Atopic dermatitis

<h2 id="signs-and-symptoms">Signs and symptoms</h2>

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 <a href="/facts/Itch/MBWq6SPc">itching</a> which can be intense. Some people experience burning or soreness or <a href="/facts/Pain/70E79oUn">pain</a>.<a class="footnote-ref" id="fnref:35" href="#fn:35">35</a>
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).<a class="footnote-ref" id="fnref:36" href="#fn:36">36</a> Surface changes include:

<ul><li>scaling cracking (<a href="/facts/Skin_fissure/QUJ3cagg">skin fissures</a>)</li>
<li>swelling (<a href="/facts/Edema/Q6MI3KdH">oedema</a>)</li>
<li>scratch marks (excoriation)</li>
<li>bumpiness (<a href="/facts/Papule/2J7QwJdE">papulation</a>)</li>
<li>oozing of clear fluid</li>
<li>thickening of the skin (<a href="/facts/Lichenification/Vkr5XpeG">lichenification</a>) where the AD has been present for a long time.<a class="footnote-ref" id="fnref:37" href="#fn:37">37</a></li></ul>
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.<a class="footnote-ref" id="fnref:38" href="#fn:38">38</a> Any part of the body can be affected by AD.<a class="footnote-ref" id="fnref:39" href="#fn:39">39</a>
Atopic dermatitis commonly affects the eyelids, where an extra prominent crease can form under the eyelid due to skin swelling known as <a href="/facts/Dennie%E2%80%93Morgan_fold/aaKPFenR">Dennie-Morgan infraorbital folds</a>.<a class="footnote-ref" id="fnref:40" href="#fn:40">40</a> Cracks can form under the ears which can be painful (infra-auricular fissure).<a class="footnote-ref" id="fnref:41" href="#fn:41">41</a><a class="footnote-ref" id="fnref:42" href="#fn:42">42</a>
The inflammation from AD often leaves "footprints" known as <a href="/facts/Postinflammatory_hypopigmentation/bcuesYsV">postinflammatory pigmentation</a> 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.<a class="footnote-ref" id="fnref:43" href="#fn:43">43</a>
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 <a href="/facts/Lesion/WJDFnyLk">lesions</a> to form in the bends of the arms or legs, face, and neck.<a class="footnote-ref" id="fnref:44" href="#fn:44">44</a><a class="footnote-ref" id="fnref:45" href="#fn:45">45</a><a class="footnote-ref" id="fnref:46" href="#fn:46">46</a><a class="footnote-ref" id="fnref:47" href="#fn:47">47</a><a class="footnote-ref" id="fnref:48" href="#fn:48">48</a>

<h2 id="causes">Causes</h2>
The cause of AD is not known, although evidence indicates environmental, immunologic, bacterial<a class="footnote-ref" id="fnref:49" href="#fn:49">49</a> and potential genetic factors.<a class="footnote-ref" id="fnref:50" href="#fn:50">50</a>

<h3>Pollution</h3>
Since 1970, the rates of atopic dermatitis in the US and UK have increased 3-6 fold.<a class="footnote-ref" id="fnref:51" href="#fn:51">51</a> Even today, people who migrate from <a href="/facts/Developing_country/eTfS4kxl">developing nations</a> before the age of 4 years to <a href="/facts/Developed_country/sqwTSDHm">industrialized nations</a> experience a dramatic rise in the risk of atopic dermatitis and have an additional risk when living in <a href="/facts/Urban_area/fu9v8h5P">urbanized areas</a> of the industrial nation.<a class="footnote-ref" id="fnref:52" href="#fn:52">52</a> Recent work has shed light on these and other data strongly suggesting that early life industrial exposures may cause atopic dermatitis.<a class="footnote-ref" id="fnref:53" href="#fn:53">53</a><a class="footnote-ref" id="fnref:54" href="#fn:54">54</a> Chemicals such as <a href="/facts/Isocyanate/YYDoDBgp">(di)isocyanates</a> and <a href="/facts/Xylene/BEGggD9s">xylene</a> prevent the skin bacteria from producing <a href="/facts/Ceramide/nLdl2GCr">ceramide</a>-<a href="/facts/Sphingolipid/qdG4l8DQ">sphingolipid</a> family <a href="/facts/Lipid/TdQR87HX">lipids</a>.<a class="footnote-ref" id="fnref:55" href="#fn:55">55</a><a class="footnote-ref" id="fnref:56" href="#fn:56">56</a> Early life deficiency in these lipids predictive which children will go on to develop atopic dermatitis.<a class="footnote-ref" id="fnref:57" href="#fn:57">57</a><a class="footnote-ref" id="fnref:58" href="#fn:58">58</a><a class="footnote-ref" id="fnref:59" href="#fn:59">59</a><a class="footnote-ref" id="fnref:60" href="#fn:60">60</a> These chemicals also directly activate an itch receptor in the skin known as <a href="/facts/TRPA1/JPYYxzfY">TRPA1</a>.<a class="footnote-ref" id="fnref:61" href="#fn:61">61</a> 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, <a href="/facts/Exhaust_gas/kLpq1eUX">automobile exhaust</a>, <a href="/facts/Wallpaper_paste/TGlrhx70">wallpaper adhesives</a>, paints, non-latex foam furniture, cigarette smoke, and are elements of fabrics like <a href="/facts/Polyester/Ivp9CHpl">polyester</a>, <a href="/facts/Nylon/hBvG9bCw">nylon</a>, and <a href="/facts/Spandex/rcId3DYb">spandex</a>.<a class="footnote-ref" id="fnref:62" href="#fn:62">62</a><a class="footnote-ref" id="fnref:63" href="#fn:63">63</a><a class="footnote-ref" id="fnref:64" href="#fn:64">64</a>

<h3>Climate</h3>
Low <a href="/facts/Humidity/Nwb28VlT">humidity</a>, and low <a href="/facts/Temperature/QyGe4gmj">temperature</a> increase the prevalence and risk of flares in people with atopic dermatitis.<a class="footnote-ref" id="fnref:65" href="#fn:65">65</a>

<h3>Genetics</h3>
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).
Immune response: Many people with AD have a family history or a personal history of <a href="/facts/Atopy/7QqBDPII">atopy</a>. Atopy is a term used to describe individuals who produce substantial amounts of <a href="/facts/Immunoglobulin_E/76uGAl7k">IgE</a>. Such individuals have an increased tendency to develop <a href="/facts/Asthma/7GkJvxn3">asthma</a>, <a href="/facts/Allergic_rhinitis/ukE6bkIs">hay fever</a>, <a href="/facts/Dermatitis/JwlyQBa2">eczema</a>, <a href="/facts/Hives/zMkVo9qL">urticaria</a> and allergic rhinitis.<a class="footnote-ref" id="fnref:66" href="#fn:66">66</a><a class="footnote-ref" id="fnref:67" href="#fn:67">67</a> Up to 80% of people with atopic dermatitis have elevated total or allergen-specific IgE levels.<a class="footnote-ref" id="fnref:68" href="#fn:68">68</a>
Skin barrier: About 30% of people with AD have mutations in the gene for the production of <a href="/facts/Filaggrin/J0B6WpBc">filaggrin</a> (FLG), which increase the risk for early onset of atopic dermatitis and developing asthma.<a class="footnote-ref" id="fnref:69" href="#fn:69">69</a><a class="footnote-ref" id="fnref:70" href="#fn:70">70</a> However, expression of filaggrin protein or breakdown products offer no predictive utility in atopic dermatitis risk.<a class="footnote-ref" id="fnref:71" href="#fn:71">71</a>
People with atopic dermatitis also have decreased expression of <a href="/facts/Tight_junction_proteins/a7TnGhc3">tight junction protein</a> <a href="/facts/CLDN1/CCd13mso">Claudin-1</a>, which deteriorates the <a href="/facts/Developmental_bioelectricity/fW8v2Szk">bioelectric</a> barrier function in the epidermis.<a class="footnote-ref" id="fnref:72" href="#fn:72">72</a>

<h3>Hygiene hypothesis</h3>
According to the <a href="/facts/Hygiene_hypothesis/3pmIpBDc">hygiene hypothesis</a>, early childhood exposure to certain microorganisms (such as <a href="/facts/Gut_flora/Xy1IWzSP">gut flora</a> and <a href="/facts/Helminth/V9wRobaA">helminth</a> parasites) protects against <a href="/facts/Allergy/dYAVosh8">allergic</a> diseases by contributing to the development of the <a href="/facts/Immune_system/HRCTf1pb">immune system</a>.<a class="footnote-ref" id="fnref:73" href="#fn:73">73</a> 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.<a class="footnote-ref" id="fnref:74" href="#fn:74">74</a> Those exposed to dogs while growing up have a lower risk of atopic dermatitis.<a class="footnote-ref" id="fnref:75" href="#fn:75">75</a> Also, epidemiological studies support a protective role for helminths against AD.<a class="footnote-ref" id="fnref:76" href="#fn:76">76</a> Likewise, children with poor hygiene are at a lower risk for developing AD, as are children who drink <a href="/facts/Raw_milk/3TSlq59T">unpasteurized milk</a>.<a class="footnote-ref" id="fnref:77" href="#fn:77">77</a>

<h3>Allergens</h3>
In a small percentage of cases, atopic dermatitis is caused by sensitization to foods<a class="footnote-ref" id="fnref:78" href="#fn:78">78</a> such as milk, but there is growing consensus that <a href="/facts/Food_allergy/Nkf1e70o">food allergy</a> most likely arises as a result of skin barrier dysfunction resulting from AD, rather than food allergy causing the skin problems.<a class="footnote-ref" id="fnref:79" href="#fn:79">79</a> Atopic dermatitis sometimes appears associated with <a href="/facts/Celiac_disease/AKd5PkTc">coeliac disease</a> and non-coeliac gluten sensitivity. Because a <a href="/facts/Gluten-free_diet/GXRvRR4K">gluten-free diet</a> (GFD) improves symptoms in these cases, <a href="/facts/Gluten/NNnUfKRU">gluten</a> seems to be the cause of AD in these cases.<a class="footnote-ref" id="fnref:80" href="#fn:80">80</a><a class="footnote-ref" id="fnref:81" href="#fn:81">81</a> A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for heavily <a href="/facts/Convenience_food/ayJbRMIt">processed foods</a>.<a class="footnote-ref" id="fnref:82" href="#fn:82">82</a>
Exposure to <a href="/facts/Allergen/bnM4cttq">allergens</a>, either from food or the environment, can exacerbate existing atopic dermatitis.<a class="footnote-ref" id="fnref:83" href="#fn:83">83</a> Exposure to <a href="/facts/House_dust_mite/CwyrgWSA">dust mites</a>, for example, is believed to contribute to the risk of developing AD.<a class="footnote-ref" id="fnref:84" href="#fn:84">84</a>

<h3>Hard water</h3>
The prevalence of atopic dermatitis in children may be linked to the level of <a href="/facts/Calcium_carbonate/UQ1wLFna">calcium carbonate</a> or "<a href="/facts/Hard_water/Ay4aksF4">hardness</a>" of household drinking water.<a class="footnote-ref" id="fnref:85" href="#fn:85">85</a><a class="footnote-ref" id="fnref:86" href="#fn:86">86</a> 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 <a href="/facts/Water_softening/66wnC1ml">water softeners</a> at home does not reduce the severity of the symptoms.<a class="footnote-ref" id="fnref:87" href="#fn:87">87</a><a class="footnote-ref" id="fnref:88" href="#fn:88">88</a>

<h2 id="role-of-staphylococcus-aureus">Role of Staphylococcus aureus</h2>
Colonization of the skin by the bacterium <a href="/facts/Staphylococcus_aureus/9yDVBMsc">S. aureus</a> is prevalent in those with atopic dermatitis.<a class="footnote-ref" id="fnref:89" href="#fn:89">89</a> Abnormalities in the skin barrier of persons with AD are exploited by S. aureus to trigger cytokine expression, thus aggravating the condition.<a class="footnote-ref" id="fnref:90" href="#fn:90">90</a>
However, atopic dermatitis is <a href="/facts/Non-communicable_disease/a3HxqDL3">non-communicable</a> and therefore could not be directly caused by a highly <a href="/facts/Infection/182XrncP">infectious</a> organism. Furthermore, there is insufficient evidence for the effectiveness of anti-staphylococcal treatments for treating S. aureus in infected or uninfected eczema.<a class="footnote-ref" id="fnref:91" href="#fn:91">91</a>
The role of S. aureus in skin irritation occurs via inflammation factors that induce <a href="/facts/Itching/MBWq6SPc">itching</a>, which may damage the skin, further driving inflammation, and facilitating the growth of S. aureus, thus promoting a chronic cycle.<a class="footnote-ref" id="fnref:92" href="#fn:92">92</a>

<h2 id="pathophysiology">Pathophysiology</h2>
Excessive <a href="/facts/Type_2_inflammation/L1srCqIE">type 2 inflammation</a> underlies the pathophysiology of atopic dermatitis.<a class="footnote-ref" id="fnref:93" href="#fn:93">93</a><a class="footnote-ref" id="fnref:94" href="#fn:94">94</a>
Disruption of the epidermal barrier is thought to play an integral role in the <a href="/facts/Pathogenesis/o9kHHK0U">pathogenesis</a> of AD.<a class="footnote-ref" id="fnref:95" href="#fn:95">95</a> Disruptions of the epidermal barrier allows allergens to penetrate the epidermis to deeper layers of the skin. This leads to activation of <a href="/facts/Dendritic_cell/19KBuKFK">epidermal inflammatory dendritic</a> and <a href="/facts/Innate_lymphoid_cell/fRNW3d80">innate lymphoid cells</a> which subsequently attracts <a href="/facts/T_helper_cell/nhwAYkDj">Th2 CD4+ helper T cells</a> to the skin.<a class="footnote-ref" id="fnref:96" href="#fn:96">96</a> This dysregulated Th2 inflammatory response is thought to lead to the eczematous lesions.<a class="footnote-ref" id="fnref:97" href="#fn:97">97</a> The Th2 helper T cells become activated, leading to the release of inflammatory cytokines including <a href="/facts/Interleukin_4/FacDJ3TY">IL-4</a>, <a href="/facts/Interleukin_13/zEaRbEqc">IL-13</a> and <a href="/facts/IL-31/0vzvz0FK">IL-31</a> which activate downstream <a href="/facts/Janus_kinase/HE2pXMJu">Janus kinase (Jak)</a> pathways. The active Jak pathways lead to inflammation and downstream activation of <a href="/facts/Plasma_cells/1fY4bFHR">plasma cells</a> and <a href="/facts/B_cells/6Y1tgwwp">B lymphocytes</a> which release antigen specific <a href="/facts/IgE/76uGAl7k">IgE</a> contributing to further inflammation.<a class="footnote-ref" id="fnref:98" href="#fn:98">98</a> Other CD4+ helper T-cell pathways thought to be involved in atopic dermatitis inflammation include the Th1, <a href="/facts/T_helper_17_cell/V3TmUNSX">Th17</a>, and Th22 pathways.<a class="footnote-ref" id="fnref:99" href="#fn:99">99</a> 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.<a class="footnote-ref" id="fnref:100" href="#fn:100">100</a>
Mutations in the filaggrin gene, FLG, also cause impairment in the skin barrier that contributes to the pathogenesis of AD.<a class="footnote-ref" id="fnref:101" href="#fn:101">101</a> Filaggrin is produced by epidermal skin cells (<a href="/facts/Keratinocytes/drqhJjuS">keratinocytes</a>) in the <a href="/facts/Stratum_corneum/7fwl4EF2">horny layer</a> 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.<a class="footnote-ref" id="fnref:102" href="#fn:102">102</a> 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 <a href="/facts/Xerosis/kJLKYrNA">xerosis</a> or dry skin commonly seen in AD) and antigen and allergen penetration of the epidermal layer.<a class="footnote-ref" id="fnref:103" href="#fn:103">103</a> 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 <a href="/facts/Staphylococcus_aureus/9yDVBMsc">Staphylococcus aureus</a> overgrowth or colonization).<a class="footnote-ref" id="fnref:104" href="#fn:104">104</a>
Atopic dermatitis is also associated with the release of pruritogens (molecules that stimulate <a href="/facts/Pruritus/MBWq6SPc">pruritus</a> or itching) in the skin.<a class="footnote-ref" id="fnref:105" href="#fn:105">105</a> Keratinocytes, <a href="/facts/Mast_cell/szfXss5q">mast cells</a>, <a href="/facts/Eosinophil/yhIKA8bE">eosinophils</a> and <a href="/facts/T_cell/5z6PQ9UN">T-cells</a> release pruritogens in the skin; leading to activation of <a href="/facts/Group_A_nerve_fiber/rWLrpWoz">Aδ fibers</a> and <a href="/facts/Group_C_nerve_fiber/9mBWCUnf">Group C nerve fibers</a> in the <a href="/facts/Epidermis/JvRABubP">epidermis</a> and <a href="/facts/Dermis/WAm7Fd6P">dermis</a> contributing to sensations of pruritus and pain.<a class="footnote-ref" id="fnref:106" href="#fn:106">106</a> The pruritogens include the Th2 cytokines IL-4, IL-13, IL-31, histamine, and various neuropeptides.<a class="footnote-ref" id="fnref:107" href="#fn:107">107</a> 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.<a class="footnote-ref" id="fnref:108" href="#fn:108">108</a> Chronic scratching of lesions can cause thickening or <a href="/facts/Lichenification/Vkr5XpeG">lichenification</a> of the skin or <a href="/facts/Prurigo_nodularis/yKAHpsgf">prurigo nodularis</a> (generalized nodules that are severely itchy).<a class="footnote-ref" id="fnref:109" href="#fn:109">109</a>
Another factor in the barrier failure and immunological dysregulation in people with atopic dermatitis may be due to decreases in <a href="/facts/Tight_junction_proteins/a7TnGhc3">tight junction protein</a> <a href="/facts/CLDN1/CCd13mso">Claudin-1</a>. Inhibiting Claudin-1 expression in human keratinocytes has been show to both reduce <a href="/facts/Tight_junction/CXxxM5H5">tight junction</a> function, as well as increase keratinocyte proliferation in vitro. It has also been discovered that this deteriorates the <a href="/facts/Developmental_bioelectricity/fW8v2Szk">bioelectric</a> barrier function in the epidermis.<a class="footnote-ref" id="fnref:110" href="#fn:110">110</a>

<h2 id="diagnosis">Diagnosis</h2>
Atopic dermatitis is typically <a href="/facts/Clinical_diagnosis/J47rvb0p">diagnosed clinically</a>, meaning it is based on signs and symptoms alone, without special testing.<a class="footnote-ref" id="fnref:111" href="#fn:111">111</a> Several different criteria developed for research have also been validated to aid in diagnosis.<a class="footnote-ref" id="fnref:112" href="#fn:112">112</a> Of these, the UK Diagnostic Criteria, based on the work of Hanifin and <a href="/facts/Georg_Rajka/8kDfJ2zN">Rajka</a>, has been the most widely validated.<a class="footnote-ref" id="fnref:113" href="#fn:113">113</a><a class="footnote-ref" id="fnref:114" href="#fn:114">114</a>

UK diagnostic criteria<a class="footnote-ref" id="fnref:115" href="#fn:115">115</a><table><tbody><tr><th>People must have <a href="/facts/Itch/MBWq6SPc">itchy skin</a>, or evidence of rubbing or scratching, plus three or more of:</th></tr><tr><td>Skin creases are involved – flexural dermatitis of fronts of <a href="/facts/Ankle/jk7FpfJs">ankles</a>, <a href="/facts/Cubital_fossa/xmrhPoTA">antecubital fossae</a>, <a href="/facts/Popliteal_fossa/mcl1blqQ">popliteal fossae</a>, skin around eyes, or neck, (or cheeks for children under 10)</td></tr><tr><td>History of <a href="/facts/Asthma/7GkJvxn3">asthma</a> or <a href="/facts/Allergic_rhinitis/ukE6bkIs">allergic rhinitis</a> (or family history of these conditions if patient is a child ≤4 years old)</td></tr><tr><td>Symptoms began before age 2 (can only be applied to people ≥4 years old)</td></tr><tr><td>History of <a href="/facts/Xeroderma/kJLKYrNA">dry skin</a> (within the past year)</td></tr><tr><td><a href="/facts/Dermatitis/JwlyQBa2">Dermatitis</a> is visible on flexural surfaces (people ≥ age 4) or on the cheeks, forehead, and extensor surfaces (people < age 4)</td></tr></tbody></table>
Other diseases that must be excluded before making a diagnosis include <a href="/facts/Contact_dermatitis/Xm6PEgcw">contact dermatitis</a>, <a href="/facts/Psoriasis/WW1k1LsH">psoriasis</a>, and <a href="/facts/Seborrheic_dermatitis/d1CfhTDG">seborrheic dermatitis</a>.<a class="footnote-ref" id="fnref:116" href="#fn:116">116</a>

<h2 id="prevention">Prevention</h2>
There are no established <a href="/facts/Evidence-based_medicine/InK1lB9l">clinical methods</a> using dietary or <a href="/facts/Topical_medication/alFfLndS">topical</a> strategies to inhibit or prevent atopic dermatitis. Specific dietary plans during pregnancy and in early childhood, such as eating fatty fish (or taking <a href="/facts/Omega-3_fatty_acid/X72Ynqov">omega-3</a> supplements), are not effective.<a class="footnote-ref" id="fnref:117" href="#fn:117">117</a> Taking <a href="/facts/Probiotic/gQNAN6ly">probiotics</a> (for example <a href="/facts/Lacticaseibacillus_rhamnosus/msxVquT6">Lactobacillus rhamnosus</a>) during pregnancy and feeding probiotics to infants are strategies under research, with only preliminary evidence that they may be preventative.<a class="footnote-ref" id="fnref:118" href="#fn:118">118</a><a class="footnote-ref" id="fnref:119" href="#fn:119">119</a>
Using <a href="/facts/Dermatitis/JwlyQBa2">moisturizers</a> 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.<a class="footnote-ref" id="fnref:120" href="#fn:120">120</a><a class="footnote-ref" id="fnref:121" href="#fn:121">121</a>

<h2 id="treatments">Treatments</h2>
No cure for AD is known, although treatments may reduce the severity and frequency of flares.<a class="footnote-ref" id="fnref:122" href="#fn:122">122</a> The most commonly used topical treatments for AD are topical corticosteroids (to get control of flare-ups) and <a href="/facts/Moisturizer/wKvt6bT2">moisturisers</a> (emollients) to help keep control.<a class="footnote-ref" id="fnref:123" href="#fn:123">123</a> Clinical trials often measure the efficacy of treatments with a severity scale such as the <a href="/facts/SCORAD/5tC5lMjM">SCORAD</a> index or the <a href="/facts/Eczema_Area_and_Severity_Index/LfGbD6hV">Eczema Area and Severity Index</a>.<a class="footnote-ref" id="fnref:124" href="#fn:124">124</a><a class="footnote-ref" id="fnref:125" href="#fn:125">125</a>

<h3>Moisturisers</h3>
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. <a href="/facts/Moisturizer/wKvt6bT2">Moisturisers</a> (or emollients) can improve skin comfort and may reduce disease flares.<a class="footnote-ref" id="fnref:126" href="#fn:126">126</a> They can be used as leave-on treatments, bath additives or <a href="/facts/Soap_substitute/E8crXogL">soap substitutes</a>. There are many different products but the majority of leave-on treatments (least to most greasy) are <a href="/facts/Lotion/GXollPbk">lotions</a>, <a href="/facts/Cream_(pharmacy)/hm2TeLhP">creams</a>, <a href="/facts/Gel/gBFE0s9G">gels</a> or <a href="/facts/Topical_medication/alFfLndS">ointments</a>. 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.<a class="footnote-ref" id="fnref:127" href="#fn:127">127</a> Non-medicated prescription moisturisers may also be no more effective than <a href="/facts/Over-the-counter_drug/QI3FcgRf">over-the-counter</a> moisturisers.<a class="footnote-ref" id="fnref:128" href="#fn:128">128</a>
The use of emollient bath additives does not provide any additional benefits.<a class="footnote-ref" id="fnref:129" href="#fn:129">129</a><a class="footnote-ref" id="fnref:130" href="#fn:130">130</a><a class="footnote-ref" id="fnref:131" href="#fn:131">131</a>

<h3>Medication</h3>
<h4>Topical</h4>
Creams and ointments containing <a href="/facts/Corticosteroid/jeL2QeIL">corticosteroids</a> applied directly on skin (<a href="/facts/Topical_steroid/jjT4BCVs">topical</a>) are effective in managing atopic dermatitis.<a class="footnote-ref" id="fnref:132" href="#fn:132">132</a><a class="footnote-ref" id="fnref:133" href="#fn:133">133</a> Newer (second generation) corticosteroids, such as <a href="/facts/Fluticasone_propionate/MfnCWC1x">fluticasone propionate</a> and <a href="/facts/Mometasone/ALWaB4xR">mometasone furoate</a>, 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 cause <a href="/facts/Steroid-induced_skin_atrophy/W0rhN7zz">skin thinning</a> 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).<a class="footnote-ref" id="fnref:134" href="#fn:134">134</a><a class="footnote-ref" id="fnref:135" href="#fn:135">135</a><a class="footnote-ref" id="fnref:136" href="#fn:136">136</a> Applying once daily is as effective as twice or more daily application.<a class="footnote-ref" id="fnref:137" href="#fn:137">137</a>
In addition to topical corticosteroids, topical <a href="/facts/Calcineurin_inhibitor/ctlB3Hda">calcineurin inhibitors</a>, such as <a href="/facts/Tacrolimus/Apj3X5S6">tacrolimus</a> or <a href="/facts/Pimecrolimus/RVtEK3Dk">pimecrolimus</a>, are also recommended as first-line therapies for managing atopic dermatitis.<a class="footnote-ref" id="fnref:138" href="#fn:138">138</a><a class="footnote-ref" id="fnref:139" href="#fn:139">139</a> Both tacrolimus and pimecrolimus are effective and safe to use in AD.<a class="footnote-ref" id="fnref:140" href="#fn:140">140</a><a class="footnote-ref" id="fnref:141" href="#fn:141">141</a> <a href="/facts/Crisaborole/KdcshgRT">Crisaborole</a>, an inhibitor of <a href="/facts/Phosphodiesterase-4_inhibitor/IgI8Dyjz">PDE-4</a>, is also effective and safe as a topical treatment for mild-to-moderate AD.<a class="footnote-ref" id="fnref:142" href="#fn:142">142</a><a class="footnote-ref" id="fnref:143" href="#fn:143">143</a> <a href="/facts/Ruxolitinib/WUkFQnnW">Ruxolitinib</a>, a <a href="/facts/Janus_kinase_inhibitor/xweMafbr">Janus kinase inhibitor</a>, has uncertain efficacy and safety.<a class="footnote-ref" id="fnref:144" href="#fn:144">144</a><a class="footnote-ref" id="fnref:145" href="#fn:145">145</a>

<h4>Systemic</h4>
When topical (on skin) treatments fail to control severe AD flares, medications taken by mouth (systemic treatment) can be used.<a class="footnote-ref" id="fnref:146" href="#fn:146">146</a>
Conventional oral medications for AD include systemic <a href="/facts/Immunosuppressive_drug/ctlB3Hda">immunosuppressants</a>, such as <a href="/facts/Ciclosporin/tcIToHvK">ciclosporin</a>, <a href="/facts/Methotrexate/LoDvhRKX">methotrexate</a>, <a href="/facts/Azathioprine/CmeIK3ca">azathioprine</a>, and <a href="/facts/Mycophenolic_acid/kHpk0USt">mycophenolate</a>.<a class="footnote-ref" id="fnref:147" href="#fn:147">147</a><a class="footnote-ref" id="fnref:148" href="#fn:148">148</a><a class="footnote-ref" id="fnref:149" href="#fn:149">149</a><a class="footnote-ref" id="fnref:150" href="#fn:150">150</a> <a href="/facts/Antidepressant/N62ND3Fa">Antidepressants</a> and <a href="/facts/Naltrexone/SVduEm3W">naltrexone</a> may be used to control pruritus (itchiness).<a class="footnote-ref" id="fnref:151" href="#fn:151">151</a>
Newer medications, such as <a href="/facts/Monoclonal_antibody/4rUBWB87">monoclonal antibodies</a> and <a href="/facts/Janus_kinase_inhibitor/xweMafbr">JAK inhibitors</a>, are highly effective for managing atopic dermatitis, but modestly increase the risk of <a href="/facts/Conjunctivitis/u1NJfh3A">conjunctivitis</a>. These include <a href="/facts/Dupilumab/EYSHml2o">dupilumab</a> (Dupixent), <a href="/facts/Tralokinumab/qdRnMEKa">tralokinumab</a> (Adtralza, Adbry), <a href="/facts/Abrocitinib/LAItpkpT">abrocitinib</a> (Cibinqo), <a href="/facts/Baricitinib/8nmqCkcL">baricitinib</a> (Olumiant) and <a href="/facts/Upadacitinib/nAgd5txm">upadacitinib</a> (Rinvoq).<a class="footnote-ref" id="fnref:152" href="#fn:152">152</a><a class="footnote-ref" id="fnref:153" href="#fn:153">153</a><a class="footnote-ref" id="fnref:154" href="#fn:154">154</a> Among monoclonal antibodies, <a href="/facts/Dupilumab/EYSHml2o">dupilumab</a> and <a href="/facts/Tralokinumab/qdRnMEKa">tralokinumab</a> are approved to treat moderate-to-severe eczema in the US and the EU.<a class="footnote-ref" id="fnref:155" href="#fn:155">155</a><a class="footnote-ref" id="fnref:156" href="#fn:156">156</a><a class="footnote-ref" id="fnref:157" href="#fn:157">157</a><a class="footnote-ref" id="fnref:158" href="#fn:158">158</a> <a href="/facts/Lebrikizumab/PTynN9um">Lebrikizumab</a> is also approved in the EU for treating moderate-to-severe AD<a class="footnote-ref" id="fnref:159" href="#fn:159">159</a> but in the US its approval was declined due to manufacturing issues.<a class="footnote-ref" id="fnref:160" href="#fn:160">160</a> <a href="/facts/Abrocitinib/LAItpkpT">Abrocitinib</a> and <a href="/facts/Upadacitinib/nAgd5txm">upadacitinib</a> have also been approved in the US for the treatment of moderate-to-severe eczema.<a class="footnote-ref" id="fnref:161" href="#fn:161">161</a><a class="footnote-ref" id="fnref:162" href="#fn:162">162</a> <a href="/facts/Nemolizumab/S9F6gSeA">Nemolizumab</a> (Nemluvio) was approved to treat atopic dermatitis in December 2024.<a class="footnote-ref" id="fnref:163" href="#fn:163">163</a>
<a href="/facts/Allergen_immunotherapy/y38xes3E">Allergen immunotherapy</a> may be effective in relieving symptoms of AD, but it also comes with an increased risk of <a href="/facts/Adverse_event/6zKwT4g5">adverse events</a>.<a class="footnote-ref" id="fnref:164" href="#fn:164">164</a> This treatment consists of a series of injections or drops under the tongue of a solution containing the allergen.<a class="footnote-ref" id="fnref:165" href="#fn:165">165</a>
The skin of people with AD can easily get infected, most commonly by the bacteria <a href="/facts/Staphylococcus_aureus/9yDVBMsc">Staphylococcus aureus</a>. 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 <a href="/facts/Antimicrobial_resistance/jsbAywgx">antimicrobial resistance</a>. For these reasons, they are only recommended for people who not only present symptoms on the skin but feel systematically unwell.<a class="footnote-ref" id="fnref:166" href="#fn:166">166</a><a class="footnote-ref" id="fnref:167" href="#fn:167">167</a><a class="footnote-ref" id="fnref:168" href="#fn:168">168</a>

<h3>Diet</h3>
The role of <a href="/facts/Vitamin_D/No0zQB2W">vitamin D</a> on atopic dermatitis is not clear, but vitamin D supplementation may improve its symptoms.<a class="footnote-ref" id="fnref:169" href="#fn:169">169</a><a class="footnote-ref" id="fnref:170" href="#fn:170">170</a><a class="footnote-ref" id="fnref:171" href="#fn:171">171</a>
There is no clear benefit for pregnant mothers taking <a href="/facts/Omega-3_fatty_acid/X72Ynqov">omega 3 long-chain polyunsaturated fatty acid</a> (LCPUFA) in preventing the development of AD in their child.<a class="footnote-ref" id="fnref:172" href="#fn:172">172</a><a class="footnote-ref" id="fnref:173" href="#fn:173">173</a>
Several <a href="/facts/Probiotics/gQNAN6ly">probiotics</a> seem to have a positive effect, with a roughly 20% reduction in the rate of AD.<a class="footnote-ref" id="fnref:174" href="#fn:174">174</a><a class="footnote-ref" id="fnref:175" href="#fn:175">175</a><a class="footnote-ref" id="fnref:176" href="#fn:176">176</a> Probiotics containing multiple <a href="/facts/Strain_(biology)/xFv4QWjN">strains</a> of bacteria seem to work the best.<a class="footnote-ref" id="fnref:177" href="#fn:177">177</a>
In people with <a href="/facts/Coeliac_disease/AKd5PkTc">celiac disease</a> or <a href="/facts/Non-celiac_gluten_sensitivity/EHktaDPW">nonceliac gluten sensitivity</a>, a gluten-free diet improves their symptoms and prevents the occurrence of new outbreaks.<a class="footnote-ref" id="fnref:178" href="#fn:178">178</a><a class="footnote-ref" id="fnref:179" href="#fn:179">179</a>
Use of blood specific <a href="/facts/Immunoglobulin_E/76uGAl7k">IgE</a> or <a href="/facts/Skin_allergy_test/qX6p7Ea0">skin prick tests</a> 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.<a class="footnote-ref" id="fnref:180" href="#fn:180">180</a>

<h3>Lifestyle</h3>
Health professionals often recommend that people with AD bathe regularly in lukewarm baths, especially in salt water, to moisten their skin.<a class="footnote-ref" id="fnref:181" href="#fn:181">181</a><a class="footnote-ref" id="fnref:182" href="#fn:182">182</a> Dilute <a href="/facts/Sodium_hypochlorite_washes/z6TjCDR3">bleach baths</a> may be helpful for people with moderate and severe eczema, but only for people with Staphylococcus aureus.<a class="footnote-ref" id="fnref:183" href="#fn:183">183</a>
Avoiding large-diameter <a href="/facts/Woolen/NAxNlgH2">woolen</a> clothing or scratchy fibres is usually recommended for people with AD as they can trigger a flare.<a class="footnote-ref" id="fnref:184" href="#fn:184">184</a><a class="footnote-ref" id="fnref:185" href="#fn:185">185</a> Safe alternatives are clothes made from fabrics with smaller diameters and smooth fibers. These include super- and ultrafine <a href="/facts/Merino/q5B0AldC">merino wool</a> and fabrics with anti-microbial textile finishes. Wearing <a href="/facts/Silk/XhxPpvvS">silk</a> is also safe but does not improve symptoms of AD.<a class="footnote-ref" id="fnref:186" href="#fn:186">186</a><a class="footnote-ref" id="fnref:187" href="#fn:187">187</a><a class="footnote-ref" id="fnref:188" href="#fn:188">188</a>

<h3>Self-management</h3>
Living with AD requires a high level of self-management (for example avoiding triggers) and <a href="/facts/Adherence_(medicine)/cC0Wfj3H">adherence</a> to treatments (regularly applying medication). Good self-management contributes to better disease outcomes and quality of life.<a class="footnote-ref" id="fnref:189" href="#fn:189">189</a><a class="footnote-ref" id="fnref:190" href="#fn:190">190</a> However, worries about topical treatments, misconceptions about the condition, unclear information and unsuitable communication from doctors can make living with AD more difficult.<a class="footnote-ref" id="fnref:191" href="#fn:191">191</a>
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.<a class="footnote-ref" id="fnref:192" href="#fn:192">192</a><a class="footnote-ref" id="fnref:193" href="#fn:193">193</a>
Appropriate communication from doctors can support self-management. Doctors need to address concerns about treatments and provide clear and consistent information about the condition.<a class="footnote-ref" id="fnref:194" href="#fn:194">194</a><a class="footnote-ref" id="fnref:195" href="#fn:195">195</a> Treatment regimens can be confusing, and written action plans may support people in knowing which treatments to use where and when.<a class="footnote-ref" id="fnref:196" href="#fn:196">196</a> A website supporting self-management has been shown to improve AD symptoms for parents, children, adolescents and young adults.<a class="footnote-ref" id="fnref:197" href="#fn:197">197</a><a class="footnote-ref" id="fnref:198" href="#fn:198">198</a>

<h3>Light</h3>
<a href="/facts/Light_therapy/yHtqwaRm">Phototherapic</a> treatment involves exposure to broad- or narrow-band <a href="/facts/Ultraviolet/kncBUqn5">ultraviolet</a> (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.<a class="footnote-ref" id="fnref:199" href="#fn:199">199</a><a class="footnote-ref" id="fnref:200" href="#fn:200">200</a> Among the different types of phototherapies only narrowband (NB) ultraviolet B (UVB) exposure might help with the severity of AD and ease itching.<a class="footnote-ref" id="fnref:201" href="#fn:201">201</a><a class="footnote-ref" id="fnref:202" href="#fn:202">202</a> However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk.<a class="footnote-ref" id="fnref:203" href="#fn:203">203</a> <a href="/facts/Phototherapy/yHtqwaRm">UV phototherapy</a> is not indicated in young adults and children due to this risk of <a href="/facts/Skin_cancer/r9BWEX7W">skin cancer</a> with prolonged use or exposure.<a class="footnote-ref" id="fnref:204" href="#fn:204">204</a>

<h3>Alternative medicine</h3>
While several <a href="/facts/Chinese_herbal_medicine/JF2XKnhH">Chinese herbal medicines</a> 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.<a class="footnote-ref" id="fnref:205" href="#fn:205">205</a>

<h2 id="impact">Impact</h2>
Atopic dermatitis significantly impairs the <a href="/facts/Quality_of_life_(healthcare)/yxMaVH3w">quality of life</a> of affected individuals.<a class="footnote-ref" id="fnref:206" href="#fn:206">206</a><a class="footnote-ref" id="fnref:207" href="#fn:207">207</a> The impact of AD extends beyond physical symptoms, encompassing substantial humanistic and <a href="/facts/Psychosocial/qKrrEQrD">psychosocial</a> effects. Its <a href="/facts/Disease_burden/0YRn1r5H">burden</a> is significant, especially given the high indirect costs and psychological impacts on quality of life.<a class="footnote-ref" id="fnref:208" href="#fn:208">208</a><a class="footnote-ref" id="fnref:209" href="#fn:209">209</a>
According to the <a href="/facts/Global_Burden_of_Disease_Study/atCSUCoC">Global Burden of Disease Study</a>, AD is the skin disease with the highest <a href="/facts/Disability-adjusted_life_year/b3oTGHg4">disability-adjusted life year</a> 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.<a class="footnote-ref" id="fnref:210" href="#fn:210">210</a>
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.<a class="footnote-ref" id="fnref:211" href="#fn:211">211</a>

<h3>Humanistic burden</h3>
Atopic dermatitis significantly decreases the quality of life by affecting various aspects of people's lives. The psychological impact, often resulting in conditions like <a href="/facts/Major_depressive_disorder/l2lQeWqr">depression</a> and <a href="/facts/Anxiety_disorder/wh9zFH1V">anxiety</a>, is a major factor leading to decreased <a href="/facts/Quality_of_life/37ljmgAH">quality of life</a>. Sleep disturbances, commonly reported in people with AD, further contribute to the humanistic burden, affecting daily productivity and concentration.<a class="footnote-ref" id="fnref:212" href="#fn:212">212</a>

<h3>Clinical and economic burden</h3>
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.<a class="footnote-ref" id="fnref:213" href="#fn:213">213</a> These figures highlight the considerable financial impact of the disease on healthcare systems and people with the condition.<a class="footnote-ref" id="fnref:214" href="#fn:214">214</a><a class="footnote-ref" id="fnref:215" href="#fn:215">215</a>

<h3>Productivity loss</h3>
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 <a href="/facts/Presenteeism/vmHb9bhx">presenteeism</a> accounting for the majority of these days.<a class="footnote-ref" id="fnref:216" href="#fn:216">216</a> The impact on productivity varies significantly with the severity of AD, with more severe cases resulting in higher numbers of days lost.<a class="footnote-ref" id="fnref:217" href="#fn:217">217</a><a class="footnote-ref" id="fnref:218" href="#fn:218">218</a>

<h3>Burden of disease in the Middle East and Africa</h3>
Atopic dermatitis leads to the highest loss in <a href="/facts/Disability-adjusted_life_year/b3oTGHg4">disability-adjusted life years</a> compared to other skin diseases in the Middle East and Africa.<a class="footnote-ref" id="fnref:219" href="#fn:219">219</a> Patients with AD in these regions lose approximately 0.19 <a href="/facts/Quality-adjusted_life_year/TT3nP7XH">quality-adjusted life years</a> (QALYs) annually due to the disease. Egypt experiences the highest QALY loss and Kuwait the lowest.<a class="footnote-ref" id="fnref:220" href="#fn:220">220</a>
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.<a class="footnote-ref" id="fnref:221" href="#fn:221">221</a>
Indirect costs, primarily due to productivity loss from <a href="/facts/Absenteeism/ftEUIM1W">absenteeism</a> and presenteeism average about 67% in these countries. Indirect costs in Saudi Arabia are the highest in the area, estimated at US $364 million.<a class="footnote-ref" id="fnref:222" href="#fn:222">222</a> 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.<a class="footnote-ref" id="fnref:223" href="#fn:223">223</a>
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.<a class="footnote-ref" id="fnref:224" href="#fn:224">224</a> 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.<a class="footnote-ref" id="fnref:225" href="#fn:225">225</a>

<h2 id="epidemiology">Epidemiology</h2>
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.<a class="footnote-ref" id="fnref:226" href="#fn:226">226</a><a class="footnote-ref" id="fnref:227" href="#fn:227">227</a> 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.<a class="footnote-ref" id="fnref:228" href="#fn:228">228</a><a class="footnote-ref" id="fnref:229" href="#fn:229">229</a> Over 15 million American adults and children have AD.<a class="footnote-ref" id="fnref:230" href="#fn:230">230</a>

<h2 id="society-and-culture">Society and culture</h2>
<h3>Conspiracy theories</h3>
A number of false and conspiratorial claims about AD have emerged on the internet and have been amplified by social media. These <a href="/facts/Conspiracy_theories/sNr2Kmh8">conspiracy theories</a> include, among others, claims that AD is caused by <a href="/facts/5G/yVb460m4">5G</a>, <a href="/facts/Formaldehyde/Ck8RLfqk">formaldehyde</a> in food, <a href="/facts/Vaccine/QcXzLug2">vaccines</a>, and topical steroids. Various unproven theories also claim that <a href="/facts/Vegan/ENrKFBzz">vegan</a> diets, <a href="/facts/Apple_cider_vinegar/sN7rhcWH">apple cider vinegar</a>, <a href="/facts/Calendula/SeqUCMoG">calendula</a>, and <a href="/facts/Witch-hazel/yDLghsWN">witch hazel</a> can cure AD and that <a href="/facts/Air_purifier/Q3rscEa7">air purifiers</a> reduce the risk of developing AD.<a class="footnote-ref" id="fnref:231" href="#fn:231">231</a>

<h2 id="research">Research</h2>
<a href="/facts/Antileukotriene/rUlYxvuc">Leukotriene receptor antagonists</a>, such as <a href="/facts/Montelukast/x26tXFtK">montelukast</a>, might be a useful for the treatment of AD but their effectiveness has not yet been proven by research.<a class="footnote-ref" id="fnref:232" href="#fn:232">232</a><a class="footnote-ref" id="fnref:233" href="#fn:233">233</a><a class="footnote-ref" id="fnref:234" href="#fn:234">234</a>

<h2 id="external-links">External links</h2>

Wikimedia Commons has media related to Atopic dermatitis.

<h2 id="references">References</h2>

<ol>
<li id="fn:1">"Handout on Health: Atopic Dermatitis (A type of eczema)". National Institute of Arthritis and Musculoskeletal and Skin Diseases. May 2013. Archived from the original on 30 May 2015. Retrieved 19 June 2015. <a href="http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp" target="_blank">http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></li>
<li id="fn:2">"Handout on Health: Atopic Dermatitis (A type of eczema)". National Institute of Arthritis and Musculoskeletal and Skin Diseases. May 2013. Archived from the original on 30 May 2015. Retrieved 19 June 2015. <a href="http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp" target="_blank">http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></li>
<li id="fn:3">Johansson SG, Bieber T, Dahl R, Friedmann PS, Lanier BQ, Lockey RF, et al. (May 2004). "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. doi:10.1016/j.jaci.2003.12.591. PMID 15131563. <a href="https://doi.org/10.1016%2Fj.jaci.2003.12.591" target="_blank">https://doi.org/10.1016%2Fj.jaci.2003.12.591</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></li>
<li id="fn:4">"Handout on Health: Atopic Dermatitis (A type of eczema)". National Institute of Arthritis and Musculoskeletal and Skin Diseases. May 2013. Archived from the original on 30 May 2015. Retrieved 19 June 2015. <a href="http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp" target="_blank">http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></li>
<li id="fn:5">"Handout on Health: Atopic Dermatitis (A type of eczema)". National Institute of Arthritis and Musculoskeletal and Skin Diseases. May 2013. Archived from the original on 30 May 2015. Retrieved 19 June 2015. <a href="http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp" target="_blank">http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></li>
<li id="fn:6">"Handout on Health: Atopic Dermatitis (A type of eczema)". National Institute of Arthritis and Musculoskeletal and Skin Diseases. May 2013. Archived from the original on 30 May 2015. Retrieved 19 June 2015. <a href="http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp" target="_blank">http://www.niams.nih.gov/Health_Info/Atopic_Dermatitis/default.asp</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></li>
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</ol>

Atopic dermatitis open-in-new

Atopic dermatitis