Contemporary Mgmt Strategies for Atopic Derm Materials

CONTEMPORARY MANAGEMENT STRATEGIES FOR ATOPIC DERMATITIS

Faculty:

L. Austin Fredrickson, MD, FACP 

L. Austin Fredrickson is an Associate Professor of Internal Medicine at Northeast Ohio Medical University, where he serves as core faculty and teaches diagnostics, therapeutics, clinical skills, and health humanities. He is board-certified in general internal medicine and practices rural primary care. 

Liz Fredrickson, PharmD, BCPS, is an Associate Professor of Pharmacy Practice and Pharmaceutical Sciences at the Northeast Ohio Medical University (NEOMED) College of Pharmacy. She has eight years of experience in medical writing and research.

Pamela Sardo, PharmD, BS

Pamela Sardo, PharmD, BS, is a freelance medical writer and licensed pharmacist. She is the founder and principal at Sardo Solutions in Texas. Pam received her BS from the University of Connecticut and her PharmD from the University of Rhode Island. Pam’s career spans many years in retail, clinics, hospitals, long-term care, Veterans Affairs, and managed health care responsibilities across a broad range of therapeutic classes and disease states.

Abstract

Atopic dermatitis (AD), also known as atopic eczema, is a chronic, relapsing inflammatory skin disorder characterized by intense pruritus, xerosis (dry skin), and eczematous lesions. It was historically considered a disease of childhood, but more recent data suggest that AD frequently persists into adulthood and may also present as a new condition in adult patients. Advances in understanding the immunopathogenesis of AD have transformed the therapeutic landscape, and the introduction of biologic therapies and oral Janus kinase (JAK) inhibitors has prompted substantial updates in national and international treatment guidelines. This continuing education activity reviews the etiology, epidemiology, and pathophysiology of AD. Additionally, common clinical presentations, diagnostic strategies, and interprofessional management plans aligned with current evidence-based recommendations will be discussed.

Accreditation Statements

In support of improving patient care, RxCe.com LLC is jointly accredited by the Accreditation Council^TM for Continuing Medical Education (ACCME^®), the Accreditation Council for Pharmacy Education (ACPE^®), and the American Nurses Credentialing Center (ANCC^®), to provide continuing education for the healthcare team.

This activity was planned by and for the healthcare team, and learners will receive 2 Interprofessional Continuing Education (IPCE) credits for learning and change.

Credits: 2 contact hour(s) (0.2 CEU(s)) of continuing education credit.

Credit Types:

IPCE Credits - 2 Credits

AAPA Category 1 Credit™️ - 2 Credits

AMA PRA Category 1 Credit™️ - 2 Credits

Type of Activity: Application

Media: Computer-Based Training (i.e., online courses)

Estimated time to complete activity: 2 contact hour(s) (0.2 CEU(s)), including Course Test and course evaluation.

Release Date: April 10, 2026 Expiration Date: April 10, 2029

Target Audience: This educational activity is for Physicians and Physician Assistants

How to Earn Credit: From April 10, 2026, through April 10, 2029, participants must:

Read the “learning objectives” and “author and planning team disclosures;”

Study the section entitled “Educational Activity;” and

Complete the Course Test and Evaluation form. The Course Test will be graded automatically. Following successful completion of the Course Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)

CME Credit: Credit for this course will be uploaded to CPE Monitor^® for pharmacists. Physicians may receive AMA PRA Category 1 Credit™️and use these credits toward Maintenance of Certification (MOC) requirements. Physician Assistants may earn AAPA Category 1 CME credit, reportable through PA Portfolio. All learners shall verify their individual licensing board’s specific requirements and eligibility criteria.

Statement of Need

Atopic dermatitis is a prevalent chronic inflammatory skin disease affecting millions of patients. It remains frequently underdiagnosed, misclassified, and inadequately controlled. Healthcare professionals may rely on body surface area to assess severity, overlooking significant quality-of-life impairments, including sleep disruption, pruritus, and psychosocial burden. Treatment selection is often inconsistent, sometimes overused, delayed, or made without full consideration of the mechanism of action, safety profiles, routes of administration, or patient-specific factors. Gaps remain in recognizing dosage forms, counseling on proper application, and optimizing the interprofessional approach to care. This activity aims to optimize classification accuracy, severity assessment, and patient-centered action plans to improve long-term disease control and adherence.

Learning Objectives: Upon completion of this educational activity, participants should be able to:

Differentiate clinical presentations and severity of atopic dermatitis

Evaluate available treatment options for atopic dermatitis based on disease severity, patient characteristics, and safety considerations

Describe patient-centered management strategies to support long-term disease control, symptom reduction, and quality-of-life improvement

Disclosures

The following individuals were involved in planning, developing, and/or authoring this activity: L. Austin Fredrickson, MD, FACP; Liz Fredrickson, PharmD, BCPS; and Pamela Sardo, PharmD, BS. None of the individuals involved in developing this activity has a conflict of interest or financial relationships related to the subject matter. There are no financial relationships or commercial or financial support relevant to this activity to report or disclose by RxCe.com or any of the individuals involved in the development of this activity. 

© RxCe.com LLC 2026: All rights reserved. No reproduction of all or part of any content herein is allowed without the prior, written permission of RxCe.com LLC.

Educational Activity Pre-Test

A 28-year-old patient presents with eczematous lesions involving 6% body surface area. They report severe pruritus with nightly sleep disturbance and a significant impact on work performance. How should this patient’s disease severity be best classified?

Mild

Severe

Cannot determine without a SCORAD score

Moderate

A patient with moderate-to-severe atopic dermatitis has failed optimized topical therapy. Which of the following is considered a first-line systemic option with a favorable safety profile and minimal routine laboratory monitoring?

Cyclosporine

Methotrexate

Dupilumab

Systemic corticosteroids

Which of the following strategies is most effective in reducing flare frequency in patients with atopic dermatitis? 

 

Discontinuing therapy once lesions resolve

Using topical corticosteroids only during severe flares

Proactive intermittent therapy to previously affected areas

Avoiding moisturizers during remission

 

Educational Activity

Contemporary Management Strategies for Atopic Dermatitis

Introduction

Atopic dermatitis (AD), also known as atopic eczema, is a chronic, relapsing inflammatory skin disorder characterized by intense pruritus, xerosis (dry skin), and eczematous lesions.^1,2 It was historically considered a disease of childhood, but more recent data suggest that AD frequently persists into adulthood and may also present as a new condition in adult patients.^1,3 This condition is notable for fluctuating severity, periods of remission and exacerbation, and significant impairment in quality of life.¹ Atopic dermatitis causes substantial physical and psychosocial burdens, and patients frequently experience sleep disturbance, fatigue, social withdrawal, anxiety, and depression.^1,2 Beyond skin involvement, AD is increasingly recognized as part of a systemic atopic phenotype associated with allergic rhinitis, asthma, and food allergies. This is often described as the “atopic march.”^2,5

Advances in understanding the immunopathogenesis of AD have transformed the therapeutic landscape, and the introduction of biologic therapies and oral Janus kinase (JAK) inhibitors has prompted substantial updates in national and international treatment guidelines.^4,5 This continuing education activity reviews the etiology, epidemiology, and pathophysiology of AD. Additionally, common clinical presentations, diagnostic strategies, and interprofessional management plans aligned with current evidence-based recommendations will be discussed.

Guideline Updates

There have been recent, important updates in AD management guidelines from the American Academy of Dermatology (AAD) and the American Academy of Allergy, Asthma and Immunology/American College of Allergy, Asthma and Immunology (AAAAI/ACAAI) Joint Task Force.³ These updates reflect the use of targeted biologics and small-molecule therapies and, importantly, emphasize shared decision-making, disease severity stratification, and long-term disease control.³ Key revisions include the following.³

Strong recommendations for dupilumab and tralokinumab in moderate-to-severe AD refractory to topical therapy

Strong or conditional recommendations for oral JAK inhibitors (abrocitinib, baricitinib, upadacitinib) in selected patients after risk assessment

Conditional recommendations for traditional systemic immunomodulators such as cyclosporine, methotrexate, azathioprine, and mycophenolate

Recommendations against routine use of systemic corticosteroids for chronic management

Emphasis on proactive maintenance therapy with topical corticosteroids (TCS) or topical calcineurin inhibitors (TCIs) to prevent flares

Clarification that prescription moisturizers offer no clear advantage over well-formulated over-the-counter moisturizers

Conditional use of dilute bleach baths in moderate-to-severe disease

Recommendation against routine elimination diets in the absence of confirmed food allergy

Additionally, the guidelines now emphasize addressing therapeutic inertia, or the failure to escalate therapy when indicated, which has historically contributed to the undertreatment of moderate-to-severe AD.³

Epidemiology of Atopic Dermatitis

Atopic dermatitis affects approximately 20% of children and 10% of adults globally.^1,3 In the United States (US), the prevalence is estimated at 18% among school-aged children and approximately 7% among adults.¹ While many cases begin in infancy, up to 25% of adults with AD report adult-onset disease.¹ AD follows a bimodal age distribution, with peaks in early childhood and middle adulthood.¹ Although it has been suggested that most children “outgrow” AD, more recent systematic reviews have found that many individuals experience persistent or recurrent disease into adulthood.¹ The disease severity distribution in adults has been reported as follows.¹

Mild: ~50%

Moderate: ~40%

Severe: <10% =

Atopic dermatitis is among the leading causes of disability-adjusted life-years (DALYs) for skin diseases worldwide.¹ It is associated with a significant economic burden. Direct and indirect costs include physician visits, prescription medications, lost productivity, and out-of-pocket expenses. In severe cases, disease-related costs may account for a substantial proportion of a patient’s household income.¹

Etiology, Risk Factors, and Pathophysiology

Atopic dermatitis is a multifactorial disorder that results from an interplay between genetic predisposition, epidermal barrier dysfunction, immune dysregulation, and environmental exposures.^1,2,6

Genetic Factors

The strongest known genetic risk factor is a mutation in the filaggrin (FLG) gene, which encodes a structural protein essential for epidermal barrier integrity.² Filaggrin deficiency leads to the following:²

Reduced ceramide production

Increased transepidermal water loss

Enhanced penetration of allergens and microbes

FLG mutations alone are not sufficient to cause AD. Multiple other genes involved in skin barrier function and immune regulation also contribute to susceptibility.²

Immune Dysregulation

AD is primarily driven by type 2 inflammation.¹ In acute lesions, keratinocytes release IL-25, IL-33, and thymic stromal lymphopoietin (TSLP), which activate dendritic cells and promote differentiation of naïve T cells into Th2 cells.¹ Th2 cells produce IL-4, IL-5, IL-13, and IL-31, leading to the following:¹

Impaired keratinocyte differentiation

Increased IgE production

Eosinophil activation

Intense pruritus

IL-13 appears to be a dominant cytokine in AD and correlates with disease severity.^1,6 Chronic disease demonstrates a broader immune profile, with involvement of Th1, Th17, and Th22 pathways contributing to epidermal thickening and lichenification.^1,6

Microbiome Alterations

Patients with AD tend to exhibit reduced microbial diversity and increased colonization with Staphylococcus aureus.^1,2 This is present in up to 90% of patients.¹ Reduced antimicrobial peptides further predispose patients to infection.^1,2s

Environmental and Lifestyle Triggers

Several environmental and lifestyle factors can exacerbate AD.³ These include the following:³

Irritants (harsh soaps, detergents)

Temperature changes

Psychological stress

Skin infections

Food allergens in selected pediatric populations

Clinical Presentation and Diagnosis

Atopic dermatitis is a clinical diagnosis based on characteristic morphology, distribution, chronicity, and associated symptoms, most notably pruritus. There is no single diagnostic laboratory test for this condition.^1,3 Instead, it is defined by a relapsing course, xerosis, and patterns of eczematous inflammation that vary by patient age.^1,3 Classic diagnostic frameworks include the Hanifin and Rajka criteria and other, simplified guidelines that emphasize essential features such as pruritus, chronic or relapsing dermatitis, and typical distribution patterns.^3,8 However, clinicians generally rely on clinical recognition rather than strict scoring systems.

Key Clinical Features

Pruritus is the hallmark of AD and often will occur before visible inflammation. Lesions are typically ill-defined, erythematous patches and plaques with excoriations and lichenification in chronic disease (Figure 1).^1,11 Acute flares may include vesicles, oozing, and crusting, whereas chronic disease is characterized by thickened skin with accentuated skin markings.^2,3 Xerosis occurs in almost all cases and reflects impaired barrier function.^2,3

Figure 1¹⁰

Distribution varies by age as follows.

Infants: Cheeks, scalp, trunk, and extensor surfaces¹⁰

Figure 2

Children: Flexural surfaces (antecubital and popliteal fossae), wrists, ankles, neck¹⁰

Figure 3

Adolescents and adults: Flexural areas, hands, eyelids, neck, and sometimes head and neck predominance¹⁰

Hand dermatitis, nipple dermatitis, and eyelid involvement are common in adults. Chronic scratching can result in prurigo nodularis–like lesions.¹⁰

Clinical recognition of atopic dermatitis in patients with darker skin tones (Fitzpatrick types IV–VI) is essential for preventing underdiagnosis and chronic undertreatment.^8,11 In these populations, the classic bright "red" erythema seen in lighter skin often appears as violaceous, grayish-brown, or deep purple patches.^8,11 There is also a higher prevalence of follicular accentuation and papular AD, particularly on the trunk and extensor surfaces, which can be misdiagnosed if clinicians only look for the classic flexural distribution.^8,11 Additionally, patients with darker skin are at significantly higher risk for post-inflammatory hyperpigmentation (PIH), which often causes more psychological distress than the dermatitis itself and requires aggressive early intervention to prevent long-term pigmentary changes.^8,11

Severity Assessment

Disease severity should be determined to guide therapeutic intensity and monitor the patient’s response. Clinician-based tools such as the Eczema Area and Severity Index (EASI) and SCORAD (Scoring Atopic Dermatitis) are used in research settings, while simpler global assessments are often used in practice.^3,11 Important elements include:¹¹

Body surface area (BSA) involvement

Degree of erythema, edema, excoriation, and lichenification

Frequency of flares

Impact on sleep

Quality-of-life impairment

Patient-reported outcomes are increasingly emphasized, particularly itch severity and sleep disturbance, which correlate strongly with disease burden.¹

Table 1

Severity Assessment

Severity	Clinical Features	Impact on Patient	Typical Management Approach
Mild	Limited BSA (<5–10%), mild erythema, minimal lichenification	Minimal sleep disturbance; mild impact on quality of life	Emollients + low- to mid-potency topical corticosteroids (TCS) or topical calcineurin inhibitors (TCIs); proactive maintenance
Moderate	More widespread involvement (10–20% BSA), frequent flares, visible inflammation	Moderate itch, sleep disruption, noticeable QoL impairment	Optimized topical therapy, wet wraps, bleach baths; consider phototherapy or escalation to systemic therapy
Severe	Extensive BSA (>20%), marked erythema, lichenification, or refractory disease	Severe pruritus, significant sleep loss, major QoL impairment	Systemic therapy (biologics, JAK inhibitors); specialist referral; comprehensive management plan
Severity	Clinical Features	Impact on Patient	Typical Management Approach
Mild	Limited BSA (<5–10%), mild erythema, minimal lichenification	Minimal sleep disturbance; mild impact on quality of life	Emollients + low- to mid-potency topical corticosteroids (TCS) or topical calcineurin inhibitors (TCIs); proactive maintenance

Laboratory Evaluation

Routine laboratory testing is not required to diagnose AD.³ However, selected tests may be useful in a specific context.^3,11

Serum IgE: often elevated but nonspecific

Peripheral eosinophilia: may be present in moderate-to-severe disease3,9

Allergy testing: considered when food allergy, allergic contact dermatitis, or environmental triggers are suspected3,9

Patch testing: appropriate in refractory disease or when allergic contact dermatitis is suspected

Skin biopsy is rarely necessary but may be considered when the diagnosis is uncertain or when alternative conditions such as cutaneous T-cell lymphoma, psoriasis, seborrheic dermatitis, scabies, or contact dermatitis are suspected.³

Systemic Comorbidities

Chronic systemic inflammation in AD is recognized as an important implicatory for broader health complications. Moderate-to-severe AD is associated with an increased risk of cardiovascular and metabolic comorbidities, including obesity, hypertension, and Type 2 diabetes.¹ Chronic inflammation has also been linked to higher rates of osteoporosis and fractures.¹ The psychosocial burden is equally severe, and there is a strong correlation with suicidal ideation, depression, and anxiety, necessitating that clinicians move beyond skin assessment to include routine mental health and metabolic screening in their long-term management plans.¹¹

Differential Diagnosis and Evaluation of Comorbidities

The differential diagnosis varies by age and distribution and includes the following.³

Contact dermatitis (allergic or irritant)

Seborrheic dermatitis

Psoriasis

Scabies

Nummular dermatitis

Cutaneous T-cell lymphoma (particularly in adults with refractory disease)

In infants, distinguishing AD from seborrheic dermatitis is important.³ Seborrheic dermatitis typically lacks significant pruritus and involves the scalp and diaper region.³

Atopic dermatitis is also associated with other atopic conditions, including asthma and allergic rhinitis (the “atopic march”).^1,2 Aside from physical symptoms, the systemic nature of AD requires a holistic approach to patient care. Screening for sleep disturbance, anxiety, depression, and reduced quality of life is recommended, particularly in cases of moderate-to-severe disease.^1,11

Management Overview

The management of AD requires a stepwise, severity-based approach with emphasis on long-term disease control and prevention of flares. The primary goals of atopic dermatitis treatment are to reduce inflammation, relieve pruritus, restore and maintain skin barrier function, prevent flares, and minimize treatment-related adverse effects.^3,4 Because atopic dermatitis is a chronic, relapsing condition, management focuses not only on acute symptom control but also on long-term disease stabilization.^5,11 Effective treatment also aims to reduce sleep disturbance, improve quality of life, and address psychosocial burden.^4,6 In moderate-to-severe disease, systemic or biologic therapies may be necessary to achieve adequate disease control while minimizing cumulative steroid exposure.^4,6

The guidelines recommend addressing several foundational elements before escalating therapy, including the following:⁵

Confirm diagnosis and rule out mimickers

Provide patient education and a written action plan

Identify and minimize triggers

Ensure correct medication use

Encourage consistent moisturization

Atopic dermatitis therapies are available in multiple dosage forms to support individualized treatment selection and patient preference. These include topical formulations such as creams, ointments, lotions, foams, and solutions; oral tablets or capsules for systemic therapies; and subcutaneous injectable biologics. Selection of the appropriate dosage form can significantly influence adherence, tolerability, and treatment success.

Pause and Ponder A 32-year-old patient reports eczema affecting 6% of body surface area but experiences nightly sleep disruption and significant work impairment. Based solely on body surface area, the disease might appear mild. However, when symptom burden and quality-of-life impact are considered, how would you classify this disease severity? Should systemic therapy be considered?

Treatment Strategies

Topical Therapies

Regular use of moisturizers is essential for all patients with atopic dermatitis, regardless of disease severity.^3,4 Emollients should be applied at least twice daily and immediately after bathing to reduce transepidermal water loss and improve barrier function.³ Ointment-based formulations (such as petrolatum-based products) provide greater occlusion and are generally more effective for severe xerosis. However, some patients prefer creams or lotions for cosmetic acceptability and daytime use.^3,4 Fragrance-free, dye-free products are preferred to reduce irritation risk. Patients should be counseled that the “best” moisturizer is the one they will use consistently and adequately.³

Topical Corticosteroids (TCS)

Topical corticosteroids are the first-line anti-inflammatory therapy for acute flares.^4,5 Potency selection should be guided by several factors, including patient age, body site, and disease severity.^4,5 Low-potency agents ( hydrocortisone 1%–2.5%) are preferred for the face, eyelids, neck, and intertriginous areas.^4,5 Medium-potency agents (triamcinolone acetonide 0.1%) are commonly used for trunk and extremities.^4,5 High-potency agents (clobetasol propionate 0.05%) may be used for thick, lichenified plaques on non-facial areas for short durations, with a typical limit of 1–2 weeks.^4,5

Typically, applying these products once a day is sufficient and may improve adherence without reducing efficacy.^4,5 Proactive therapy, which involves intermittent application (twice weekly) to previously affected areas after disease control, has been shown to reduce flare frequency.^4,5 Adverse effects include skin atrophy, striae, telangiectasias, perioral dermatitis, and, rarely, hypothalamic–pituitary–adrenal axis suppression with extensive or prolonged high-potency use.^4,5 Caution is warranted in pediatric patients due to higher surface-area-to-body-weight ratios.^4,5

Topical corticosteroid withdrawal, sometimes referred to as “red skin syndrome,” is a controversial and incompletely understood phenomenon noted by erythema, burning, and rebound inflammation after prolonged, inappropriate use of medium- to high-potency topical corticosteroids.^4,9 While uncommon, widespread discussion on social media has led to increased patient concerns and may contribute to avoidance of appropriate therapies.^1,4 Current evidence suggests that most patients can use topical corticosteroids safely when prescribed at appropriate potency, duration, and anatomical site.⁴ Clinicians should provide balanced counseling, reinforce safe use practices, avoid prolonged continuous high-potency steroid exposure on sensitive areas, and monitor for signs of misuse. An evidence-informed approach helps prevent both overtreatment and undertreatment.^3,5

Topical Calcineurin Inhibitors (TCIs)

Tacrolimus 0.1% for adults and pimecrolimus 1% cream are steroid-sparing agents appropriate for sensitive areas such as the face, eyelids, and intertriginous regions.^4,9 They may be applied twice daily during active disease and used intermittently for maintenance therapy. The most common adverse effect is transient burning or stinging at the application site, particularly during early treatment.³ Although boxed warnings regarding theoretical malignancy risk exist, long-term safety data and large observational studies have not demonstrated a causal association when used as directed.^4,9 TCIs do not cause skin atrophy and are suitable for long-term use in appropriate patients.^3,5

Topical PDE-4 Inhibitor

Crisaborole 2% ointment is indicated for mild-to-moderate atopic dermatitis in patients aged 3 months and older.³ It is applied twice daily to affected areas. Clinical trials have demonstrated modest reductions in inflammation and pruritus.⁴ The most common adverse effect is application-site burning or stinging, which is typically mild and transient.^4,6 It may be particularly useful in patients who want to avoid corticosteroids.⁴

Topical JAK Inhibitors

Topical ruxolitinib 1.5% cream is approved for short-term, noncontinuous treatment of mild-to-moderate atopic dermatitis in non-immunocompromised patients aged 12 years and older with limited body surface area involvement (typically ≤20%).^4,11 It is applied twice daily, and rapid itch reduction is a notable benefit. However, as a Janus kinase inhibitor, it carries boxed warnings for serious infections, malignancy, major adverse cardiovascular events, and thrombosis, although systemic exposure is lower than with oral formulations.⁴ It should not be used in combination with biologics, systemic JAK inhibitors, or potent immunosuppressants. Current guidelines suggest reserving topical JAK inhibitors for appropriate candidates rather than routine early use.^4,5

Adjunctive Measures

Wet wrap therapy can be effective during moderate-to-severe flares, particularly in pediatric populations.^3,4 It enhances topical medication penetration and improves hydration, but should be supervised to avoid infection risk.^3,4

Dilute bleach baths (typically 0.005% sodium hypochlorite solution, e.g., ¼–½ cup household bleach in a full bathtub of water twice weekly) may reduce Staphylococcus aureus colonization in moderate-to-severe disease.³ When recommending these for moderate-to-severe disease, clinicians must provide precise instructions to avoid the risk of chemical burns or sub-therapeutic dosing.³ Patients should soak for exactly 10 minutes, no more than twice weekly, and must rinse their skin thoroughly with fresh water afterward.³ To maximize the benefit, the "Soak and Seal" method should be followed immediately, applying a thick emollient while the skin is still damp to lock in hydration and maintain the barrier.³

Routine use of topical or systemic antimicrobials is not recommended unless clinical infection is present.^4,5 While sedating antihistamines are sometimes used short-term to improve sleep quality by addressing nocturnal scratching, patients should be counseled that they do not directly treat the underlying skin inflammation.^1,3

Systemic Therapies

Systemic therapy is indicated for moderate-to-severe atopic dermatitis that is inadequately controlled with optimized topical regimens and adjunctive measures.

Biologic Therapies

Dupilumab, an IL-4 receptor alpha antagonist that inhibits IL-4 and IL-13 signaling, is approved for moderate-to-severe atopic dermatitis in adults and children (age-dependent approvals).^4,6 Typical adult dosing is a 600 mg loading dose followed by 300 mg subcutaneously every two weeks.^1,6 It significantly improves EASI scores, pruritus, and quality-of-life measures.^1,6

Tralokinumab, an IL-13 inhibitor, is administered as a 600 mg loading dose followed by 300 mg every two weeks.^4,5 Common adverse effects of biologics include injection-site reactions and conjunctivitis. Routine laboratory monitoring is generally not required.⁴ Live vaccines should be avoided during therapy.^4,5

Oral JAK Inhibitors

Abrocitinib (100–200 mg daily), upadacitinib (15–30 mg daily), and baricitinib (dose varies) provide rapid itch reduction and notable clinical improvement.^4,11 They are generally reserved for moderate-to-severe disease following shared decision-making and careful risk assessment.⁴ Boxed warnings include risks of serious infection (including herpes zoster), malignancy, thrombosis, and major cardiovascular events.^4,6 Baseline and periodic laboratory monitoring (CBC, liver enzymes, lipids) is recommended.⁴ They should be avoided in patients with significant cardiovascular risk factors or prior thromboembolic events unless the benefits outweigh risks.^4,5

Traditional Immunosuppressants

Cyclosporine (typically 3–5 mg/kg/day divided doses) may be used as short-term rescue therapy in severe refractory disease, with monitoring for nephrotoxicity and hypertension.^5,6 Methotrexate (10–25 mg weekly), azathioprine (1–3 mg/kg/day), and mycophenolate mofetil are conditionally recommended off-label options requiring laboratory monitoring for hematologic and hepatic toxicity.^4,5 Systemic corticosteroids are discouraged for long-term management due to rebound flares and significant adverse effects. However, brief courses may be used in select acute circumstances.^3,5

Emerging Biologic Therapies: Lebrikizumab and Nemolizumab

Lebrikizumab is a monoclonal antibody that selectively targets interleukin-13 (IL-13), which is a central cytokine in the Th2 inflammatory pathway of atopic dermatitis.¹¹ This agent has demonstrated significant improvements in pruritus reduction and quality-of-life measures in patients with moderate-to-severe disease.^4,11 Its mechanism is similar to tralokinumab; however, it binds IL-13 with high affinity and prevents receptor complex formation.⁴ Lebrikizumab is administered via subcutaneous (SQ) injection following a loading dose, then maintenance dosing every two to four weeks, depending on clinical response.¹¹ Adverse effects are generally mild and include injection-site reactions and conjunctivitis.¹¹ Routine laboratory monitoring is not typically required.¹¹

Nemolizumab is a monoclonal antibody targeting the interleukin-31 (IL-31) receptor A, a pathway strongly associated with pruritus signaling.¹¹ Clinical trials have demonstrated both rapid and meaningful reductions in pruritus scores along with improvements in skin inflammation.^1,11 Nemolizumab is administered subcutaneously at intervals determined by labeling and patient response.⁴ Common adverse effects include injection-site reactions and mild upper respiratory symptoms.⁴

Table 2

Comparing Biologics to Other Therapies

Feature	Biologics (e.g., dupilumab, tralokinumab)	Oral JAK Inhibitors (e.g., upadacitinib, abrocitinib)	Traditional Systemics (e.g., cyclosporine, methotrexate)
Mechanism	Targeted cytokine inhibition (IL-4, IL-13)	Broad intracellular signaling inhibition (JAK pathways)	Broad immunosuppression
Onset of Action	Moderate (weeks)	Rapid (days to weeks)	Variable
Administration	Subcutaneous injection	Oral	Oral
Monitoring	Minimal routine lab monitoring	Requires CBC, LFTs, lipids	Requires frequent lab monitoring
Safety Profile	Favorable overall; conjunctivitis common	Boxed warnings (infection, MACE, thrombosis)	Organ toxicity (renal, hepatic), infection risk
Best Use	Long-term control, steroid-sparing	Rapid control or refractory disease	Short-term or select refractory cases
Adherence Considerations	Injection training required	Daily oral adherence required	Monitoring burden may limit use

Biologic therapies generally have a favorable safety profile and require minimal routine laboratory monitoring, which may simplify long-term management. In contrast, oral JAK inhibitors provide more rapid symptom relief but require baseline and ongoing laboratory monitoring and carry boxed warnings that necessitate careful patient selection and counseling. Traditional systemic immunosuppressants are effective but are associated with greater toxicity and monitoring burden, making them less desirable for long-term use. Cost, insurance coverage, and access may significantly influence therapy selection, and primary care physicians may collaborate with pharmacists to help balance efficacy, safety, and affordability while supporting adherence.

Safety Considerations

The initiation of advanced systemic therapies, especially Janus kinase (JAK) inhibitors and biologics, requires a standardized screening and preparation protocol to ensure patient safety. For JAK inhibitors such as upadacitinib or abrocitinib, mandatory pre-screening must include a tuberculosis (TB) test, hepatitis B or C serology, a complete blood count (CBC), liver function tests, and a lipid panel.⁴ In contrast, while biologics like dupilumab require minimal laboratory monitoring, a thorough clinical eye exam is recommended to identify baseline dry eye or keratitis.⁴ Regardless of therapy, clinicians should ensure that all age-appropriate live vaccines are administered before the commencement of treatment, as live vaccines are generally contraindicated once these systemic immunomodulators are started.⁴

Before initiating or dispensing advanced systemic therapy, pharmacists should assess:

Infection risk (active infection, history of recurrent infections)

Tuberculosis (TB) and hepatitis B/C screening status (especially for JAK inhibitors)

Baseline laboratory results (CBC, liver function tests, lipid panel)

Drug–drug interactions

Vaccination status (avoid live vaccines during therapy)

Pregnancy status and reproductive considerations

Patient-specific risks (cardiovascular disease, thromboembolism, and malignancy history)

Phototherapy

Narrowband UVB phototherapy is conditionally recommended for moderate-to-severe atopic dermatitis refractory to topical therapy.^4,5 Treatments are typically administered two to three times weekly. Phototherapy can reduce inflammation and pruritus but requires consistent attendance and carries cumulative ultraviolet exposure risks, including photoaging and a theoretical increased risk of skin cancer with prolonged use.^3,4

Table 3

Medications for the Management of AD^3-6

Therapy class	Examples	Common AEs / cautions	Practical counseling pearls
Moisturizers / emollients	OTC ointments/creams (fragrance-free)	Irritation with fragranced products; adherence is main barrier	“Soak and seal”: moisturize within minutes after bathing; keep it simple and consistent
Topical corticosteroids (TCS)	Low potency (face/folds), mid–high potency (body flares)	Skin atrophy/striae/telangiectasia risk increases with potency, duration, and thin skin areas	Provide a simple action plan: which steroid, where + how long; fingertip-unit teaching reduces underuse
Topical calcineurin inhibitors (TCI)	Tacrolimus (0.03%, 0.1%), pimecrolimus	Transient burning/stinging; historical boxed warning—JTF cites large linked evidence base showing no credible increased cancer risk with typical use	Warn about initial stinging; using after moisturizer and on calmer skin reduces discomfort
Topical PDE-4 inhibitor	Crisaborole 2% ointment	Application site burning/stinging	Good for steroid-avoidant patients; cost/coverage often limits use
Topical JAK inhibitor	Ruxolitinib cream (where available/appropriate)	Labeling restrictions; infection risk considerations	If used, emphasize limited BSA, duration, and monitoring per labeling
Occlusive therapy (“wet wraps”)	Low–mid potency TCS under wet layer	Folliculitis, discomfort; potential increased absorption of TCS	Teach technique; use for a defined, short burst during flares
Topical antimicrobials (routine use)	e.g., mupirocin (only if infection)	Resistance; irritation	Frame clearly: treat infection, not baseline inflammation
Therapy	Where it fits	Typical dosing (adult)	Monitoring / key risks
Narrowband UVB (NB-UVB)	Consider it for refractory disease when topical therapy is insufficient and systemic therapy is undesirable	Usually 2–3x/week for ~10–14 weeks (logistical burden)	Sunburn-like reactions, heat intolerance; long-term skin cancer risk is less concerning than PUVA, but still UV exposure considerations
Cyclosporine	Short-term control for moderate–severe AD, especially as a bridge	3–5 mg/kg/day PO	BP, renal function, drug interactions
Methotrexate	Alternative systemic option in selected patients	10–25 mg weekly PO/SC	CBC, LFTs; teratogenic; folate supplementation
Azathioprine	Less favored; select cases only	2.5–5 mg/kg/day PO; check TPMT before starting	CBC/LFT; infection risk
Mycophenolate mofetil	Selected refractory cases	Up to 3000 mg/day divided BID	CBC, infection risk; teratogenic
Systemic corticosteroids	Avoid except in rare, exceptional circumstances	Not preferred	Rebound flares, metabolic/bone effects, infection

Pause and Ponder   When a patient’s atopic dermatitis fails to improve, do you first question the efficacy of the drug or the patient's comfort in using it?

 

Treatment Algorithm⁴

Step 0: The "Good Practice" Foundation (All Severities)

Before escalating therapy, primary care physicians must verify these five pillars:

Confirm Diagnosis: Rule out mimickers (Contact dermatitis, Scabies, CTCL).

Education: Provide a written Eczema Action Plan.

Trigger Management: Identify and minimize irritants, heat, and allergens.

Adherence Check: Ensure the patient is using the medications correctly.

Skin Barrier Support: Encourage liberal, daily use of bland moisturizers.

Step 1: Mild AD (Localized, Limited Impact)

Goal: Rapid symptom control and relapse prevention with minimal treatment burden.

Barrier Optimization: "Soak and Seal": Apply moisturizer immediately after bathing.

Active Inflammation: First-line: Topical Corticosteroids (TCS)

Sensitive Areas: Topical Calcineurin Inhibitors (TCI) for face, neck, and folds

Maintenance: "Proactive Therapy": apply TCS or TCI twice weekly to common flare sites.

Alternatives: Consider Crisaborole (PDE-4 inhibitor) for mild-to-moderate disease

Avoid: Routine topical antibiotics unless clinical signs of infection are present.

Step 2: Moderate AD (Widespread or Quality of Life Impairment)

Goal: Gain control quickly, then simplify for long-term adherence.

Optimize Topicals: Move to once-daily application of higher-potency TCS to improve adherence

Crisis Management: Wet Wrap Therapy: Short-term (3–5 days) during acute flares

Dilute Bleach Baths: Use for moderate-to-severe disease to reduce colonization

Advance Therapy (Shared Decision-Making):

Phototherapy (NB-UVB): If feasible and available

Transition to Systemic: When topicals no longer provide adequate control or cause side effects.

Step 3: Moderate-to-Severe / Refractory AD (High Burden)

Goal: Rapid itch reduction, clear skin, and a sustainable long-term systemic plan.

Preferred Advanced Options (Biologics)

Dupilumab (>/6 months old): Strong recommendation from both AAD and JTF.

Tralokinumab (>/12 years old): Strong recommendation for patients refractory to topicals.

Lebrikizumab / Nemolizumab: Consider as newer Th2-targeted or itch-targeted alternatives.

Advanced Options (Oral JAK Inhibitors)

Abrocitinib / Upadacitinib: Reserved for patients requiring rapid control or those who fail biologics.

Safety: Must perform shared risk-benefit assessment regarding MACE, thrombosis, and infection; requires baseline and periodic blood monitoring.

Alternative Systemic & Warnings

Traditional Agents: Conditional use of cyclosporine (short-term), methotrexate, azathioprine, or mycophenolate.

Critical Warning: Avoid systemic corticosteroids for chronic management due to high rebound rates and cumulative toxicity.

Atopic Dermatitis Action Plan^4,5

Atopic Dermatitis (Eczema) Action Plan

Patient Name: ____________________ Date: __________

Provider: ____________________

GREEN ZONE: All Clear (Maintenance)

Skin looks: Clear, no redness, no itching, no rough patches.

Your Goal: Keep the skin barrier strong and prevent flares.

Bathing: Lukewarm bath or shower (5–10 minutes) once daily. Use a soap-free, fragrance-free cleanser.

Moisturizing: Apply thick moisturizer (ointment or cream) within 3 minutes of patting skin dry ("Soak and Seal"). Apply at least twice daily.

Proactive Therapy: Apply [Name of Medication] to common flare sites (e.g., inner elbows, behind knees) twice weekly (e.g., Saturdays and Sundays).

YELLOW ZONE: Caution (Flare-Up)

Skin looks: Red, itchy, rough, or bumpy in specific areas.

Your Goal: Stop the inflammation quickly before it spreads.

Continue: All Green Zone bathing and moisturizing steps.

Face/Folds (Sensitive areas): Apply [Low Potency Steroid or TCI] to red/itchy areas twice daily until clear.

Body (Trunk/Arms/Legs): Apply [Medium/High Potency Steroid] to red/itchy areas twice daily.

When to stop: Once the skin is smooth and no longer itchy (usually 1–2 weeks), return to the Green Zone.

RED ZONE: Emergency (Severe Flare or Infection)

Skin looks: Widespread redness, intense itching that prevents sleep, oozing, "honey-colored" crusting, or painful blisters.

Your Goal: Crisis control and medical evaluation.

Advanced Treatment: Apply [Specific High-Potency Medication] as directed.

Wet Wraps: Apply medicated ointment followed by a damp layer of gauze/pajamas and a dry top layer for [X] hours or overnight.

Call the Office if:

Skin is oozing, crusting, or has painful blisters (signs of infection).

No improvement after 48 hours of Yellow Zone treatment.

Fever or chills develop.

Practical Tips for Success^4,5

The Fingertip Unit (FTU): One FTU is the amount of cream squeezed from the tip of the finger to the first crease. This covers an area the size of two adult palms.

Quantity Matters: A standard 30g tube should cover the entire adult body roughly once. If you are treating the whole body, ensure you have an adequate supply.

Steroid Safety: When used as directed in the Yellow Zone, topical steroids are safe and effective. Avoid long-term continuous use of high-potency steroids on the face or skin folds without a provider's supervision.

Treatment Adherence and Therapeutic Failure

Treatment failure in atopic dermatitis is frequently related to inadequate adherence rather than true pharmacologic inefficacy. Multiple studies demonstrate that patients often underuse prescribed topical corticosteroids due to fear of adverse effects, a phenomenon commonly referred to as “steroid phobia.”^4,11 Concerns about skin thinning, systemic absorption, and long-term harm may lead patients or caregivers to apply insufficient amounts, prematurely shorten treatment duration, or avoid therapy altogether.

In addition, clinicians frequently prescribe inadequate amounts of medication. For example, approximately 30 grams of topical medication are required to cover the entire adult body once.^3,5 Clear instructions using fingertip unit guidance can improve proper dosing. Primary prescription nonadherence, or failure to fill prescribed medications, also contributes significantly to poor disease control.^3,5 Addressing adherence requires open discussion of safety, realistic risk framing, proactive follow-up, and shared decision-making.^4,5 Emphasizing proactive maintenance therapy and setting expectations that atopic dermatitis is a chronic condition requiring ongoing management can reduce therapeutic inertia and improve long-term outcomes.^4,5,11

Clinical Counseling Pearls

Atopic dermatitis is a chronic condition requiring ongoing maintenance therapy—even when skin appears clear

Moisturizers are the foundation of treatment and should be used consistently

Apply topical medications before moisturizers unless otherwise directed

Use the fingertip unit (FTU) guidance to ensure adequate dosing

Mild burning or stinging with TCIs or crisaborole is common and often improves with continued use

Biologic therapies may take several weeks for full effect

JAK inhibitors may provide faster itch relief but require closer monitoring

Fear of topical corticosteroids (“steroid phobia”) often leads to undertreatment and poor outcomes

Interprofessional Considerations

Effective management of atopic dermatitis requires coordinated care among healthcare team members. Physicians and advanced practice providers are responsible for establishing the diagnosis, assessing disease severity, initiating and escalating therapy, and monitoring for complications and treatment response. Pharmacists may play a key role in optimizing medication selection, identifying potential drug interactions, providing detailed counseling on proper use and expected outcomes, and addressing adherence barriers. This interprofessional approach improves treatment adherence, enhances patient education, and supports long-term disease control.

Summary

Atopic dermatitis is a chronic inflammatory disease driven by epidermal barrier dysfunction and type 2 immune dysregulation. It affects millions worldwide and significantly impairs the quality of life for many patients. Recent advances in understanding immunopathogenesis have led to targeted biologic and small-molecule therapies that have reshaped treatment paradigms.

Management requires accurate severity assessment, proactive maintenance strategies, patient education, and shared decision-making. Topical therapies remain foundational, but systemic biologics and JAK inhibitors provide effective options for moderate-to-severe disease. Updated guidelines emphasize individualized care, avoidance of therapeutic inertia, and long-term disease control.

Through interprofessional collaboration, including physicians, pharmacists, and pharmacy technicians, patients with atopic dermatitis can achieve meaningful symptom reduction, improved sleep, enhanced quality of life, and sustained disease stability.

References

Langan SM, Irvine AD, Weidinger S. Atopic dermatitis. Lancet. 2020;396(10247):345-360. doi:10.1016/S0140-6736(20)31286-1

Weidinger S, Novak N. Atopic dermatitis. Lancet. 2016;387(10023):1109-1122. doi:10.1016/S0140-6736(15)00149-X

Sidbury R, Alikhan A, Bercovitch L, et al. Guidelines of care for the management of atopic dermatitis in adults with phototherapy and systemic therapies. J Am Acad Dermatol. 2024;90(2):e43-e56. doi:10.1016/j.jaad.2023.08.029

Boguniewicz M, Fonacier L, Guttman-Yassky E, Ong PY, Silverberg JI. Atopic Dermatitis Yardstick update. Ann Allergy Asthma Immunol. 2023;130(6):811-820. doi:10.1016/j.anai.2023.03.010

Wollenberg A, Flohr C, Simon D, et al. European guideline (EuroGuiDerm) on atopic eczema – part I: systemic therapy. J Eur Acad Dermatol Venereol. 2022;36(9):1409-1431. doi:10.1111/jdv.18345

Kim J, Kim BE, Leung DYM. Pathophysiology of atopic dermatitis: Clinical implications. Allergy Asthma Proc. 2019;40(2):84-92. doi:10.2500/aap.2019.40.4202

Drucker AM, Lam M, Prieto-Merino D, et al. Systemic Immunomodulatory Treatments for Atopic Dermatitis: Living Systematic Review and Network Meta-Analysis Update. JAMA Dermatol. 2024;160(9):936-944. doi:10.1001/jamadermatol.2024.2192

Hanifin JM, Rajka G. Diagnostic features of atopic dermatitis. Acta Derm Venereol Suppl (Stockh). 1980;92:44-47.

Silverberg JI. Atopic dermatitis in adults. J Am Acad Dermatol. 2019;80(3):655-668. doi:10.1016/j.jaad.2018.02.001

Stanway A, Jarrett P. Atopic dermatitis [Atopic eczema]. DermNet New Zealand. Updated Feb 2021. Accessed February 24, 2026. https://dermnetnz.org/topics/atopic-dermatitis

Wollenberg A, Christen-Zäch S, Taieb A, et al. ETFAD/EADV Eczema Task Force 2020 position paper on diagnosis and treatment of atopic dermatitis. J Eur Acad Dermatol Venereol. 2020;34(12):2717-2744. doi:10.1111/jdv.16892

DISCLAIMER

The information provided in this course is general in nature, and it is designed solely to provide participants with continuing education credit(s). This course and materials are not meant to substitute for the independent, professional judgment of any participant regarding that participant’s professional practice, including but not limited to patient assessment, diagnosis, treatment, and/or health management. Medical and pharmacy practices, rules, and laws vary from state to state, and this course does not cover the laws of each state; therefore, participants must consult the laws of their state as they relate to their professional practice.

Healthcare professionals must consult their employer, healthcare facility, hospital, or other organization for guidelines, protocols, and procedures to follow. The information provided in this course does not replace those guidelines, protocols, and procedures, but is for academic purposes only, and this course’s limited purpose is for the completion of continuing education credits.

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