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REVIEW ARTICLE
Year : 2020  |  Volume : 18  |  Issue : 4  |  Page : 317-325

Atopic dermatitis in children: An update for pediatricians


Department of Dermatology, Venereology, Leprosy and Pediatric Dermatology, Christian Medical College and Hospital, Vellore, Tamil Nadu, India

Date of Submission16-May-2020
Date of Decision26-Jun-2020
Date of Acceptance18-Jul-2020
Date of Web Publication19-Oct-2020

Correspondence Address:
Dr. Dharshini Sathishkumar
Department of Dermatology, Venereology, Leprosy and Pediatric Dermatology, Christian Medical College and Hospital, Vellore, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmi.cmi_81_20

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  Abstract 


Atopic dermatitis (AD), also known as atopic eczema, is a chronic, relapsing, inflammatory skin disorder commonly affecting children, and its hallmark is constant pruritus. The etiopathogenesis is complex, involving genetics and environmental triggers. There is skin barrier dysfunction along with an aberrant helper T-cell type 2 immune response. Diagnosis is primarily clinical, and a simplified version of the United Kingdom Working Party's diagnostic criteria can be helpful. The disease can be debilitating and significantly impairs the quality of life of the patients and family. The treatment has to be tailored to an individual patient, and the various components include education, identification and avoidance of triggers, skin barrier repair and maintenance, control of inflammation, management of secondary infection, and prevention of flares. The mainstay of treatment includes emollients to maintain the skin barrier, as well as topical anti-inflamamtory agents to control inflammation. However, in moderate-to-severe disease, systemic agents might be required. We hope to provide an overview of the pathogenesis, clinical features, and pharmacological and nonpharmacological treatment of AD, which will help a family physician or a pediatrician to manage children with AD preting to them.

Keywords: Atopic dermatitis, atopic eczema, topical therapy


How to cite this article:
Sathishkumar D, Gupta A, Saini K. Atopic dermatitis in children: An update for pediatricians. Curr Med Issues 2020;18:317-25

How to cite this URL:
Sathishkumar D, Gupta A, Saini K. Atopic dermatitis in children: An update for pediatricians. Curr Med Issues [serial online] 2020 [cited 2020 Nov 26];18:317-25. Available from: https://www.cmijournal.org/text.asp?2020/18/4/317/298600




  Introduction Top


Atopic dermatitis (AD), also known as atopic eczema, is a chronic, relapsing, inflammatory skin disorder, and its hallmark is constant pruritus. It usually starts in infancy and most patients have a personal or family history of atopy. The triad of AD, allergic rhinitis, and asthma is called atopy.[1] As pediatricians are the first “port of call” for most children, it is prudent for them to be aware of salient clinical features and basic approach to manage a child with AD.


  Epidemiology Top


In children, the lifetime prevalence of AD is estimated to be 15%–20%.[2] Over the past 30 years, there has been a twofold to threefold increase in the incidence,[2] which is probably due to environmental factors such as lifestyle “westernization.”[3] The higher risk of development of AD is seen in areas of industrialization, urbanization, and higher affluent class, whereas those living in more tropical latitudes and rural areas have a lower risk of developing AD.[1] Overall prevalence of AD in India (0.9%), is much lower than the west[4] which is attributed to the protective effect of breastfeeding, longer weaning, and introduction of solid foods later in the diet that exposes the child to food allergies at a relatively older age.[5]


  Pathogenesis Top


The major risk factors for the development of AD include a family history of atopy and defect in the FLG gene which codes for filaggrin.[6] The pathogenesis of AD is complex and multifactorial and includes genetic factors, skin barrier defects, environmental factors, microbiome alterations, and immune dysfunction. Filaggrin is involved in the maintenance of the skin barrier, and its defect leads to increased transepidermal water loss (TEWL), easy entry of the aeroallergens, and alteration in the skin pH, which leads to bacterial overgrowth such as Staphylococcus aureus, which in turn triggers the innate immune response. When compared to healthy individuals, the cutaneous microbiome in AD is not heterogeneous and predominantly has S. aureus.[1],[6]

Loss-of-function mutations in FLG gene have been noted in up to 50% of patients with moderate-to-severe AD and poses risk for an early-onset, more severe, and persistent disease.[7]

AD shows a biphasic inflammatory response; initially there is helper T-cell type 2 (Th2) lymphocyte-dominant response with increased Th2 cytokines, interleukin 4 (IL-4), IL-5 and IL-13 before converting to a Th1 response. The interplay of psychological stress and environmental factors has an important role in causing AD.[6]


  Common Triggers Top


Common triggers include infections, physical or psychological stress, sweating, extremes of temperature, physical factors in the form of clothes (woolen or nylon), dry air, low humidity, alkaline soaps, detergents, fragrances, cosmetics, house dust mites, animal dander, and pollen allergens in specific seasons.[8] Periocular changes are commonly observed during airborne pollen seasons.[9] About one-third of the children with moderate/severe AD can have associated food allergy; nevertheless, food allergy[1]; does not cause AD. Assumption of food allergy as a cause of AD can lead to unwarranted elimination of essential nutrients from the diet, causing potential nutritional concerns for the child.


  Clinical Features Top


The cardinal features of AD are itching which is often referred to as “itch that rashes” and dryness of the skin.[10] The clinical features manifest before the age of 2 years in most children and are extremely heterogeneous and vary based on the patient's age and disease activity. Eczema can be acute in the form of oozing and exudation; subacute exhibiting dry scaly minimally crusted plaques [Figure 1]a; or chronic [Figure 1]b, [Figure 1]c, [Figure 1]d in the form of lichenification (thickening of the skin with exaggerated skin markings due to prolonged rubbing).[1],[6] Based on the age at presentation, AD can have three stages as shown in [Table 1].[1]
Figure 1: (a) Crusted plaques involving the legs. (b) Eczematous plaques with lichenification of the lower limbs. (c and d) Flexural lichenification.

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Table 1: Clinical features of atopic dermatitis according to the age of presentation[1]

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Patients with AD can have other cutaneous findings such as centrofacial pallor, white dermographism (blanching response following stroking of the skin with the back of a fingernail that leads to white streaks), keratosis pilaris (small, rough bumps, generally on the cheeks, upper arms, and thighs), palmar hyperlinearity [Figure 2]a and [Figure 2]b, pityriasis alba (multiple ill-defined hypopigmented patches with fine scaling that are often located on the face and neck) [Figure 2]c, periorbital darkening (allergic shiners), Dennie–Morgan fold (dark, symmetric, double horizontal folds below the lower eyelids), thinning or loss of lateral portion of the eyebrows (Hertoghe sign), and follicular prominence (seen predominantly in dark-skinned individuals and trunk of children).[1],[6]
Figure 2: (a and b) Hyperlinear palms and soles. (c) Pityriasis alba. (d) Facial eczema.

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There can be regional and morphologic variants of AD. Regional variants depend on the area affected such as atopic hand dermatitis, nipple eczema, atopic cheilitis (inflammation of the lips and surrounding skin), eyelid eczema, facial eczema [Figure 2]d, and anogenital eczema. Morphological variants include nummular (coin-shaped) lesions usually seen on the extremities [Figure 3], prurigo, and follicular eczema. Severe cases can present as erythroderma which is erythema involving >90% body surface area [Figure 4].[1],[6]
Figure 3: Nummular eczema.

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Figure 4 : Erythrodermic atopic eczema.

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  Associated Comorbidities and Quality of Life Top


Children with AD can have associated atopic march(AD preceding other atopic conditions such as food allergies, asthma, and allergic rhinitis in temporal sequence), ichthyosis vulgaris, and various eye diseases, such as cataract, blepharitis, keratoconjunctivitis, and keratoconus.[9] Children with AD develop obesity and tend to have poor health behaviors, leading to increased cardiovascular risk factors, such as hypertension later in life.[11] They can have low bone mineral density and increased risk of fractures.[6]

Itch can cause sleep cycle disturbance, frequent awakenings at night affecting the quality of life (QOL) of the children and parents. The widespread skin rash can provoke teasing in the school, leading to poor scholastic performance and isolation. Many psychiatric disorders such as attention-deficit hyperactivity disorder, depression, and anxiety disorders are common in AD children.[12]


  Diagnosis Top


There is no single test to diagnose AD, and it is based on a constellation of physical findings and history of chronic, relapsing, pruritic dermatitis in the classical distribution [Figure 5]. The differentials include contact dermatitis, seborrheic dermatitis, psoriasis, scabies, cutaneous T-cell lymphoma, primary immunodeficiencies, and metabolic disorders, which ought to be ruled out before making a diagnosis of AD.[6],[13] There are various clinical criteria proposed such as the Hanifin and Rajka criteria, presented in 1980,[14] and the United Kingdom Working Party's diagnostic criteria introduced by Williams et al. The UK Working Party's diagnostic criteria is the most extensively validated criteria and is shown in [Table 2].[15]
Figure 5: Approach to diagnosis of atopic dermatitis. LDH-Lactate Dehydogenase, TARC- Thymus and activation-regulated chemokine

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Table 2: UK Working Party's diagnostic criteria for atopic dermatitis[15]

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Laboratory investigations

There is no single biomarker which will help in the diagnosis and differentiate AD from other similar skin conditions.[6] A high serum IgE (immunoglobulin E) level is seen in about 80% of extrinsic AD.[16] Eosinophilia is seen in blood and tissue, and since it changes more rapidly than IgE, it can serve as a marker to assess the progression of the disease.[9] Thymus and activation-regulated chemokine is a Th2 chemokine, and its serum level is a useful auxiliary marker to assess disease activity in children with AD.[13] The other simple laboratory parameter to assess the disease severity is lactate dehydrogenase.[17] The possibility of coexistent allergic contact dermatitis has to be ruled out in atypical and recalcitrant cases by patch testing.[18] A skin biopsy helps to rule out noneczematous conditions that can mimic AD.

Severity assessment

Clinical scoring is a noninvasive method to assess disease activity. Among the various available scores, EASI (Eczema Area and Severity Index), POEM (Patient-Oriented Eczema Measure), and SCORAD (Severity SCORing of Atopic Dermatitis) index have been validated adequately.[19] The Three-Item Severity score is based on the evaluation of erythema, edema/papulation, and excoriation on a scale from 0 to 3 and is easy to use in daily practice.[19] QOL tools used include Children's Dermatology Life Quality Index, Dermatitis Family Impact, Dermatology Life Quality Index, and the Infant's Dermatology Life Quality Index.[20]

Skin testing

Although exacerbation following exposure to certain allergens is reported, there is no conclusive evidence. Skin prick tests or specific IgE to allergens does not correlate with disease severity and is not routinely done in clinical practice.[18]

Food allergen testing has no clinical consequences if done in children without a history of immediate-type noneczematous reactions.[19] The National Institute of Allergy and Infectious Diseases guidelines state that allergy evaluation, in particular, to milk, egg, peanut, wheat, and soy should be considered only in children younger than 5 years with severe/persistent disease despite optimal management or if there is a highly reliable history of an immediate cutaneous reaction after ingestion of specific food or both.[21] A restrictive diet is recommended only for those with a positive oral challenge test, the gold standard assay for food allergy.[18] Reactivity to aeroallergens such as house dust mites, pollens, and animal dander increases with age, and diagnosis is based on relevant history such as exacerbation of symptoms following contact, demonstration of clinical relevance, and dermatitis exacerbated on the exposed areas.[22]


  Management Top


Ideal treatment is targeted toward long-term disease control with a reduction of flares and maintenance of good QOL. Single therapeutic approach is hardly capable of achieving disease control, and generally, a multipronged approach [Figure 6] is used which is as follows:[16]
Figure 6: Approach to management of atopic dermatitis. TCS: Topical corticosteroids, TCI: Topical calcineurin inhibitors, CsA: Cyclosporine, Mtx Methotrexate, AZA: Azathioprine, MMF: Mycophenolate mofetil

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  • General measures and education
  • Trigger avoidance
  • Barrier repair
  • Control of acute flare
  • Treatment of secondary bacterial infection
  • Maintenance treatment.


General measures and education

Education is an important part of AD management and parents/caregivers need to be counseled regarding the natural course of the disease and what is expected is control rather than cure. They should be educated to recognize signs and symptoms of an acute flare, secondary infection and trigger avoidance. Information can be provided in various forms such as live demonstrations, videos, hand-outs, links to useful websites (e.g., www.nationaleczema.org), and introduction to support groups. Providing a written treatment plan improves treatment adherence and reduces failures.[22]

The following aspects need to be discussed with the patient and their family members:[1]

  1. Avoidance of triggers: May be unavoidable, but exposure time can be minimized; e.g., washing off the allergens immediately
  2. Use of loose, cotton clothing which reduces overheating and avoid synthetic clothes
  3. Double rinsing of the clothes to wash the residual detergents and laundry the new clothes before using
  4. Bathing: There are various thoughts with regard to bathing in AD. Bathing increases hydration, reduces the scales and crusts, and helps remove bacteria. A once-daily short shower (5–10 min) with lukewarm water (27°C–30°C) is preferred. The cleansers used should be soap-free, close to the skin pH, and free of fragrances and allergens. Moisturizers have to be applied immediately (preferably within 3 min) after shower to reduce the TEWL
  5. Trimming and filing of the nails to prevent damage to the skin from scratching.


Topical therapies

The topical formulation should always be applied in a downward motion along the direction of hair growth to prevent folliculitis. The body surface area to weight ratio is higher in children, and hence, the systemic absorption will be more for the same amount of cream applied in adults.

Moisturizers[1],[23]

The key measure in the management of AD is the use of moisturizers to replenish the damaged barrier, thereby reducing TEWL and protecting from the penetration of allergens/microorganisms from outside. Moisturizers also help reduce the inflammation and severity by its own. They form the primary treatment for mild disease and an integral part in the management of moderate-to-severe disease.

Moisturizers are available in various formulations including lotion, cream, ointment, or gels. The choice of the moisturizers is based on the individual's preference and various aspects such as safety, effectiveness, and cost. Moisturizers should be free of additives, fragrances, and other common allergens (e.g., lanolin). Lighter ones such as lotions/creams can be used in the daytime/summer season, and ointments can be tried in the night/winters. Creams are well tolerated, but the added preservatives can cause sensitization. In contrast, ointments have very less water content and cause less stinging, but they can be very greasy and occlusive, particularly in hot and humid weather. Moisturizers have to be used liberally and frequently (every 2–4 h) and preferably immediately after bathing all over the body and not only on the areas of eczema to minimize xerosis.

Topical anti-inflammatory therapy[24]

Topical anti-inflammatory therapy forms the mainstay of AD treatment and includes topical corticosteroids (TCSs) and topical calcineurin inhibitors (TCIs). They should have sufficient potency, applied according to the recommended quantity per day, and used only on the affected skin [Table 3].[12]
Table 3: Recommendation of topical therapy according to body sites[12]

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Topical corticosteroids

TCSs form the first-line treatment in AD and are classified based on their vasoconstrictive potential [Table 4].[25] The choice of the TCS depends on the patient's age, site of application, the skin thickness/relative absorption, and the severity and the clinical phase of the eczema.
Table 4: Classification of topical corticosteroids[25]

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A thorough explanation of the risks and benefits of TCS should be given to the parents. The various side effects of TCS include skin atrophy, telangiectasia, striae, glaucoma, rebound flare, TCS dependence, tachyphylaxis, Cushing syndrome, adrenocortical suppression, and decreased growth rate. The risk is higher for thinner skin (younger skin, flexures and face), high-potency TCS, prolonged and continuous usage, and with occlusion. High-potency TCSs should not be routinely used on thin skin such as the face, body folds, and groin because of the risk of cutaneous atrophy.[26] The amount of medication applied depends on the age of the patient and the body surface area involved. Finger-tip unit (FTU) can be used as an index of adequate and safe use of TCS. One FTU is the quantity of TCS delivered from a tube with a 5-mm nozzle onto the distal end on the pulp side of an adult's forefinger (from the distal crease to the tip) and is approximately equivalent to 0.5 g.[8] One FTU can cover two palms of an adult (2% of the body surface area), and a simple way to explain this to patients is “4 hand areas = 2 FTUs = 1 g ointment.” The amount of cream used on different body parts for different age groups is shown in [Table 5].[8]
Table 5: Quantity of topical corticosteroids to be used according to age and anatomical location[8]

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With regard to the frequency of application, TCS should be used once or twice as more frequent administration does not provide improved efficacy. Patients should be taught to apply the TCS to active, noninfected eczema, and once the severity decreases/lesions resolve, the frequency of application of the TCS should be slowly tapered to once daily/every other day before beginning the maintenance therapy.[13]

Soak and smear technique[23]

For those areas that are significantly inflamed, soaking in water for about 10 min followed by the immediate application of the TCS to these areas without towel drying can reduce inflammation significantly.

Wet-wrap therapy[23]

This is one of the methods of delivering topical agents and is used in very severe or recalcitrant cases or during flares. Wet-wrap therapy (WWT) can be done with or without TCS but should not be used on infected lesions. The skin is dab dried after a short shower followed by application of the topical agent, which is then covered by a wetted first layer of tubular bandages/gauze/cotton suit, which is followed by a dry second layer. WWT increases the absorption of the topical agent due to occlusion, reduces TEWL, and forms a physical barrier which reduces scratching. The use of WWT with TCS should be limited to 2 weeks, particularly in very small children. The possibility of infection and suppression of the hypothalamic-pituitary-adrenal axis should be borne in mind when using WWT with TCS.

Topical calcineurin inhibitors[23]

The two TCIs available are tacrolimus ointment (0.03% and 0.1%) and pimecrolimus cream (1%). Although the Food and Drug Administration has officially approved the use of TCIs only above 2 years of age, the recent American guidelines have recommended the off-label use in <2 years.[23] Tacrolimus 0.1% is used in children above 15 years of age. The most common side effects include burning and stinging sensation, which can be alleviated by refrigerating the tube for 15–20 min before application.[27] Although there is a black box warning stating the theoretical risk of development of lymphoma due to TCIs based on animal studies, it is not proven in humans.[23]

TCIs are mainly used for the treatment of eczema on the face, eyelids, neck, flexures, and genitalia and also for proactive therapy as discussed below. TCIs should not be used for acute infected eczema or under occlusion and is better avoided for prolonged continuous use.

Antihistamines

The aim of systemic antihistamines is to allow better quality of sleep, since their role as anti-inflammatory agents in AD is controversial. First-generation sedative agents are useful due to their sedative effect and helps relieve symptoms of other AD-related conditions such as asthma, rhinoconjunctivitis, and urticaria.[18]

Maintenance therapy

Proactive therapy is based on the observation that the previously involved lesional skin is far from normal and has subclinical signs of inflammation, epidermal barrier defects, and damage. Patients with frequent relapses can use proactive therapy which is the application of the TCI or medium-potency topical corticosteroid twice-weekly in the areas prone for flares, in addition to the regular use of emollients.[23]

A sample approach to the use of the topical anti-inflammatory agents is shown in [Table 6].[1]
Table 6: Approach to the use of the topical anti-inflammatory agents[1]

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Management of infections

Oral antibiotics should be used only for a short duration during active infection to avoid bacterial resistance. Topical treatment with antiseptics minimizes the risk of antibiotic resistance, and suitable agents include dilute bleach (0.005% sodium hypochlorite) bath twice weekly which is prepared by adding 120 ml (0.5 cup) of 6% household bleach in 150 L of water,[12] dilute chlorhexidine baths, and dilute KMnO4 baths.[5]

Necessary swabs are required to rule out methicillin-resistant S. aureus infection in those presenting with secondary bacterial infection. Chronic Staphylococcal carriage has to be ruled out by doing a nasal and perianal swab in children with recurrent skin infections, and decolonization should be considered.[1]

Children with AD are also prone to viral infections such as molluscum contagiosum and herpes infections.[9]

Failure of first-line treatment

In patients who fail to respond to topical treatment, the following causes should be ruled out before proceeding to the second-line treatment:[18]

  • Different diagnosis or conditions coexisting with AD which are not addressed
  • Lack of adherence
  • Steroid phobia
  • Failure to adhere to general measures in AD management or breach in patient education
  • Secondary infection
  • Severity of disease indicating need for systemic therapy.


Second-line treatment

Phototherapy is a second-line treatment and can be used as a maintenance therapy as well. It improves clinical signs and reduces pruritus and bacterial colonization.[28] The common side effects include actinic damage, local erythema and tenderness, pruritus, burning, and stinging, and the less common adverse effects include nonmelanoma skin cancer and melanoma. A limiting factor for this therapeutic modality is lack of adherence to long-term treatment as patients have to come frequently to the hospital. It is important to avoid phototherapy in patients with recurrent herpes simplex infection/history of eczema herpeticum and is better not to combine with other immunosuppressive agents to avoid the synergistic risk of inducing skin malignancy.[29],[30]

Systemic anti-inflammatory agents

Systemic anti-inflammatory agents need to be considered in patients not responding to first line topical therapy or phototherapy and the skin disease has a significant negative physical, emotional or social impact. As much as possible, the use of systemic steroids should be avoided in AD and should be reserved for acute, severe exacerbations as a bridge therapy to other systemic agents and limited to a week.[31] Salient features of other systemic drugs used in AD management are shown in [Table 7].[29],[30],[31]
Table 7: Systemic agents used for management of severe atopic dermatitis[29],[30],[31]

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Newer agents

Topical crisaborole ointment inhibits phosphodiesterase 4 and is used in patients ≥2 years with mild/moderate AD.[32] Dupilumab, a monoclonal antibody, targets the IL-4 receptor alpha, thus blocking IL-4 and IL-13 pathway and is used to treat children 6-11 years old with severe AD.[33] Several topical and oral Janus kinase inhibitors have been found to reduce AD severity.[18],[32]


  Conclusion Top


Since AD can severely affect the QOL of the children and family, effective management can make a major difference and improve the family harmony. Primary treatment for AD includes skin hydration using moisturizers, topical anti-inflammatory therapy, avoidance of aggravating factors, and educational programs with a multidisciplinary approach. Proactive use of TCIs/TCS helps to minimize flares. Systemic therapy should be only indicated for refractory or severe disease after attempts with topical therapy. Secondary infections must be diagnosed early and treated promptly.

Declaration of patient consent

We have obtained an informed written consent from all the patients for publication.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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Abstract
Introduction
Epidemiology
Pathogenesis
Common Triggers
Clinical Features
Associated Comor...
Diagnosis
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