoms of AD, but it also comes with an increased risk of adverse events. This treatment consists of a series of injections or drops under the tongue of a solution containing the allergen. The skin of people with AD can easily get infected, most commonly by the bacteria Staphylococcus 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 of S. aureus, but their benefit is limited, and they increase the risk of antimicrobial resistance. For these reasons, they are only recommended for people who not only present symptoms on the skin but also feel systemically unwell. Diet The role of vitamin D on atopic dermatitis is not clear, but vitamin D supplementation may improve its symptoms. 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. Several probiotics seem to have a positive effect, with a roughly 20% reduction in the rate of AD. Probiotics containing multiple strains of bacteria seem to work the best. In people with celiac disease or nonceliac gluten sensitivity, a gluten-free diet improves their symptoms and prevents the occurrence of new outbreaks. Lifestyle Health professionals often recommend that people with AD bathe regularly in lukewarm baths, especially in saltwater, to moisten their skin. Dilute bleach baths may be helpful for people with moderate and severe eczema, but only for people with Staphylococcus aureus. Avoiding large-diameter woolen clothing or scratchy fibres is usually recommended for people with AD as they can trigger a flare. Safe alternatives are clothes made from fabrics with smaller diameters and smooth fibers. These include super- and ultrafine merino wool and fabrics with anti-microbial textile finishes. Wearing silk is also safe but does not improve symptoms of AD. Self-management Living with AD requires a high level of self-management (for example, avoiding triggers) and adherence to treatments (regularly applying medication). Good self-management contributes to better disease outcomes and quality of life. However, worries about topical treatments, misconceptions about the condition, unclear information, and unsuitable communication from doctors can make living with AD more difficult. A website supporting self-management has been shown to improve AD symptoms for parents, children, adolescents and young adults. 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. Among the different types of phototherapies only narrowband (NB) ultraviolet B (UVB) exposure might help with the severity of AD and ease itching. However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk. UV phototherapy is not indicated in young adults and children due to this risk of skin cancer with prolonged use or exposure. Research into microbiome-based approaches to restoring the skin barrier has also been explored, including formulations developed by companies such as Codex Labs, which focus on supporting skin microbiota balance in atopic dermatitis. == Impact ==

Atopic dermatitis significantly impairs the quality of life of affected individuals. 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. According to the Global Burden of Disease Study, AD is the skin disease with the highest disability-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. Humanistic burden Atopic dermatitis significantly decreases the quality of life by affecting various aspects of people's 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 people with AD, further contribute to the humanistic burden, affecting daily productivity and concentration. Productivity loss 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, with presenteeism accounting for the majority of these days. Burden of disease in the Middle East and Africa Atopic dermatitis leads to the highest loss in disability-adjusted life years compared to other skin diseases in the Middle East and Africa. 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 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. 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. 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. == 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. 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. Over 15 million American adults and children have AD. == 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. == Research ==

Leukotriene receptor antagonists, such as montelukast, might be useful for the treatment of AD but their effectiveness has not yet been proven by research. == References ==