Atopic Dermatitis: Update on Skin-Directed Management: Clinical Report Free

Atopic dermatitis (AD) is a common chronic skin condition often seen in children and adolescents. Its prevalence has been increasing in industrialized countries, including the United States and may reach as high as 25% in some populations.^1,2 The number of health care visits for AD in the United States is also increasing; however, the burden of those visits is disproportionately on general pediatricians and other pediatric primary care providers, in part because of lack of access to subspecialists.^3,4 Outpatient primary care visits for AD have nearly doubled over the last 20 years, while during that same period of time, outpatient dermatology visits for AD have decreased. Children account for most of these visits, with approximately one-third of visits being for children younger than 5 years.

Many pediatricians may not feel comfortable treating AD or other dermatologic conditions. Studies show that most pediatricians believe that their residency training in the management of AD was “enough to get by or inadequate.”⁵ In addition, variability in practice recommendations, especially regarding bathing, moisturizing, topical medications, and the role of food allergies in AD, can lead to frustration for both pediatricians and families. Because the professional competence of the physician treating AD has been shown to be an important determinant of treatment satisfaction, improving primary care provider comfort with treating pediatric AD is of paramount importance.

Since the American Academy of Pediatrics published its initial clinical report on AD in 2014,⁶ the landscape of pediatric AD has been rapidly changing, particularly as it relates to comorbidities and treatment options. This clinical report reviews pediatric AD and provides an up-to-date approach to skin-directed management that incorporates recent advances, including mental health and quality of life in children with AD, implications of the Learning Early About Peanut allergy (LEAP) trial for children with AD, and emerging topical therapies. This information will allow pediatricians and other pediatric primary care clinicians to provide effective and up-to-date care for most children with AD.

The diagnosis of AD remains primarily clinical, based on the presence of characteristic features (Table 1).⁶ Major clinical features include relapsing and remitting dermatitis that is pruritic, with onset of the disease usually occurring before 1 year of age. A family history of atopic dermatitis and/or a personal or family history of other atopic conditions may be supportive. Erythema, scaling, excoriations, and lichenification are often present in typical plaques of AD (Figure 1). In patients with darkly-pigmented skin, erythema may be more subtle (Figure 2), while dyspigmentation and follicular eczema may be more prominent. The distribution of the eczematous plaques varies with age, with cheeks, trunk, and extremities being the most characteristic areas of involvement in infancy (Figure 3), flexures being most characteristic in childhood, and hands and feet being most characteristic in teenagers and young adults.⁷ It is important to consider other skin conditions that may mimic AD, including scabies, contact dermatitis, psoriasis, and seborrheic dermatitis. In young infants, there may be an overlap of concurrent seborrheic dermatitis and AD, consisting of characteristic features of both conditions.⁸ Generally, tests such as laboratory testing and skin biopsies are not needed nor helpful in confirming the diagnosis of AD but may be useful when alternate diagnoses are being considered.

Black and Hispanic children are disproportionally affected by AD. Black infants are more likely to develop AD.² Compared with white children, eczema severity is increased in both Black and Hispanic children,⁹ and both groups are more likely to miss school because of AD.¹⁰ Black and Hispanic children are also more likely to receive medical care for AD in the primary care and emergency settings, although Black children are significantly less likely than white children to be referred to a dermatologist for poorly controlled AD.¹¹ 

The pathogenesis of AD is complex and multifactorial, involving an interplay of genetic predisposition, skin barrier disruption, environmental triggers, and immune dysfunction. Skin barrier dysfunction is central to the pathophysiology of AD.^12,13 While early studies identified increased stratum corneum lipids in Black patients compared with patients of other races, more recent and larger studies have shown lower ceramide levels in Black patients compared with white and Asian patients.^14–16 Studies examining racial differences in transepidermal water loss and stratum corneum hydration are conflicting.^15,17–20 Differences in skin barrier physiology may explain morphologic variations in the appearance of AD between patients of different races. However, it is unclear whether the disparity in AD severity between racial groups is explained by differences in the skin barrier or attributable to contextual differences including socioeconomic, health care, and/or environmental factors.^14,21 Loss-of-function mutations in the gene that encodes filaggrin (FLG) have also been found in those with AD and other atopic disorders, likely attributable to impact on the function of the skin barrier. Inheritance of this loss-of-function mutation increases the risk of developing AD and allergic disorders, potentially by allowing the entry of external antigens, which then trigger a systemic immune response.¹³ Children of parents with a history of atopic disease have an increased risk of developing AD.²² 

The most recent advances in understanding the pathogenesis of AD have been regarding the accompanying complex immune dysfunction, particularly the Th2 immune response and its impact on AD. The initial immune dysfunction triggered in AD has been identified in the Th2 immune response, which includes the cytokines IL-4 and IL-13, both of which are involved in the development of AD.²³ This Th2-mediated inflammation continues in chronic lesions of AD, along with upregulation of Th1 cytokines such as interferon gamma.²⁴ In addition, the Th2 immune response is involved in driving the synthesis of immunoglobulin E (IgE); however, IgE is not consistently elevated in patients with AD.²⁵ Recent therapeutic advances have focused on targets along the Th2 immune response.

In the majority of children, AD starts before 1 year of age and before 5 years of age in nearly all children.¹ Many will outgrow the disease, but the specific predictors of prognosis are not yet understood. A prospective study in a cohort of children followed longitudinally indicated that approximately 60% of children who developed AD by the age of 2 years had resolution of their symptoms by 4 years of age.²⁶ Those who have mutations in the filaggrin gene are more likely to have persistent disease.²⁷ 

The effects of AD extend beyond the skin, influencing quality of life and mental health. AD impacts quality of life in multiple domains in affected children and their families.²⁸ Itching, treatment burden, sleep, embarrassment related to appearance of the skin, and ability to participate in sports have the most bearing on quality of life.²⁹ Not surprisingly, impact on quality of life correlates with severity of disease. AD also affects mental health and has been linked to depression and anxiety in both patients and parents.^30–32 Cognitive behavioral therapy may be effective in reducing self-reported symptoms of eczema and anxiety.³³ 

Sleep disturbance affects approximately two-thirds of pediatric patients with AD, and disturbed sleep is associated with increased depression, anxiety, and inattention.³⁴ Lower nocturnal melatonin secretion was also associated with sleep disturbance in children with AD.³⁵ A randomized, double-blinded, placebo-controlled trial of melatonin in children 6 to 12 years old demonstrated subjective improvement in AD severity and sleep quality.³⁶ Behavioral therapy, including progressive muscle relaxation and optimization of sleep hygiene, can serve as an effective adjunct in the care of patients with AD.³⁷ 

Although sedating antihistamines have historically been used as adjunctive treatment of eczema, there is limited evidence to support their efficacy in the treatment of AD.³⁸ Children with AD have increased attention-deficit symptoms compared with healthy controls, which have been linked to sedating antihistamine use. It is unclear whether there is a causal relationship between early antihistamine exposure and increased attention deficit, or whether antihistamine use is a surrogate for more severe AD or poor sleep quality.³⁹ Infantile exposure to H1-antihistamines has been linked to development of attention-deficit/hyperactivity disorder (ADHD).⁴⁰ Nonsedating second-generation antihistamines are not associated with the same side effect profile as first-generation antihistamines and have been shown to be safe to use long-term, particularly in patients who also have comorbid environmental allergies.⁴¹ 

AD has been viewed as the first step in the “atopic march,” whereby the defective skin barrier leads to immune sensitization to antigens, resulting in food allergy, asthma, and allergic rhinitis.⁴² Although parents may suspect food allergies as a cause of AD, food-induced AD is rare. Instead, the conditions tend to co-occur in patients with atopic disease, and up to 40% of children with AD develop food allergy.⁴² Food allergy typically manifests with IgE-mediated hypersensitivity, with symptoms including urticaria and angioedema. In the rare patient in whom food allergy drives eczematous dermatitis (delayed-type hypersensitivity), an immediate-type hypersensitivity reaction has preceded it.⁴³ Food allergy testing should only be pursued in children with a history consistent with immediate-type allergy, because more than half of children with AD will have high food-specific IgE concentrations (even without true food allergy).⁴⁴ Overemphasis on food allergy as a cause of AD leads to unnecessary, and potentially dangerous, elimination diets⁴⁵ and may result in intolerance of previously tolerated foods.⁴³ Avoidance diets should only be recommended in patients who have failed a diagnostic food challenge. Treatment should instead focus on skin-directed therapies.

Increasing rates of food allergy prompted the hypothesis that decreased exposure to antigens leads to decreased immune tolerance and, thus, increased sensitization (the “hygiene hypothesis”). The Learning Early About Peanut allergy (LEAP) trial demonstrated that early exposure to peanut in a cohort of at-risk infants reduced the risk of peanut allergy compared with a control group.⁴⁶ The effect was persistent after 12 months of peanut avoidance, strengthening the argument for induction of immune tolerance via early exposure to the antigen.⁴⁷ This landmark study led to changes in clinical practice, emphasizing early antigen exposure to the gastrointestinal tract (rather than through the skin) to induce tolerance. New guidelines from the National Institute of Allergy and Infectious Disease (NIAID) for early peanut introduction⁴⁸ relied heavily on the results of the LEAP trial. In these guidelines, infants are stratified based on their risk for peanut allergy, which is determined by the presence and severity of AD as well as the presence of egg allergy. In the highest-risk group—infants with severe eczema and/or egg allergy—a peanut-specific IgE and/or skin prick test is recommended before introduction of peanut; if infants do not show evidence of sensitization, then peanut introduction is recommended at 4 to 6 months of age. Infants with mild to moderate eczema comprise the moderate-risk group, and introduction of peanut-containing foods is recommended around 6 months of age to reduce the risk of peanut allergy. In low-risk infants (infants without eczema or any food allergy), peanut-containing foods may be introduced according to family preference.

Successful treatment of AD revolves around the triad of maintenance skin care, topical anti-inflammatory medications, and avoidance of triggers. For most patients with mild to moderate AD, following these treatment principles results in good disease control. However, for a subset of patients with severe or treatment-refractory AD, systemic therapies such as phototherapy, immunosuppressants, or biologic medications are warranted, necessitating referral to a pediatric subspecialist. It is worth noting that many cases of perceived treatment failure are attributable to misunderstanding of the recommended treatment plan or difficulty in adhering to the treatment regimen. Barriers to adherence include fear of adverse medication effects, misunderstanding of the chronic nature of the disease, and lack of time and/or resources needed to follow treatment recommendations. Educating families about the expected disease course and safety of treatments can build a therapeutic foundation of trust and understanding. Individual patient circumstances, including socioeconomic status, work/time constraints, language preference, cultural practices, and beliefs, may all contribute to treatment adherence and should be considered when designing a treatment regimen. Online resources may help increase patient and family engagement.⁴⁹ The use of a written action plan has been shown to increase parent understanding of AD treatment and may positively impact patient outcomes.⁵⁰ Older children and adolescents can also participate in action plan development as a way to support chronic disease understanding, self-management, and treatment adherence.⁵¹ Additionally, physicians have found action plans to be useful in their own understanding and management of AD.⁵² Therefore, consideration should be given to the use of a written AD action plan, such as the sample shown in Figure 4.

The mainstay of preventive care in AD is moisturization. Moisturizers work by enhancing the skin barrier to protect from allergens, pathogens, and injury while simultaneously reducing transepidermal water loss. Regular use of moisturizers has been shown to reduce the frequency of flares in AD and the amount of topical corticosteroid needed to control disease.⁵³ Ideally, moisturizers should be applied liberally to the entire body skin surface at least daily in patients with AD, especially after a bath, shower, or hand washing. Younger children should be encouraged to assist in the application process, empowering them to help manage their skin disease. To increase adherence to the treatment plan and include adolescents in decision making, adolescents should be encouraged to trial various emollients and choose one that they feel most comfortable applying to their skin.

Moisturizers are emulsions of oil and water and can be categorized based on water content as lotions (higher water content) or creams (lower water content). Moisturizer selection should consider cost, accessibility, and tolerability. Evidence has not strongly supported any specific brand or formulation over another. In general, moisturizers should be fragrance free and thick in texture with low water content (creams). If a stinging sensation is encountered, ointments such as petrolatum may be substituted to allow for greater patient comfort. Although emollients have also historically been used as bath additives, evidence does not support their efficacy in reducing severity of skin disease in patients with AD.⁵⁴ 

Although moisturizers are beneficial in patients with AD, recent data suggest that they may not have a role in preventing the disease. This finding is in contrast to previously published studies that suggested a preventive benefit.^55,56 In the BEEP (Barrier Enhancement for Eczema Protection) and PreventADALL (Preventing Atopic Dermatitis and Allergy in Children) studies, two large randomized controlled trials of prophylactic emollients, there was no statistically significant change in incidence of AD in those who were treated with daily emollient vs those that used only routine infant skin care.^57,58 In the preterm infant population, application of petrolatum-based ointments in the neonatal intensive care unit has been associated with increased rates of candidemia and coagulase-negative Staphylococcus infection.^59–61 Together, these data suggest that there is currently no role for recommendation of daily emollient application to all infants, because doing so does not appear to prevent AD.⁶² 

Historically, bleach (sodium hypochlorite) baths have been considered part of maintenance skin care for patients with AD. However, the research regarding the efficacy of dilute bleach baths has been conflicting. Patients with AD have higher rates of skin surface colonization with Staphylococcus aureus than their non-AD counterparts, with increased density of S aureus associated with greater severity of AD.^63–65 Bleach theoretically may help reduce the skin surface colonization of S aureus without inducing bacterial resistance. One systematic review and meta-analysis concluded that, although dilute bleach baths were helpful in decreasing AD severity, they showed no statistical advantage over water baths alone,⁶⁶ whereas another review found slight improvement in AD with bleach baths.⁶⁷ Dilute bleach baths appear to be safe and relatively well-tolerated, although some patients may experience transient burning, stinging, or xerosis. Thus, dilute unscented bleach baths may be recommended as an adjunct in the care of AD, because they are unlikely to cause harm; however, further well-designed studies are needed to determine their efficacy.

Frequency of bathing has been a controversial topic in AD, and parents often receive conflicting advice from different providers. Although good quality studies are generally lacking, studies favor more frequent bathing,^68,69 with daily baths being the most common recommendation made by pediatric dermatologists.⁷⁰ In general, it is reasonable to recommend frequent, short baths with lukewarm water and gentle cleansers. Emphasis should be given to the importance of moisturizer application immediately after the bath.

Environmental triggers may precipitate or worsen an AD flare and should, therefore, be avoided if possible. These include low humidity, skin irritants such as harsh soaps or detergents, and contact allergens. Although the data are conflicting,⁷¹ some studies find contact allergies to be more common in people with AD than in those without atopic disease.^72,73 Patients with AD may become sensitized to various allergens via application of topical products to nonintact skin. Although not necessary for all patients with atopic disease, it is reasonable to consider patch testing in patients with dermatitis that is unresponsive to usual treatment measures, extends beyond the typical skin locations, or is temporally flared after application of a specific product. As a preventative measure, patients with AD should be counseled to avoid products with added fragrance, dyes, or essential oils, as these do little to treat AD and are known potential contact allergens.

For decades, topical corticosteroids have been the standard of care for treatment of AD.⁷⁴ Despite concerns about potential side effects, topical corticosteroids have long been an effective and safe treatment for eczema when used with appropriate supervision.⁷⁵ A common misconception about topical steroids in the treatment of eczema is that steroids discolor or bleach the skin. Although rare cases of hypopigmentation secondary to intralesional corticosteroid use have been reported,⁷⁶ typical use of topical steroids does not alter skin pigmentation. Instead, the skin affected by the AD can be lightened either because of the inflammation associated with the eczema and/or tanning of the skin around the actively inflamed eczema patch. Hypopigmentation is, thus, a secondary feature of the eczema itself rather than an adverse effect of the topical medications.

Topical steroids are available in a variety of vehicles, including cream, ointment, solution, foam, oil, and spray. Potency of topical corticosteroids is ranked from class I (superpotent) to class VII (least potent). In some instances, the vehicle affects the potency of the corticosteroid. For example, mometasone 0.1% cream is a “mid-strength” topical steroid, and mometasone 0.1% ointment is classified as “potent.”⁷⁷ In addition to potency, body site should be considered when selecting topical corticosteroids in the treatment of AD. For example, a solution, foam, or scalp oil may be preferable for treatment of scalp dermatitis rather than a cream.

Wet wrap therapy, with or without topical corticosteroids, is a useful adjunctive therapy in patients with moderate-severe or focally recalcitrant AD. Wet wraps are performed by applying topical corticosteroid or emollient to affected areas and then covering the area with damp wet wraps (typically cotton pajamas, tight-fitting clothing, or gauze wraps). Distilled white vinegar is sometimes added to the wet wrap as an antimicrobial. If desired for comfort, an additional dry layer of clothing or a blanket may be applied on top of the wet wraps. Wet wraps may be left on for a minimum of 20 to 30 minutes or as long as overnight. The proposed mechanism of wet wrap therapy is that the occlusion and moisture of the wrap enhances penetration of the topical steroid.⁷⁸ 

Topical calcineurin inhibitors (TCIs), tacrolimus 0.03% and 0.1% ointments, and pimecrolimus 1% cream, are steroid-sparing topical immunosuppressive agents that are approved as second-line therapy in the treatment of atopic dermatitis (for children 2 years and older). Both tacrolimus and pimecrolimus are effective in the treatment of mild to moderate AD, although tacrolimus is more effective than pimecrolimus.⁷⁹ However, TCIs are rarely effective in cases of AD that are recalcitrant to topical steroids. TCIs have a favorable side effect profile in that there is no concern for striae, atrophy, or adrenal suppression. They are particularly useful in patients with AD in locations where concern for long-term topical steroid side effects is highest, such as the face and eyelids. However, TCI use is associated with burning and pruritus, primarily in the first few days of use. This, combined with the cost of these medications and US Food and Drug Administration (FDA) approval down to only 2 years of age, may limit use of TCIs for some patients.

Concern has been raised regarding the safety of TCIs because of their immunosuppressive properties. The FDA issued a “black box” warning for TCIs because of the observation that laboratory animals exposed to high systemic doses of calcineurin inhibitors developed malignancies and because of isolated reports of melanoma and lymphoma in adults who were using TCIs.⁸⁰ Further studies did not identify an association between TCIs and malignancy risk, although there may be a baseline increased lymphoma risk in those with more severe AD.^81,82 A recent study found no increased long-term cancer risk in children who used topical tacrolimus for AD.⁸³ Similarly reassuring findings have been reported regarding the use of pimecrolimus in children with AD.⁸⁴ Thus, TCIs are believed to be extremely safe in the management of pediatric AD, with little evidence to support increased risk of malignancy.

There is increasing interest in and demand for nonsteroidal topical therapies in the treatment of AD because of concerns and perceptions regarding potential side effects. The first nonsteroidal/non-TCI topical medication to be approved to treat AD was topical crisaborole 2%. Crisaborole is a phosphodiesterase (PDE) 4 inhibitor that has been shown to be safe and have some efficacy in the treatment of mild to moderate AD in patients 3 months or older.⁸⁵ The effect, however, was modest when compared with vehicle; only 32.8% with improvement of AD in the crisaborole group vs 25.4% improvement rate in the vehicle group.⁸⁶ Because crisaborole has not been compared head-to-head against topical steroids or TCIs, the relative efficacy is difficult to determine, although it appears to be considerably lower than either of those medications. Thus, because of lower relative efficacy, cost, and a higher prevalence of side effects of application site burning and stinging, use of crisaborole in the treatment of AD is somewhat limited.

There are multiple emerging topical therapies that have the potential for safe and efficacious use in the treatment of AD. Topical ruxolitinib, a topical Janus kinase (JAK) inhibitor, was approved for use in people 12 years and older in 2022, although cost currently limits access for many patients. In addition, alternative PDE4 inhibitors and medications with other mechanisms, such as aryl hydrocarbon receptor agonists, are currently being developed and studied. It is likely that the number of topical medications available to treat AD will increase in the coming years.

Standard dogma in the treatment of AD has been to use topical prescription medications to areas of active, eczema-involved skin only. However, recent evidence indicates a role for so-called “proactive” treatment, especially in children who experience recurrent flares at the same body site. This strategy has been both efficacious and cost-effective in patients with moderate to severe AD. Twice weekly treatment with topical tacrolimus to areas of previously recurrent AD was found to reduce the number of AD flares and to increase the time between flares, with potential cost-savings.^87,88 In addition, topical steroids used in proactive fashion in children with moderate to severe AD led to improved disease severity and quality of life scores when compared with similar children not using topical steroids proactively.⁸⁹ This strategy should be considered in children with recurrent flares in similar locations of involvement. Specific medication and dosing may depend on individual characteristics, such as patient’s age, location of disease, and cost.

Spurred in part by the Human Microbiome Project initiative sponsored by the National Institutes of Health,⁹⁰ there has been an increased emphasis on the interplay between the human microbiome and disease. The microbiome includes the bacteria, viruses, fungi, and other sources of external genetic material present on the host. Researchers hypothesize that inflammatory diseases, such as AD, are caused or sustained by dysbiosis, resulting in a proinflammatory state.⁹¹ A randomized controlled trial of children with AD treated with 12 weeks of oral probiotics demonstrated reduced severity of AD and reduction in topical corticosteroid use compared with children who received a placebo.⁹² However the evidence for oral probiotics in prevention of AD is conflicting, and administration of probiotics to a group of preterm infants did not result in reduction of AD incidence.⁹³ Larger prospective placebo-controlled trials are needed to better understand the complex relationship between manipulation of the gut microbiome via probiotics and AD.

When skin-directed therapies fail to adequately control AD, systemic therapies are considered. Pediatricians should consider referral to subspecialists when a patient’s AD is not controlled with the use of topical corticosteroids for flares, plus proactive treatment to reduce flares. Until recently, oral immunosuppressants were the only options but were suboptimal in the treatment of AD, with modest efficacy and considerable risk of side effects. Dupilumab, a human monoclonal interleukin-4 and interleukin-13 blocker, has recently been approved in the treatment of moderate to severe AD in patients 6 months or older, with demonstration of good efficacy and a favorable side effect profile, thus changing the AD treatment landscape.^94,95 Tralokinumab, which targets IL-13, was approved in 2023 for moderate to severe AD in patients 12 years and older. JAK inhibitors have also recently gained FDA approval for refractory moderate to severe AD in people 12 years and older, including upadacitinib in 2022 and abrocitinib in 2023. There are multiple other systemic agents showing promise in the treatment of AD in various stages of development and testing, including several other biologic agents (eg, lebrikizumab and nemolizumab).

Pruritus is significantly disruptive for affected patients and their families and is one of the most difficult components of AD. The associated pruritus may contribute to ongoing damage to the skin barrier, superinfection, sleep disturbance, and decreased quality of life. The factors contributing to itch are multiple, and there is a complex interplay of both physical and immunologic factors.⁹⁶ It can be difficult to eliminate itch; however, some supportive measures include avoiding contact with irritants such as wool and aeroallergens, minimizing other triggers, and continuing skin-directed treatments aimed at reducing inflammation and restoring the skin barrier. Treatment of active AD has the greatest impact on improvement of itch. The role of histamine in AD-related itch is not completely clear, and although oral antihistamines do not have a direct effect on dermatitis, some patients may find benefit from antihistamines. Nonsedating second-generation antihistamines are not associated with the same side effect profile as first-generation antihistamines and have been shown to be safe to use long-term, particularly in patients who also have comorbid environmental allergies or dermatographism.⁹⁷ Emerging treatments for AD have shown promise in having a directly beneficial effect on the associated pruritus.⁹⁶ 

Advances in skin microbiome research have led to an increased understanding of the pathophysiology of AD.⁹⁸ AD flares are associated with a reduction of skin microbial diversity and increased prevalence of Staphylococcus species.⁹⁹ Patients with intermittent treatment between AD flares, including either maintenance application of topical corticosteroids or dilute bleach baths, had higher microbial diversity and decreased S aureus prevalence. For this reason, intermittent/maintenance treatment (“proactive” treatment) with topical corticosteroids and/or topical calcineurin inhibitors can lead to a reduction in AD flares. Commensal Staphylococcal species protect from pathogenic Staphylococcal strains,¹⁰⁰ supporting the notion that widespread eradication of cutaneous Staphylococcus does not lead to long-term improvement in AD. Treatment of S aureus in AD has, thus, moved toward treatment of underlying eczema and utilization of maintenance therapies rather than focusing on eradication of Staphylococcus. However, in patients with clear impetiginization, short-term anti-staphylococcal oral or topical antibiotics may be appropriate in treatment of severe AD flares. Other bacteria, particularly group A Streptococcus species, have also been implicated in severe flares of AD. In one retrospective, culture-based study, children with AD and streptococcal infection were more likely to have herpetiform lesions and invasive disease compared with children infected by staphylococcal species.¹⁰¹ However, prospective, microbiome-based studies are needed to corroborate this finding, which may have been biased by culture-based and retrospective methodology.

Children with AD also have increased risk of viral skin infections. Molluscum contagiosum (MC) is a common viral infection in children and is 5 times more prevalent in patients with AD vs those without eczema.¹⁰² MC can trigger or flare eczema in patients with AD, often leading to dermatitis concentrated around MC lesions.¹⁰³ Children with AD are at increased risk for MC because of their compromised skin barrier and tend to have more widespread disease, in part resulting from autoinoculation via scratching. MC may persist from weeks to years, and there are currently no consistently effective treatments, which can be a source of significant frustration for parents.

Eczema herpeticum, which occurs nearly exclusively in patients with AD, can rarely lead to life-threatening disseminated herpes simplex virus infection. Eczema herpeticum presents as monomorphic, grouped vesicles and shallow erosions, concentrated in areas of underlying AD. In patients who require hospitalization, early recognition and treatment with systemic antivirals shortens hospitalization.¹⁰⁴ Treatment of underlying AD with topical corticosteroids does not prolong hospitalization and, therefore, should not be withheld during eczema herpeticum.

Children with AD may have flares of eczema with enteroviral infection, described as “eczema coxsackium.”¹⁰⁵ Eczema coxsackium is characterized by polymorphous vesicles and bullae, distributed in areas previously or currently involved with AD, as well as an acral distribution (cheeks, buttocks, hands, and feet). The irregular and larger vesicles, as well as the presence of lesions on the palms and soles, may be helpful clues in distinguishing eczema coxsackium from eczema herpeticum. There may be an eczematous background surrounding the vesicular or bullous lesions. A similar presentation may occur in patients without a history of AD, but without flaring of background eczema, and is termed “atypical hand, foot, and mouth disease.” Patients often have concurrent oral lesions and/or exposure to hand, foot, and mouth disease, which helps to distinguish the disease from eczema herpeticum. Supportive care and treatment of the underlying AD often leads to resolution in 1 to 2 weeks without sequelae.

AD is one of the most common skin complaints presenting to the pediatric primary care provider. The information reviewed here will equip pediatricians with the tools required to diagnose and treat the majority of patients with AD. Treatment recommendations are summarized in Table 2. Patients with severe, recalcitrant, and/or complicated AD should be referred to subspecialists, such as pediatric dermatologists. In some regions, wait times to see subspecialists exceed many months; thus, pediatric primary care providers should feel comfortable prescribing standard of care treatments, including topical corticosteroids. Ongoing collaboration between pediatric primary care providers and AD specialists can optimize care for patients with complex AD.

Jennifer J. Schoch, MD, FAAD, FAAP

Katelyn R. Anderson, MD, FAAP, FAAD

Amie E. Jones, MD, FAAP

Megha M. Tollefson, MD, FAAP, FAAD

Teresa Wright, MD, FAAP, Chairperson

Raegan Hunt, MD, PhD, FAAP

Christine Lauren, MD, FAAP

Christina Boull, MD, FAAP

Deepti Gupta, MD, FAAP

Brandi Kenner-Bell, MD, FAAP

Sheilagh Maguiness, MD, FAAP

Megha M. Tollefson, MD, FAAP

Miriam Weinstein, MD, FRCPC, FAAP

Albert Yan, MD, FAAP

Kim Horii, MD, FAAP

Melissa Marx

AD

atopic dermatitis

IgE

immunoglobulin E

JAK

Janus kinase

LEAP

Learning Early About Peanut (allergy)

MC

molluscum contagiosum

PDE

phosphodiesterase

TCI

topical calcineurin inhibitor