Version July 2025
INTRODUCTION —
Atopic dermatitis (AD; eczema) is often associated with elevated levels of serum immunoglobulin E (IgE) and positive tests for allergen-specific IgE. AD commonly occurs in conjunction with other atopic disorders, including asthma, allergic rhinitis, and food allergy [1], that are known to be exacerbated or caused by specific allergens. These observations strongly suggest a shared pathophysiologic relationship among these atopic disorders and suggest a role for allergy in AD.
However, the causal role of specific allergens (ie, allergy to foods or aeroallergens) in the occurrence, exacerbation, or severity of AD is controversial. Studies suggest that allergens play a role in a subset of patients with AD and may therefore provide a therapeutic target.
The epidemiology, pathogenesis, clinical manifestations, diagnosis, and treatment of AD, as well as the role of delayed-type hypersensitivity to chemicals in topical medications and skin care products in exacerbating AD, are discussed separately. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis" and "Treatment of atopic dermatitis (eczema)".)
ATOPIC ASSOCIATIONS AND SENSITIZATION
Relationships of AD with other allergic diseases — Children with AD have higher rates of comorbid atopic disease, such as asthma, allergic rhinitis, and food allergy, than the general population and, on an individual basis, may progress to develop these diseases [1]. However, allergy and AD are not always linked. The majority of children with AD do not progress to develop comorbid atopic conditions, and adult-onset asthma is not commonly associated with AD [1-4]. (See "The relationship between IgE and allergic disease", section on 'The atopic march'.)
A higher risk of asthma and allergic rhinitis in children with AD is associated with earlier age of AD onset and AD severity. Analysis of a US pediatric claims database of >240,000 AD and matched non-AD patients showed a more than doubled prevalence of asthma and rhinitis in those with AD, with increased prevalence related to AD severity [5]. Early-onset AD may be a risk for developing comorbid respiratory allergy. In a cohort study of 3966 children, earlier onset, under age two years, of pediatric AD was associated with increased risk for respiratory allergy [6].
In addition, children with AD who are sensitized to inhalant or food allergens may be at particularly high risk for asthma and other comorbid atopic disease. In a longitudinal study of 2311 Canadian children with AD compared with those without, allergen sensitization increased the risk of asthma sevenfold [7]. In a study of 640 infants enrolled into a prevention study of peanut allergy with moderate-severe AD, hen's egg allergy, or both, the rates of asthma were 15 to 18 percent and seasonal rhinoconjunctivitis 46 to 47 percent at a follow-up at five years of age [8].
Many studies demonstrate a risk of AD for the development of food allergy [1,9-11]. As an example, in an Australian population-based study of 4453 one-year-old children, the odds ratio of food allergy to peanut, egg, or sesame was 6.2 (95% CI 4.9-7.9) in those with compared with those without eczema [11]. A systematic review and meta-analysis identified a pooled prevalence of food allergy in AD of 32.7 percent and AD prevalence among those with food allergy of 45.3 percent [12]. This systematic review also noted higher rates of food allergy in AD among children compared with adults and among those with more severe AD than milder AD and an apparent decrease in prevalence over time among studies since the 1980s.
Allergen sensitization in AD — Allergen-specific IgE, detected by allergen skin prick testing (SPT) or serum tests, is commonly identified in persons with AD [1,12,13]. As an example, in a US National Health and Nutrition Examination Survey of children, median total IgE levels were higher in children with eczema, as were the percentage with detectable allergen-specific IgE to food and environmental allergens (eg, egg sensitization 13 versus 6.4 percent and dog sensitization in 23 versus 12 percent in those with and without eczema, respectively) [13]. The high rates of sensitization have been attributed to the disrupted skin barrier and inflammatory milieu of the skin, where topical/environmental exposure may result in systemic sensitization. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis" and "Treatment of atopic dermatitis (eczema)".)
However, allergen sensitization is not synonymous with a diagnosis of allergen-exacerbated or induced AD. Although some patients who are sensitized to a food or aeroallergen may experience exacerbations of their eczematous rash from exposure, most will not. (See "The relationship between IgE and allergic disease", section on 'Sensitization' and "The relationship between IgE and allergic disease", section on 'Allergy'.)
FOOD ALLERGIES
Types of food-induced allergic response in the skin — The pathogenesis of food-exacerbated AD is not well understood but may involve IgE-mediated and non-IgE-mediated allergic responses [14-16].
IgE-mediated, acute-onset allergic reactions to foods are typically characterized by urticaria and angioedema. Urticaria and angioedema may occur from direct skin contact with the food allergen or via ingestion, and, for the latter, the skin response may be isolated or may occur along with the involvement of additional organ systems. These types of dermatologic responses are discussed elsewhere. (See "Food-induced anaphylaxis" and "New-onset urticaria (hives)".)
Another possible allergic response from food is the exacerbation/flaring of eczematous lesions from an isolated ingestion or the contribution of ingestion of an allergen to chronic AD [16-19]. Food additives or components (eg, propylene glycol, cinnamic aldehyde) and metals (eg, nickel) or proteins (eg, carmine) in food could cause systemic contact dermatitis from ingestion [20]. This subject is discussed elsewhere. (See "Allergic contact dermatitis in children" and "Allergic contact dermatitis: Clinical features and diagnosis".)
Prevalence and features of food-exacerbated AD — The prevalence of food-exacerbated AD is not well established, and studies of this phenomenon are typically small and vary with regard to methodology and target population. The published observations of this phenomenon are primarily reported from pediatric referral populations and identify hen's egg and cow's milk as common triggers [15-18]. More recent studies of children, compared with studies performed decades before, have not disclosed high rates of food-exacerbated AD even though all the studies included children with AD and suspected food allergy.
In one early study published in 1985, 84 percent of 63 children with AD and reactions during double-blind, placebo-controlled oral food challenges (DBPCFC) experienced eczematous rashes [17]. Two other early studies were performed in Germany. The first, published in 1999, reviewed 387 DBPCFCs (131 positive) performed in 107 children with AD, with exacerbation of eczema observed in 41 percent of 81 early (<2 hours) reactions, 19 percent of 29 delayed (2 to 48 hours) reactions, and all cases of combined early and delayed reactions [21]. In the second study, published in 2004, of 106 DBPCFCs (49 positive) in 64 children with AD, early (within six hours) isolated eczematous reactions occurred in 43 percent, late eczematous reactions following immediate reactions in 45 percent, and isolated late eczematous reactions in 12 percent [22].
By contrast, a study from the Netherlands published in 2016 [18] reviewed DBPCFCs from 2001 to 2011 in 682 children with AD for suspected food allergy. Clinical reactions occurred in 272. On challenge with the food, 5 percent had exacerbation of AD within two hours, 3 percent in two to six hours (mostly having immediate reaction symptoms as well), and 2 percent later than six hours. The late reaction rate was similar between the food tested and placebo. Among children having a history of isolated AD exacerbations to specific foods, no reactions were substantiated from the DBPCFCs.
A retrospective single-center study from Germany published in 2018 included 182 patients with AD (median age of the study population was 26 years, range 3 to 70 years; 82 percent ≥12 years) who were also birch pollen allergic and suspected birch pollen-related food allergy who were evaluated by DBPCFC to birch pollen-related foods (apple, hazelnut, carrot, celery) [19]. Of 261 DBPCFCs in 182 patients, 103 were positive in 65 patients, primarily with immediate-type reactions. They recorded late eczematous responses in 32 of these patients, overall 18 percent of this specific patient population.
Efficacy of food elimination diets to improve AD — A systematic review and meta-analysis of data from clinical trials of DBPCFCs performed to determine whether foods could exacerbate AD concluded that any improvements seen in AD due to dietary elimination were slight and potentially unimportant. The reviewers identified 10 randomized trials that overall included 599 participants with mild-to-moderate AD, primarily infants and young children [23]. The studies included in the analysis varied in design, most had a high risk of bias, and the targeted foods included milk and egg (two studies), egg alone (one), selected few foods (one), test-guided elimination (one), and various hypoallergenic formulas (five). The data provided low certainty evidence supporting the conclusion that dietary elimination only slightly improved eczema severity (50 percent with versus 41 percent without dietary elimination) measured by the SCOring Atopic Dermatitis (SCORAD) index and did so by a minimally important difference of 8.7 points. There were also small improvements in pruritus and sleep scores that were considered unimportant. Additionally, the study identified potential risks of these approaches such as developing acute IgE-mediated reactions to the food(s). (See 'Risks of elimination diets to treat food-exacerbated AD' below.)
Evaluation of food allergy as a trigger of AD — The general approach to the diagnosis of food allergy is described elsewhere and focuses upon acute allergic reactions, but the same general principles apply to diagnosing food allergy as a trigger of AD. Patients with AD have higher risks for IgE-mediated food allergy (eg, acute urticaria or other symptoms of IgE-mediated food allergy) that may not also result in AD flares. Determining whether food allergy is triggering AD for an individual patient requires the additional consideration of the epidemiologic data, as well as particular aspects of the personal history, test results, and, possibly, oral food challenges (preferably DBPCFCs). (See "Diagnostic evaluation of IgE-mediated food allergy" and "Overview of skin testing for IgE-mediated allergic disease", section on 'Skin conditions' and "Overview of in vitro allergy tests".)
●Epidemiologic data – As described above, patient/caregiver-suspected exacerbations of AD from foods are not typically confirmed by DBPCFCs, and dietary elimination does not significantly improve AD in most patients (see 'Prevalence and features of food-exacerbated AD' above and 'Efficacy of food elimination diets to improve AD' above). In addition, flaring of AD is not a common side effect of oral immunotherapy despite patients ingesting an allergen, also suggesting a low prior probability that food will exacerbate or cause AD (see "Food allergy management: Allergen-specific immunotherapy", section on 'Adverse events'). Thus, the prior probability that identifying and eliminating food allergen(s) will result in improvement of AD or reduction of AD flares is low.
●Personal history – AD waxes and wanes, and there are many potential non-food triggers. If the rash improves at times without a change in the diet, it is not likely that food is contributing. If there is a history that the rash flares consistently following a particular food ingestion, especially a food such as milk, egg, or wheat, the possibility of food allergy as a trigger is increased. When a food that is a current component of the diet is suspected to be a cause of AD, the food may be discontinued or reduced in the diet for a few days and then tried again to ascertain whether the rash improves with avoidance and flares when it is added back into the diet. For reasons described below (see 'Risks of elimination diets to treat food-exacerbated AD' below), we discourage elimination of foods that appear to be tolerated.
●Test results – As described above, patients with AD are often sensitized to many food allergens, but clinical reactivity due to this sensitization is low (see 'Allergen sensitization in AD' above). The limitations of skin testing and in vitro tests for IgE-mediated food allergy, namely a high rate of positive tests without clinical implication, is especially a concern when evaluating the potential for food-exacerbated AD given that AD flares from food are far less common than immediate-type reactions (eg, urticaria).
●Oral food challenges – The oral food challenge (OFC) can be used to determine if a food triggers a flaring of AD (see "Oral food challenges for diagnosis and management of food allergies"). However, as described above, patients may have late eczematous reactions at the same rate after placebo (see 'Prevalence and features of food-exacerbated AD' above). Thus, undertaking DBPCFCs may be required. If the food is a routine component of the diet, the food is generally avoided for a period of time prior to the DBPCFC. However, for reasons described below, caution is needed in not eliminating the food for long periods (see 'Risks of elimination diets to treat food-exacerbated AD' below). Thus, we advise not avoiding the food for more than one to two weeks prior to an oral challenge.
Risks of elimination diets to treat food-exacerbated AD — A systematic review of 10 randomized trials of dietary elimination to treat AD concluded that there were risks of developing IgE-mediated food allergy to the avoided foods and withholding more effective treatment options for AD [23]. (See 'Efficacy of food elimination diets to improve AD' above.)
Risks of approaching the treatment of AD through dietary elimination include:
●New onset of acute allergic reactions to foods that were eliminated for treatment of AD – Dietary elimination of a food that ostensibly had been tolerated in the diet or is thought to be triggering chronic eczematous eruptions can result in acute and potentially severe allergic reactions upon reexposure, particularly if there is evidence of sensitization to the food, with rare fatalities reported [23-26]. The pathophysiology of this observation is likely related to a loss of desensitization during a period of avoidance [26].
As an example, a review of 298 patients evaluated at an allergy clinic for concerns of food-triggered AD found that 19 percent with food-triggered AD and no prior history of immediate reactions developed new acute reactions to the eliminated food. Seventy percent of the reactions were cutaneous, and 30 percent were anaphylaxis [24]. In another review, 45 of 442 pediatric OFCs to egg, milk, peanut, soy, or wheat were performed after elimination of a suspected AD trigger, with a reaction rate of 13 percent [25]. This rate was similar to that seen for other circumstances that led to OFCs (history of prior reaction, sensitized with no prior exposure).
●Nutritional risk – Dietary elimination carries nutritional risks, especially for children, and particularly if milk or multiple food allergens are eliminated [27-29]. (See "Management of food allergy: Nutritional issues".)
●Decreased quality of life and increased anxiety – Dietary elimination can lead to social isolation, negative impact on quality of life (QoL), and increased anxiety for patients and caregivers [30-33]. (See "Food allergy: Impact on health-related quality of life" and "Management of food allergy-related anxiety in children and their parents/caregivers".)
Role of dietary management — The low prevalence of food-exacerbated AD and the risks of dietary elimination have led to the deemphasis of evaluating foods as a cause or trigger of AD and a shift away from the use of elimination diets, in the absence of a strong suspicion, in favor of unrestricted diets and a focus on optimizing skin care regimens and medical treatment for the skin [15,16,34,35]. For most patients with AD, we suggest against the use of elimination diets in the management of AD, consistent with the 2023 AD guidelines [35]. Inclusion of allergens in the diet of young children may be important for allergy prevention and reducing the risk of malnutrition. Additionally, a systematic review identified that parents/caregivers valued nonpharmacologic therapies and understanding the role of food allergens but also put a high value on safe interventions and avoiding acquisition of another chronic condition such as food allergy [36]. Thus, shared decision making with discussion of patient and family preferences in addition to the risks and benefits of dietary management is important. (See 'Prevalence and features of food-exacerbated AD' above and 'Risks of elimination diets to treat food-exacerbated AD' above and "Treatment of atopic dermatitis (eczema)".)
Although IgE-mediated, acute allergic reactions to foods (ie, urticaria, anaphylaxis) and evidence of sensitization to foods are increased in those with AD, the potential for foods to substantially contribute to chronic AD and acute AD flares is relatively low. Food elimination diets are likely to only slightly improve eczema severity, and dietary elimination carries risks, including nutritional deficiencies and poor growth, negative impacts on QoL and social activities, and the immunologic risk of experiencing immediate-type anaphylactic reactions to foods that were previously included in the diet. In general, medical management of AD should be pursued ahead of dietary elimination because of these risks and the relatively low chance of success with dietary elimination. (See 'Risks of elimination diets to treat food-exacerbated AD' above.)
AD rashes wax and wane and have many nonallergic exacerbating factors. Foods should not be eliminated from the diet randomly without any clinical suspicion, nor should foods be excluded from the diet long term (as opposed to short term for diagnostic purposes) based upon positive skin or in vitro tests or patient history alone. Food allergy testing should be performed judiciously, based upon the clinical history and pretest likelihood that the food is a trigger of AD. Clinical reactivity should be confirmed when necessary by DBPCFC. Suspicion of a specific food trigger is usually excluded when diagnostic testing with medically supervised feeding tests is employed. The use of elimination diets and OFCs in the diagnosis and management of food allergy are discussed in greater detail separately (See 'Evaluation of food allergy as a trigger of AD' above and "Oral food challenges for diagnosis and management of food allergies".)
Two cases illustrate our approach:
●Case 1 – A nine-month-old infant with moderate AD had a significant acute allergic reaction to peanut when it was first introduced at six months of age. He is currently tolerating a milk-based formula and routinely consumes egg and wheat. His AD is treated only with occasional moisturizers as the parents/caregivers are averse to using medications such as topical corticosteroids. They would like to introduce infant-safe forms of tree nuts to "avoid more allergies" but are worried about introducing them and want allergy testing to tree nuts first. They also want allergy testing to milk, egg, and wheat because of concerns that these foods are causing the AD.
In shared decision-making discussions, we would offer to perform allergy tests to select tree nuts. The risk of tree nut allergy in this infant with peanut allergy and moderate AD is increased, and the parents/caregivers are uncomfortable introducing the foods without testing. Regarding their request to test for milk, egg, and wheat, we would discuss with the parents/caregivers that these foods are already in the diet, and they did not notice any specific AD flare related to these foods, suggesting a low probability of a relationship. As such, we would not offer testing to these foods. We would inform the parents/caregivers of the low likelihood that these foods are triggering his AD and discuss the risks of elimination (nutritional, social, and the potential for de novo allergy, including anaphylaxis). We would also discuss the safety of medications, a hydrating regimen to treat the AD, and the potential benefits of medical management without altering the diet. (See "Treatment of atopic dermatitis (eczema)".)
●Case 2 – A nine-month-old infant has moderate AD, and the parents/caregivers note that the AD flares about two to three hours following ingestion of scrambled egg. AD flares occurred after all of the eight trials of scrambled egg. They removed egg from the diet one week ago and think that the eczema is about 50 percent improved.
We would discuss with the parents/caregivers that they have identified egg as a potential trigger of AD flares but also discuss that complete avoidance may not be the best or only approach available given that strict avoidance might result in acute allergic reactions to egg with reexposure as well as potential effects on nutrition and QoL. We would review the risks and benefits of complete egg avoidance, including reasons to keep egg in the diet, and would emphasize the importance of a good skin care regimen. We would offer allergy testing to confirm sensitization to egg and to have a baseline to follow if some degree of avoidance is maintained. Although they observed a very clear relationship, we would discuss how AD waxes and wanes and offer evaluation of the relationship of the AD to whole egg through an OFC (a DBPCFC to egg would be least likely biased) if they are hesitant to fully reintroduce egg. Alternatively, or in addition, it would be safe to have them home trial egg in bakery foods to maintain at least some egg in the diet given that the infant was tolerating scrambled egg just one week before. We would explain that their child is likely to tolerate egg in baked foods even if we confirmed through food challenge that lightly cooked egg causes AD flares and that regular ingestion of egg in baked goods is often associated with eventual tolerance of whole egg [37].
ENVIRONMENTAL ALLERGIES
Pathogenesis of aeroallergen-exacerbated AD — The pathogenesis of aeroallergen-exacerbated AD is not well understood but may involve IgE-mediated and non-IgE-mediated allergic responses. Patients with AD have an impaired skin barrier and an inflammatory milieu. In this setting, direct skin contact with allergens or systemic exposure by inhalation may result in activation of allergen-specific IgE and non-IgE pathways that further promote inflammation. Aeroallergens, such as pollens, house dust mites (HDM), and animal danders, may trigger exacerbations of AD or contribute to chronic rash. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis" and "Treatment of atopic dermatitis (eczema)".)
Evaluation of aeroallergens as a trigger of AD — The potential for aeroallergen-induced AD may be tested by atopy patch test (APT) for non-IgE-mediated reactions or by skin prick testing (SPT) or serum-specific IgE (sIgE) for IgE-mediated reactions. However, sensitivity and specificity for diagnosis in the context of AD have not been established, and APT is not standardized [34,38-41].
Associations between aeroallergens and AD — Observational studies suggest a relationship between environmental allergens and AD, particularly perennial aeroallergens. In one study of adults with AD, sensitization to HDM by APT, SPT, and sIgE was most common, especially in patients with severe face, eyelid, and neck rash [38]. In this same study, cat sensitization was second most common, and adults with positive APT and SPT to cat report AD flares with exposure. Another study found that adults living with a cat had worse AD relative to their degree of cat sensitization [42]. In a study of children with AD tested by APT and SPT to multiple aeroallergens, 49 percent tested positive to HDM by APT, and strong APT positivity correlated with the extent of the disease [41]. The degree of HDM SPT positivity correlated with subjective symptom scores and AD severity scores.
Severity of AD is also correlated with total pollen count [43]. A study of adults followed through the birch pollen season found that both birch-sensitized and nonsensitized subjects experienced exacerbations of rash on exposed areas when pollen counts rose, but the sensitized group had greater improvements when pollen counts decreased [44].
Aeroallergen exposure inducing AD flares — The few challenge studies that examine the effect of aeroallergen exposure on AD suggest that allergen exposure can induce AD flares in some patients. In one trial of 17 grass pollen-sensitized adults exposed in a random blinded manner in an environmental chamber to either grass pollen or clean air over two days, those exposed to grass pollen experienced exacerbations in AD, particularly on air-exposed skin rather than covered skin, suggesting that direct skin contact was a trigger (rather than via inhalation) [45]. In another trial of 20 patients with AD who underwent bronchial challenge with HDM in a random blinded manner, nine experienced skin symptoms, with three having a flare of preexisting lesions, three developing new lesions, and three experiencing both. All nine of these patients had a history of asthma, and eight of them had asthma symptoms that preceded the skin symptoms [46].
Effects of decreasing aeroallergen exposure on AD — Interventional studies to reduce allergen exposure have explored the impact on AD outcomes, focusing on HDM remediation [47,48]. A systematic review identified seven randomized trials involving a total of 324 children and adults [47]. Studies included single or combined approaches of remediation such as mattress or bedding allergen covers, vacuuming carpets, and use of acaricides. The variability in the patient populations and interventions as well as the paucity of data precluded a meta-analysis. The evidence was considered very low quality, with the authors concluding an inability to inform clinical practice, although one included trial evaluating a combined approach (covers, acaricide, and high-filtration vacuuming) in adults and children with AD noted a modest treatment benefit [49].
Impact of allergen immunotherapy on AD — Multiple trials, primarily focusing on HDM, have evaluated the impact of allergen immunotherapy on AD [50-52]. A systematic review of 23 randomized trials of sublingual (SLIT) or subcutaneous (SCIT) immunotherapy for AD including 1957 children and adults primarily sensitized to HDM found that both SCIT and SLIT added on to standard AD therapy resulted in improvements in AD severity that were likely clinical significant [52]. The SCORing Atopic Dermatitis (SCORAD) index was reduced by at least 50 percent in 40 percent of those treated with allergen immunotherapy compared with 26 percent in the placebo group (absolute difference 14 percent; risk ratio 1.53, 95% CI 1.31-1.78) and improved quality-of-life (QoL) scores by 56 versus 39 percent, respectively (absolute difference 17 percent; risk ratio 1.44, 95% CI 1.03-2.01). Results were similar for SLIT versus SCIT, across AD severities, and among children and adults. More limited data suggested that immunotherapy reduced itch scores, but the impact on sleep disturbance and flares was uncertain. Both SCIT and SLIT increased adverse events (66 percent with SCIT versus 41 percent with placebo, absolute difference 25 percent; 13 percent with SLIT versus 8 percent with placebo, absolute difference 5 percent). Limitations of the available data include a focus on HDM with insufficient studies addressing additional allergens, lack of long-term outcome data, limited data regarding patient-reported outcomes, and variability in the baseline severity of AD that may influence the clinical impact of an improvement.
Role of allergen immunotherapy — Results of clinical trials suggest that allergen immunotherapy may be a helpful modality for AD [35,52] (see 'Impact of allergen immunotherapy on AD' above). For patients with moderate-to-severe AD who are who are still symptomatic despite standard therapy and who have aeroallergen sensitization, we suggest allergen immunotherapy. The patients who are most likely to benefit from this therapy are those with HDM sensitization and those with associated respiratory allergies (eg, asthma, allergic rhinitis). Factors to take into consideration include the risks and benefits, with SLIT having a more favorable risk profile than SCIT, and that response can take many months of treatment to achieve. The positive results of immunotherapy also suggest an important role of aeroallergens in AD and that multidisciplinary care should be considered. The approach to allergen immunotherapy for AD is the same as for other indications and is reviewed in greater detail separately. (See "Subcutaneous immunotherapy (SCIT) for allergic rhinoconjunctivitis and asthma: Indications and efficacy" and "Sublingual immunotherapy for allergic rhinitis and conjunctivitis: SLIT-tablets" and "SCIT: Standard schedules, administration techniques, adverse reactions, and monitoring".)
INFECTION AND ALLERGY TO INFECTIOUS AGENTS
Role and management of skin infections in AD — Bacterial, viral, and fungal infections are more common in AD and may represent a complication or, in some cases, a trigger for AD or may be related to pathogenesis. The role of allergy to bacterial or fungal agents is uncertain. Management of skin infection in AD is discussed in greater detail separately. (See "Treatment of atopic dermatitis (eczema)", section on 'Management of infection'.)
Staphylococcus — Patients with AD are frequently colonized with Staphylococcus aureus, which has both pathophysiologic and treatment implications. In addition, patients with AD have a higher prevalence of IgE against staphylococcal enterotoxin A and B than controls [53]. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis" and "Treatment of atopic dermatitis (eczema)", section on 'Staphylococcus aureus'.)
Malassezia — Malassezia yeast is a normal commensal of the skin but has been attributed a pathogenic role in AD related to immune reactions, both IgE and T cell mediated, to a variety of immunogenic proteins produced by the yeast [54]. A pathogenic role may be particularly likely for those presenting with head and neck lesions, those presenting during adolescence, and those having lesions that are persistent despite standard therapy [55]. These patients may respond to topical antifungals (eg, ketoconazole or ciclopirox) or combinations of antifungals with topical corticosteroids [34,56]. (See "Treatment of atopic dermatitis (eczema)", section on 'Fungal infections'.)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Atopic dermatitis".)
SUMMARY AND RECOMMENDATIONS
●Atopic associations and sensitization in AD – Patients with atopic dermatitis (AD), particularly those with increasingly severe AD, are more likely to have or develop comorbid atopic conditions such as allergic asthma, rhinoconjunctivitis, and food allergies and to be sensitized to food and environmental allergens. However, allergen sensitization in isolation does not indicate that the allergen is a cause or trigger of the AD. (See 'Atopic associations and sensitization' above.)
●Food allergy in AD – For most patients with AD, we suggest against the use of elimination diets in the management of AD (Grade 2C). Although immunoglobulin E (IgE) mediated, acute allergic reactions to foods (ie, urticaria, anaphylaxis) and evidence of sensitization to foods are increased in those with AD, the potential for foods to substantially contribute to chronic AD and acute AD flares is relatively low. Food elimination diets are likely to only slightly improve eczema severity, and dietary elimination carries risks. (See 'Food allergies' above and 'Role of dietary management' above.)
•Food allergy diagnosis and elimination diets – AD rashes wax and wane and have many nonallergic exacerbating factors. Foods should not be eliminated from the diet randomly without a consistent history of reactions specific to the food(s), nor should foods be excluded from the diet long term (as opposed to short term for diagnostic purposes) based upon positive skin or in vitro tests or patient history alone. Food allergy testing should be performed judiciously, based upon the clinical history and pretest likelihood that the food is a trigger of AD. Clinical reactivity should be confirmed, when necessary, by double-blind, placebo-controlled food challenge (DBPCFC). Suspicion of a specific food trigger is usually excluded when diagnostic testing with medically supervised feeding tests is employed. (See 'Evaluation of food allergy as a trigger of AD' above.)
•Risks of dietary avoidance to treat food-exacerbated AD – The risks of dietary avoidance include nutritional deficiencies and poor growth, negative impacts on quality of life (QoL) and social activities, and the immunologic risk of experiencing immediate-type anaphylactic reactions to foods that were previously included in the diet. Medical management of AD is typically pursued ahead of dietary elimination because of these risks and the relatively low chance of success with dietary elimination. (See 'Risks of elimination diets to treat food-exacerbated AD' above.)
●Environmental allergies and AD – There are compelling data to suggest a relationship between sensitization to environmental allergens and AD severity and flares in at least a subset of patients. Studies of approaches to house dust mite (HDM) remediation have mostly shown no improvements in AD. However, studies of allergen immunotherapy, particularly regarding HDM, have shown improvements in AD severity and QoL. (See 'Environmental allergies' above.)
For patients with moderate-to-severe AD who are still symptomatic despite standard therapy and who have aeroallergen sensitization, we suggest allergen immunotherapy (Grade 2B). The patients who are most likely to benefit from this therapy are those with HDM sensitization and those with associated respiratory allergies (eg, asthma, allergic rhinitis). (See 'Role of allergen immunotherapy' above and 'Impact of allergen immunotherapy on AD' above.)
●Infections and allergies in AD – Bacterial, viral, and fungal infections are common in AD and may have a pathogenic role related to allergic responses. Immune reactions, both IgE and T cell mediated, to staphylococcal and Malassezia species may worsen AD. (See 'Infection and allergy to infectious agents' above.)
ACKNOWLEDGMENT —
The UpToDate editorial staff acknowledges Jonathan M Spergel, MD, PhD, FAAAAI, who contributed to earlier versions of this topic review.
