Atopic Dermatitis (Pediatric) Management

Disease Severity

A holistic approach may be applied when assessing the severity of disease.

Severity	Skin	Quality of Life and Social Wellbeing
Mild	With areas of dry skin, infrequent pruritus with or without areas of redness	Minimal impact on quality of life (some disturbance during the day and during sleep, mild changes in psychosocial wellbeing)
Moderate	With areas of dry skin, frequent pruritus, redness with or without excoriation and skin thickening	Moderately affects quality of life including everyday activities and psychosocial wellbeing, sleep frequently disrupted
Severe	Extensive areas (>20%) of dry skin, intensely pruritic, erythema with or without excoriation and skin thickening; often complicated by persistent infections	Significant disruption of quality of life; sleepless nights; lost school days

Ocular or infectious complications may also be present in severe atopic dermatitis. This may require hospitalization for severe eczema or skin infections. Severity may also be assessed using different scoring methods (eg Scoring of Atopic Dermatitis [SCORAD], Eczema Area and Severity Index [EASI], Patient Oriented Eczema Measure [POEM]).

Topical Corticosteroids

Topical corticosteroids are generally regarded as the first-line option in most situations because they are both affordable and readily accessible. This is an additional treatment for patients ≥3 months old with uncontrolled mild to severe atopic dermatitis refractory to moisturization alone. There is an anti-inflammatory and antipruritic activity through several mechanisms such as alteration in leukocyte number and activity; suppression of mediator release (histamine, prostaglandins); and enhanced response to agents that increase cyclic adenosine monophosphate (prostaglandin E₂ and histamine via the histamine-2 receptor).

Topical corticosteroids provide rapid symptomatic relief of acute flare-ups and prevention of flare relapses. These are available in different potencies from mild to very potent. Moderately potent and potent corticosteroids should be used for the treatment of clinical exacerbation over short periods of time. Mildly potent corticosteroids are recommended for maintenance therapy. A trial of mildly to moderately potent corticosteroids under occlusive dressing may be considered in patients with localized uncontrolled atopic dermatitis refractory to moderately to highly potent topical treatment. The use of super-potent topical corticosteroids is not recommended in children because of increased risk of adverse events. Potency is also affected by the vehicle the product is formulated in (eg cream, ointment).

The choice of product will depend on the severity of the flare-up, distribution of lesions, and other factors (eg humidity). The least potent but effective product should be used. Prolonged continuous use (>4 weeks) can lead to adverse effects; thus, recommended restrictions regarding intensity and duration of use on delicate skin areas (eg face, groin, neck, and skin folds) should be followed. Intermittent use (1-2 times/week) in combination with moisturizers is historically the standard therapy for atopic dermatitis. Continued intermittent or proactive therapy may also be used. Intermittent use of low- to medium-potency topical corticosteroids is recommended in patients up to 18 years of age as maintenance therapy.

Topical corticosteroids may occasionally cause hypersensitivity reactions in non-resolving or worsening atopic dermatitis despite good compliance with application. Rebound flaring can occur if higher potency preparations are discontinued abruptly. A gradual decrease in potency should follow the use of higher potency preparations. Therapy-resistant lesions may require potent topical corticosteroids used under occlusion for a short period of time and under close supervision.

Calcineurin Inhibitors (Topical)

Example drugs: Pimecrolimus, Tacrolimus

Calcineurin inhibitors inhibit inflammatory cytokine transcription in activated T cells and other inflammatory cells through inhibition of calcineurin. This is a second-line therapy for children ≥2 years of age with mild to moderate atopic dermatitis. Pimecrolimus may be used as second-line therapy for patients ≥3 months old with chronic atopic dermatitis unresponsive to, intolerant of, or with contraindications to moisturization alone. This helps reduce subsequent flare-ups or relapses with intermittent use.

Calcineurin inhibitors are equated to the medium potency strength of topical corticosteroids. These are effective for flares and as maintenance therapy. Continued intermittent or proactive therapy may be used.  Intermittent use is recommended for children and adolescents up to 18 years of age as maintenance therapy. These are especially useful for patients with atopic dermatitis in areas where long-term topical steroid adverse effects (eg skin atrophy) are most concerning (eg face, eyelids, anogenital areas, intertriginous sites). These may be used on all body locations for extended periods of time, especially the face, hands, and feet. All preparations are of a standard potency.

Common side effects include transient burning, erythema, and pruritus. Avoid the use of these agents in children younger than 2 years of age. Use only for short periods of time using the minimum amount necessary to control symptoms. Avoid continuous use and avoid its use in patients with compromised immune systems.

Pimecrolimus

The safety and efficacy of Pimecrolimus have been shown in children >2 years of age with mild to moderate atopic dermatitis. Pruritus relief has been seen as early as day 3 of use. This prevents flare-ups and results in a significant steroid-sparing effect when used for up to 12 months. When used in early stages of disease, it has shown to be therapeutically advantageous over typical moisturizers plus topical corticosteroids in long-term use.

Tacrolimus

Tacrolimus is indicated for moderate-severe atopic dermatitis. This may be used for up to 1 year without loss of effectiveness, increase in infection risk, or other non-application-site adverse effects. This is well-tolerated with transient skin burning or irritation. Studies have confirmed the efficacy of Tacrolimus 0.03% compared to low-potency topical corticosteroids in children.

Phosphodiesterase-4 (PDE4) Inhibitors (Topical)

Crisaborole

Crisaborole is a selective PDE4 inhibitor that prevents pro-inflammatory cytokine production. This is approved by the United States Food and Drug Administration (US FDA) for the treatment of mild-moderate atopic dermatitis in patients ≥3 months old refractory to moisturization alone.

Difamilast

Difamilast is a selective PDE4 inhibitor approved by the US FDA for patients ≥2 years old with mild to moderate atopic dermatitis.

Roflumilast

Roflumilast is a selective, highly potent PDE4 inhibitor with anti-inflammatory properties. Topical 0.05% cream is recommended for patients aged 2-5 years old, and topical 0.15% cream is recommended for patients ≥6 years old with mild to moderate atopic dermatitis who are unresponsive to topical corticosteroids or topical calcineurin inhibitors and/or prefer not to use topical corticosteroids.

Other PDE4 Inhibitor

Lotamilast is being studied for treatment of atopic dermatitis.

Aryl Hydrocarbon Receptor Agonist (Topical)

Tapinarof

Tapinarof is recommended in patients ≥2 years old with mild, moderate, or severe atopic dermatitis. This has been shown to enhance barrier function, reduce inflammation, and alleviate itch.

Biological Agents

Dupilumab

Dupilumab blocks the IL-4 receptor alpha subunit and inhibits signaling from IL-4 and IL-13. The first human monoclonal antibody approved for patients ≥6 months with moderate to severe atopic dermatitis refractory, intolerant, or unable to use topical treatments and cannot tolerate systemic treatments. Significant improvements in disease activity, symptoms, and quality of life were seen in patients given Dupilumab involved in several clinical studies.

Lebrikizumab

Lebrikizumab is a subcutaneous recombinant humanized IgG4 anti-IL-13 monoclonal antibody approved for the treatment of moderate to severe atopic dermatitis in patients ≥12 years with a body weight of at least 40 kg who are candidates for systemic therapy.

Nemolizumab

Nemolizumab is a humanized IgG2 monoclonal antibody that inhibits IL-31 signaling by binding selectively to IL-31 receptor alpha. This is a treatment option for patients ≥12 years of age with moderate to severe atopic dermatitis refractory to topical therapies alone who are candidates for systemic therapy, given in combination with topical corticosteroids and/or calcineurin inhibitors.

Tralokinumab

Nemolizumab is a human, high-affinity IgG4 monoclonal antibody that acts by neutralizing IL-13. This is recommended for children ≥12 years with moderate to severe atopic dermatitis uncontrolled by topical therapies and who are candidates for systemic therapy. Combination treatment with topical corticosteroids, topical calcineurin inhibitors, and UV light is possible.

Other Biological Agents

Other biologicals undergoing clinical trials or currently being used as off-label therapy for atopic dermatitis include Astegolimab, Benralizumab, Fezakinumab, Itepekimab, Mepolizumab, Omalizumab, Rituximab, Tezepelumab and Ustekinumab.

Skin Infections¹

Clinical infections at treatment sites should be cleared before starting anti-inflammatory agents. This may need to treat reservoirs of the infection to prevent recurrence (eg nose, groin).

Bacterial Infections

Staphylococcus aureus is commonly cultured from eczematous skin and is often the cause of localized infections.

Topical Therapy

Topical therapy may be used to treat mild and localized secondary infection. Fusidic acid, Mupirocin and Retapamulin are treatment options. Retapamulin is recommended for children ≥9 months. Prolonged use should be avoided to decrease the risk of bacterial resistance.

Oral Therapy

Oral therapy is usually necessary to treat widespread infected lesions. Anti-staphylococcal penicillins, macrolides, first- and second-generation cephalosporins, and Clindamycin are treatment options.

Viral Infections

Patients may develop secondary herpes infections inclusive of eczema herpeticum (Kaposi’s varicelliform eruption) and may require systemic Acyclovir treatment in a hospital setting. Prophylactic oral antiviral agents may be used to suppress recurrent cutaneous herpetic infections.

Fungal Infections

The role of fungi in atopic dermatitis is questionable. Topical or systemic antifungal therapy may be considered in selected patients with atopic dermatitis, particularly those with the head and neck variant and with documented IgE sensitization to Malassezia spp. Superficial dermatophytosis and Pityrosporum ovale may be treated with systemic or topical antifungals.

Antihistamines¹

Oral sedating antihistamines may be useful if the patient has comorbidities (allergic rhinitis, urticaria, or dermatographism) and sleep disturbance. They are best used at bedtime since pruritus is typically worse at night. Studies of oral non-sedating antihistamines have shown variable results in controlling pruritus; however, they may be useful in a small group of patients with associated urticaria. Topical antihistamines are usually not helpful in relieving pruritus and may cause allergic contact dermatitis.

Systemic Corticosteroids¹

Systemic corticosteroids should only be considered in treatment-resistant atopic dermatitis. The American Academy of Allergy, Asthma and Immunology (AAAAI) does not recommend using systemic corticosteroids since its benefit versus risk of adverse effects cannot be justified. This should be limited to short-term bridge use during acute, severe flares and is not appropriate for long-term maintenance, especially in children. The most commonly used formulations are Prednisone and Prednisolone for oral and IV administration, with dosing based on body weight and a tapering course to decrease the risk of adrenal suppression.

Routine use in children and adolescents is discouraged but may be used for severe atopic dermatitis with the following conditions: Lack of or contraindications to other treatment options; as a bridge to phototherapy or other systemic therapies; for the provision of immediate relief during acute flares; and when a major life event is anticipated. Systemic corticosteroids improve lesions, but rebound flare-ups usually occur upon discontinuation. This should be used short-term and decrease the chance of rebound effect by tapering oral form slowly while increasing topical corticosteroid treatment and continuously hydrating the skin. A decreased linear growth may be observed with long-term administration of systemic corticosteroids in children and adolescents.

¹Various anti-infectives, antihistamines, and corticosteroids are available. Please see the latest MIMS for specific formulations and prescribing information.

Janus kinase (JAK) Inhibitors

Abrocitinib

Abrocitinib is an oral JAK1 inhibitor used in patients ≥12 years old for the treatment of refractory moderate to severe atopic dermatitis that is inadequately controlled with other systemic drugs (including biologics) or when use of those therapies is not advisable. This may be used with or without topical corticosteroids. This is not recommended to be used in combination with other JAK inhibitors, biologic immunomodulators or other immunosuppressants. A large, randomized, safety clinical trial showed an increased risk of malignancy (lymphoma and lung cancer), all-cause mortality (including sudden cardiovascular death), major adverse cardiovascular events ([MACE] defined as cardiovascular death, myocardial infarction, and stroke), and thrombosis (including pulmonary embolism and venous and arterial thrombosis) with another JAK inhibitor compared to tumor necrosis factor (TNF) inhibitors in patients with rheumatoid arthritis.

Baricitinib

Baricitinib is an oral selective JAK1 and JAK2 inhibitor that blocks signals of immune response and inflammation. In European countries, Baricitinib is a treatment option for patients ≥2 years of age with moderate to severe atopic dermatitis who are candidates for systemic therapy. This is only approved for use in adults in the US.

Delgocitinib

Delgocitinib is a topical JAK inhibitor approved in Japan for the treatment of atopic dermatitis in patients aged ≥2 years.

Ruxolitinib (Topical)

Ruxolitinib is a topical JAK1/2 inhibitor. This is recommended by the American Academy of Dermatology (AAD) and the US FDA for short-term treatment of mild to moderate atopic dermatitis in immunocompetent patients aged ≥2 years old who are unresponsive to other topical agents or for whom those therapies are not advisable. The AAAAI prefers that patients use other topical therapies than topical Ruxolitinib unless the patient has not responded to other topical therapies and/or highly values its modest benefits over other topical treatments and consents to its known side effects.

Upadacitinib

Upadacitinib is an oral selective and reversible inhibitor of JAK enzymes (preferentially JAK1 or JAK1/3), which are intracellular enzymes involved in the stimulation of hematopoiesis and immune cell function through a signaling pathway. This is used in patients ≥12 years old with refractory moderate to severe atopic dermatitis that is inadequately controlled with other systemic drugs (including biologics) or when use of those therapies is not advisable. This is not recommended to be used in combination with other JAK inhibitors, biologic immunomodulators, or other immunosuppressants.

Systemic Immunosuppressants¹

A minimal effective dose should be applied once a response is attained and sustained. Continued adjunctive therapy allows the use of the lowest dose and duration of systemic agent.

Azathioprine

The AAAAI recommends against the use of Azathioprine in patients with moderate- to severe-atopic dermatitis refractory, intolerant, or unable to use moderate- to high-potency topical treatment and systemic treatment inclusive of biologics. This may be considered for severe or refractory disease, especially for children with significant psychosocial impact. Thiopurine methyltransferase (TMPT) levels should be taken pretreatment and while on treatment to determine dose and test for myelosuppression to decrease risk of myelotoxicity. Monitor hematologic and liver function parameters. Azathioprine is safer than Ciclosporin and has been used for long-term. Most patients respond to low doses. Adverse reactions include nausea, fatigue, myalgia, liver dysfunction, and bone marrow depression in patients deficient in thiopurine methyltransferase. The mechanism of action involves generating 6-mercaptopurine (6MP) metabolites, thioguanine nucleotides (TGNs), which are incorporated into DNA and thereby inhibit DNA synthesis, producing the drug’s primary immunosuppressive effect.

Ciclosporin

Ciclosporin is an alternative treatment option for children and adolescents with refractory atopic dermatitis when moderate- to high-potency topical treatment and systemic treatment or phototherapy are not desirable, accessible, or effective. This is effective for short-term use in severe refractory disease. Condition tends to return after discontinuation of therapy but not always at the original severity level. Long-term use is not justified because of risks of hypertension and renal dysfunction. Mechanism of action involves inhibiting T‑cell activation and proliferation by blocking nuclear factor of activated T cells (NFAT)-dependent cytokine production.

Methotrexate

Methotrexate is an alternative treatment option for children with severe atopic dermatitis and intolerant or with contraindications to Ciclosporin, however, the AAAAI recommends against the use of Methotrexate in patients with moderate- to severe-atopic dermatitis refractory, intolerant, or unable to use moderate- to high-potency topical treatment and systemic treatment inclusive of biologics. Folate supplementation is recommended during treatment with Methotrexate. The mechanism of action involves antagonizing folic acid, thereby impairing cell division, DNA/RNA synthesis and repair, and protein synthesis, ultimately suppressing immune system activity.

Mycophenolate Mofetil (Mycophenolic Acid)

Mycophenolate mofetil is an alternative treatment option for children with severe refractory atopic dermatitis and intolerance to or contraindications to Ciclosporin. The AAAAI recommends against the use of Mycophenolate in patients with moderate- to severe-atopic dermatitis refractory, intolerant, or unable to use moderate- to high-potency topical treatment and systemic treatment inclusive of biologics.

¹Various immunosuppressants are available. Please see the latest MIMS for specific formulations and prescribing information.

Other Pharmacotherapeutic Options

Allergen immunotherapy may benefit patients with moderate to severe atopic dermatitis, especially those with a history of other allergic diseases. Further studies are needed to prove the efficacy of probiotics, topical sodium cromoglycate, vitamin D, Tofacitinib, mast cell stabilizers, and leukotriene antagonists (eg Montelukast) in atopic dermatitis. Vitamin D supplementation and use of prebiotics/probiotics may reduce symptoms but are not routinely recommended. 

Patient and Caregiver Education

Discuss the chronic nature of atopic dermatitis, exacerbating factors, and appropriate treatment options. Emphasize that atopic dermatitis tends to improve over time. Teach the patient or caregiver how to monitor disease progression and when to seek medical help. Teach the patient or caregiver how to recognize flares and give instructions on how to manage flares. Educate the patient about good skin care practices (eg bathing, hydration, and use of moisturizers). Explain potential side effects of medications when used over extended periods of time. The patient or caregiver should be instructed to apply topical steroids thinly to skin lesions only and emollients over unaffected areas. Keep fingernails trimmed short. Use cotton gloves at night to limit scratching. Corticophobia may be addressed by communicating to parents the proper application and need for good compliance for the best clinical outcome. Emphasis should be made against corticosteroid addiction, which may result in rosacea-like perioral dermatitis and genital steroid-induced folliculitis.

Avoidance of Trigger Factors

All Irritants

Lipid solvents (soaps, detergents) may be a trigger factor for atopic dermatitis. New clothes should be laundered before wearing to decrease levels of formaldehyde and other chemicals added. When washing, use liquid instead of powder detergent, and do another rinse cycle to remove detergent completely from clothes. Other irritants include disinfectants (eg swimming pool chlorine), occupational irritants, and household fluids (eg meats, juices from fresh fruits).

Contact and Aeroallergens

Allergens include furry animals (eg cats, dogs), molds, human dander (dandruff) resulting in overgrowth of yeast, and dust mites. Avoidance includes use of dust mite-proof encasings on pillows and mattresses, washing bedding in hot water weekly, removing bedroom carpeting and curtains, decreasing indoor humidity level by air conditioning, and avoiding upholstered sofas.

Other Triggers

Foods

Flaring or occurrence of atopic dermatitis with a specific food may warrant an elimination diet in patients with moderate-severe atopic dermatitis. Skin prick tests (SPT) and measurement of specific IgE are used to determine sensitization to a particular food. Limited food allergy testing may be considered in children <5 years with moderate-severe atopic dermatitis and disease unresponsive to previous therapies and/or with a history of an allergic reaction to a specific food. Negative results are useful for ruling out suspected allergens.

Climate

Consider temperature and humidity control to avoid increased pruritus due to heat and perspiration. Prolonged sun exposure may increase evaporative losses due to sweating.

Hormones (Menstrual Cycle)

Hormonal changes during the menstrual cycle may trigger or exacerbate atopic dermatitis.

Psychological factors

Emotional factors (eg anxiety and anger) cause disease exacerbation, induce immune activation, and increase pruritus and scratching. Psychological evaluation and counseling should be considered in patients who have difficulty with emotional triggers or who have psychological problems.

Skin Care

Hydration of skin with emollients and restoration of skin barrier function are essential in atopic dermatitis treatment. Regular skin cleansing with the use of soaps, synthetic detergent (syndet) bars, and topical antiseptics and antibiotics help reduce abnormal microbial colonization to restore the skin microbiome.

Bathing¹ 

Soap substitutes with minimal defatting activity, hypoallergenic, fragrance-free, and with neutral to low pH are preferred. Soak in a bath or shower daily for 10-15 minutes using lukewarm water and the “soak-and-seal” approach, not exceeding two baths in 1 day. Bathing should be frequent (daily to every other day) and short, using lukewarm water and a gentle cleanser. “Soak-and-seal” is the immediate application of prescribed topicals and emollients after bathing. Consider using bath oils within the last 2 minutes of bathing.

Topical medications are best applied after bathing or soaking for 20 minutes without toweling dry because of greater penetration of hydrated skin. Bleach baths with intranasal Mupirocin may be used for moderate to severe disease with frequent bacterial infections. Salt baths may be used in patients with heavily impetiginized or ichthyotic skin. Oatmeal products added to a bath may be soothing but do not increase water absorption by the skin.

Moisturizers¹ 







Moisturizers strengthen the skin barrier protecting against allergens, pathogens, and physical injury while reducing transepidermal water loss. Consistent use has been shown to decrease flare frequency and lower the amount of topical corticosteroid required for disease control. Oil-in-water emulsions can be classified by their water content as lotions (higher water content) or creams (lower water content), and their selection should take into account cost, availability, and individual tolerability. Fragrance-free non-prescription moisturizers are preferred over prescription moisturizers.

Emollients (eg Glycerol stearate, lanolin, soy sterols) provide lubrication, improve the epidermal barrier, and help soften the skin surface. Newly developed emollients contain ingredients that positively influence the skin microbiome of atopic dermatitis patients.

Occlusive agents (eg Dimeticone, Mineral oil, petrolatum) provide a physical barrier against water evaporation. Humectants (eg Urea, Glycerol, Lactic acid, pyrrolidone carboxylic acid [PCA]) help retain moisture in the stratum corneum. Urea, lactate, PCA, and amino acids (eg Arginine) are components of natural moisturizing factors (NMF) which maintain adequate hydration of the skin, thus optimizing the barrier function of the stratum corneum.

Patient preference and treatment area will determine the formula used in moisturizers (eg Ceramides, Hydroxypalmitoyl sphinganine, Palmitoylethanolamide [PEA], Liquid paraffin, Mineral oils, Glycerin, Hyaluronic acid, Shea [Butyrospermum parkii] butter, Telmesteine, Glycyrrhetinic acid, Lactic acid). Urea-containing moisturizers reduce the rate of flares but may cause transient burning and stinging after application. Oat- and Glycerol-containing moisturizers also reduce the rate of flares but with lesser side effects and lessen the use of topical corticosteroids. Glycyrrhetinic acid and Allantoin have anti-inflammatory properties that help reduce pruritus. The anti-inflammatory and antibacterial properties of Licochalcone contained in some moisturizers are comparable to the efficacy of the combination therapy of moisturizers and 1% Hydrocortisone acetate cream. Niacinamide and sunflower seed oil improve skin barrier function by reducing transepidermal water loss. Olive oil application is not recommended, as it may aggravate xerosis and atopic dermatitis.

Emollients should be applied liberally to the entire body skin surface at least three times daily (in the morning and afternoon immediately after a bath and at night before bedtime) or in flare-up conditions every 3-4 hours. If the product stings, it should not be used.

¹Various products are available. Please see the latest MIMS for specific formulations and prescribing information.

Wet Dressings

Wet dressings may be used on weeping lesions, localized recalcitrant lesions, or moderately to severely affected areas. Discomfort, folliculitis, and impetigo are reported as common adverse effects. These can help reduce water loss and disease severity in patients with moderate to severe atopic dermatitis. Combined with topical corticosteroids, it can be effective in treating refractory cases. Temporary increased systemic absorption of corticosteroids was reported. These are recommended during flares rather than as maintenance therapy for atopic dermatitis. Topical corticosteroids or emollients applied on the affected area and then wrapped with damp wet wraps should be left on for a minimum of 20 to 30 minutes or overnight. The mechanism of action involves providing moisture and occlusion that enhance the penetration of topical treatments (eg corticosteroids, emollients).

Phototherapy

Broad-band UVB and UVA, narrow-band UVB and UVA-1, or combined UVA and UVB can be useful in atopic dermatitis. Narrowband UVB is the initial phototherapy of choice due to its safety profile and availability. If accessible and acceptable, it represents a viable adjunct to topical corticosteroids for adolescents with moderate to severe atopic dermatitis who prefer to avoid systemic agents or have contraindications to systemic immunosuppressive or immunomodulatory therapies. Effects of phototherapy include acceleration of wound healing, cell migration and barrier repair, suppression of pro-inflammatory cytokines, and promotion of antimicrobial peptide production. Phototherapy should be avoided in infants and young children.

Photochemotherapy with Psoralens and UVA should be restricted to patients with widespread severe atopic dermatitis. Ultraviolet (UV) therapy should be reserved for pediatric patients >6 years of age who present with severe refractory atopic dermatitis. A yearly skin exam is recommended with continued phototherapy. Relapse following cessation of therapy frequently occurs. Adverse reactions may be short-term (erythema, skin pain, pigmentation, itching) and long-term (premature skin aging and potential cutaneous malignant diseases). 

Identification and elimination of triggering factors is the mainstay for prevention of flares and long-term treatment of atopic dermatitis. Breastfeeding or feeding with hypoallergenic hydrolyzed formula milk was shown to be beneficial. If the patient with atopic dermatitis is also diagnosed with a food allergy, the mother should be advised to eliminate all identified food allergens from her diet. Probiotics may also reduce the incidence or severity of atopic dermatitis; however, more studies are needed to prove this benefit.