Download Free Medical Emerging Treatments in Moderate to Severe Atopic Dermatitis PowerPoint Presentation

Emerging Treatments in Moderate to Severe Atopic Dermatitis PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Emerging Treatments in Moderate to Severe Atopic Dermatitis" by David I. Bernstein, MD and Amy S. Paller, MD.

This medical PowerPoint presentation talks about atopic dermatitis, also known as eczema. Atopic dermatitis is a chronic inflammatory skin condition that affects millions of people worldwide. It is characterized by dry, itchy, and inflamed skin, and it can have a significant impact on quality of life. While there is no cure for atopic dermatitis, there are emerging treatments that can help manage the symptoms of moderate to severe cases.

Dupilumab: This is a monoclonal antibody that targets a protein called interleukin-4 receptor alpha (IL-4RA), which is involved in the inflammatory process that drives atopic dermatitis. Dupilumab is administered via injection and has been shown to significantly reduce symptoms in clinical trials.

Janus kinase inhibitors (JAK inhibitors): These are oral medications that block certain enzymes involved in the inflammatory process. Two JAK inhibitors, baricitinib and abrocitinib, have been approved by the FDA for the treatment of atopic dermatitis.

Topical phosphodiesterase-4 (PDE4) inhibitors: These are creams or ointments that inhibit the PDE4 enzyme, which plays a role in the inflammation associated with atopic dermatitis. A topical PDE4 inhibitor called crisaborole has been approved by the FDA for the treatment of mild to moderate atopic dermatitis.

Topical JAK inhibitors: These are creams or ointments that contain JAK inhibitors and are applied directly to the affected skin. Topical JAK inhibitors are still being studied, but early results have been promising.

Biologic therapies: These are medications that target specific molecules involved in the inflammatory process. A number of biologic therapies are currently being studied for the treatment of atopic dermatitis, including nemolizumab, lebrikizumab, and tralokinumab.

Its important to note that these emerging treatments may not be appropriate or effective for everyone with moderate to severe atopic dermatitis. Its essential to work closely with a healthcare professional to determine the best course of treatment for your individual needs.

Tags : Atopic Dermatitis, eczema, chronic inflammatory skin condition, Dermatology, Dermatology PowerPoint presentation

Published on : Apr 03, 2023 | Views : 1306 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

ppt slide no 1 content not found
Slide 2-

Faculty David I. Bernstein, MD Professor of Medicine and Environmental Health Division of Immunology, Allergy and Rheumatology University of Cincinnati College of Medicine Cincinnati, Ohio Amy S. Paller, MD Walter J. Hamlin Professor and Chair of Dermatology Professor of Pediatrics Northwestern University Feinberg School of Medicine Chicago, Illinois
Slide 3-

Program Overview Video 1. Epidemiology Video 2. Pathophysiology Video 3. Clinical Assessment Video 4. Medical Management: Overview Video 5. Medical Management 1 Video 6. Medical Management 2 Video 7. Prevention of Flares Video 8. Emerging Therapies
Slide 4-

Learning Objectives After participating in this program, the participant will be able to: Examine the epidemiology and pathogenesis of AD and the relevance to the management of patients with AD . Integrate a proactive approach to long-term disease management in AD, with a focus on prevention of flares, assessment of disease activity, and patient education. Discuss the mechanisms, efficacy, and safety data for emerging biologic therapies and which patients are likely to benefit.
Slide 5-

Epidemiology Video 1
Slide 6-

Atopic Dermatitis: Definition Chronic, pruritic, eczematous skin disease1,2 Often associated with elevated serum IgE levels and a personal or family history of type I allergies, allergic rhinitis, and asthma Atopic dermatitis = atopic eczema1 Atopic dermatitis ≠ eczema ICD codes for atopic dermatitis and eczema are different 1. Eichenfield LF, et al. J Am Acad Dermatol. 2014;70(2):338-351. 2. Whiteley J, et al. Curr Med Res Opin. 2016;doi:10.1080/03007995.2016.1195733.
Slide 7-

Case Scenario: Emily HPI: Emily is being seen for her 6-month well-child visit Red cheeks with edema and exudation Emily has dry skin with generalized itching, sometimes making it difficult for her to fall asleep Medications: none Allergies: dairy products aggravate skin itching and rash FH: father and mother with seasonal allergic rhinitis PE: skin – facial eczema, xerosis of face, as well extensor surfaces of joints
Slide 8-

Atopic Dermatitis: Epidemiology Occurs most frequently in children, but also affects adults1,2 Up to 25% of children Up to 7% of adults Prevalence higher in women than men2,3 Onset commonly between ages of 3 and 6 months1,2 60% by age 1 year 85% to 90% by age 5 years 1. Eichenfield LF, et al. J Am Acad Dermatol. 2014;70(2):338-351. 2. Guttman-Yassky E, et al. J Allergy Clin Immunol. 2011;127(5):1110-1118. 3. Whiteley J, et al. Curr Med Res Opin. 2016;doi:10.1080/03007995.2016.1195733.
Slide 9-

Atopic Dermatitis: Epidemiology (cont) Severity1 In children Mild (two-thirds), moderate (one-quarter); severe (<10%) Percentage of people with severe AD increases with age Pooled analysis of 45 studies (N=110,651) showed2 Children who developed AD by age 2 y had less persistent disease 80% of children with AD had disease resolution by 8 years after diagnosis, >95% by 20 years after diagnosis Later age of onset and greater severity  more persistent AD 1. Chernyshov PV, et al. Clin Cosmet Investig Dermatol. 2016;9:159-166. 2. Kim JP, et al. J Am Acad Dermatol. 2016;75(4):681-687.
Slide 10-

Atopic Dermatitis: Epidemiology (cont) Study of infants (age 3-18 mos) with recent onset AD (≤3 mos) showed many developed an allergic condition over 3 years Asthma (10.7%) Allergic rhinitis (22.4%) Food allergy (15.9%) Allergic conjunctivitis (14.1%) ≥1 atopic comorbidity (37.0%) Schneider L, et al. Pediatr Dermatol. 2016;33(4):388-398.
Slide 11-

Atopic Dermatitis: Epidemiology (cont) Impact on children varies over time 0-3 years: parental exhaustion, emotional distress  impaired mother-child attachment 3-10 years: teasing, bullying, avoid social interactions and sports 10 years to adulthood: low self-esteem Chernyshov PV, et al. Clin Cosmet Investig Dermatol. 2016;9:159-166.
Slide 12-

Pathophysiology Video 2
Slide 13-

Immune triggers stimulate the release of inflammatory mediators Peng W, et al. Clin Exper Allergy. 2015;45:566-574. Pathogenic Mechanisms in Acute Atopic Dermatitis
Slide 14-

Pathophysiology Complex interplay of 3 factors Barrier dysfunction Immunological Environmental Egawa G, et al. Cogent Biol. 2015;1;1103459.
Slide 15-

Disease Biomarkers Are Needed Biomarkers are being identified to1,2: Facilitate diagnosis Assess disease severity Identify AD disease phenotypes  targeted therapy Predict individual responses to medications 1. Mansouri Y, et al. J Clin Med. 2015;4:858-87. 2. Thijs JL, et al. J Clin Med. 2015:4:479-487.
Slide 16-

Clinical Assessment Video 3
Slide 17-

Case Scenario: Jack Jack is a 13-year-old male, accompanied by his mother. During the visit, he is noted to frequently scratch the flexural areas of his arms. History: Jack has complained of dry, itchy skin on his arms for many years that worsened over the past 2 years. Symptoms are worse in the winter. Mother had asthma and father has seasonal allergies Jack has asthma since 4 years of age PE: Dry skin Erythema, dryness, lichenification noted in flexural areas of both arms Hyperlinear palms and increased scaling on legs Mom also shows hyperlinear palms/dry legs Image courtesy of DermNetNZ.org under the Creative Commons Attribution-NonCommercial-NoDerivs 3.0 (http://creativecommons.org/licenses/by-nc-nd/3.0/nz/) with no changes.
Slide 18-

Patient Assessment in Routine Clinical Practice Not recommended in practice Disease severity measurement scales* Quality of life measurement scales Recommended as part of PE General questions Itch Impact on daily activity, sleep Disease persistence Associated conditions Rhinitis/Rhinoconjunctivitis Asthma Food allergy Sleep disturbance Depression *Not recommended outside of a clinical trial. US Food and Drug Administration requires Investigator Global Assessment that is used for product labeling. Eichenfield LF, et al. J Am Acad Dermatol. 2014;70:338-351.
Slide 19-

Risk Factors Strong association Family history of atopy Odds of developing atopic dermatitis Both parents are atopic: 3 to 5-fold higher risk Loss of function mutations in the FLG gene (minority – 10% or less) Earlier onset More severe, persistent disease Eczema herpeticum Moderate association African-American race Higher parental education Unclear association Pet exposure Urban living Daycare Eichenfield LF, et al. J Am Acad Dermatol. 2014;70:338-351. Kelleher et al. JACI 2015;135:930-935.
Slide 20-

Transepidermal Water Loss at 2 Days of Life as a Predictor of Atopic Dermatitis Kelleher M, et al. J Allergy Clin Immunol. 2015;135(4):930-935. *Patients were grouped by percentiles based on history of parental atopy and transepidermal water loss test reading score at 2 days. TEWL threshold scores were 5.0 gwater/m2/h (25th percentile), 7.0 gwater/m2/h (50th percentile), and 9.0 gwater/m2/h (75th percentile). †1597 infants screened. At 6 months, 18.7% were diagnosed with AD. At 12 months, 15.5% were diagnosed with AD N=1903 infants† Interpretation: Infants in top quartile at 2 days are 7.1 times more likely to be diagnosed with AD at 1 year.
Slide 21-

Diagnostic Features Essential Features Pruritus Eczematous dermatitis (acute, subacute, chronic) Typical morphology and age-specific patterns Facial, neck, and extensor involvement in infants and children Current or previous flexural lesions at any age Sparing of the groin and axillary regions Chronic or relapsing history Eichenfield LF, et al. J Am Acad Dermatol. 2014;70:338-351.
Slide 22-

Diagnostic Features (cont) Important Features (seen in most) Early age of onset Atopy Personal and/or family history IgE reactivity Xerosis Eichenfield LF, et al. J Am Acad Dermatol. 2014;70:338-351.
Slide 23-

Distribution
Slide 24-

Atopic Dermatitis: Differential Diagnosis Other eczematous disorders Contact dermatitis Seborrheic dermatitis Dyshidrotic eczema Hand eczema Nummular dermatitis Psoriasis Scabies Unusual disorders Ichthyoses Immune deficiency diseases Photosensitivity dermatoses Erythroderma of other causes Cutaneous T-cell lymphoma Eichenfield LF, et al. J Am Acad Dermatol. 2014;70:338-351.
Slide 25-

Role of the Laboratory Laboratory testing not needed for most patients1 IgE level not elevated in 5% to 37%2,3 Numerous biomarkers, but none are reliable to distinguish atopic dermatitis from other inflammatory diseases4,5 Allergen skin testing helpful in those with Respiratory allergies (allergic rhinitis or asthma) Food allergies: screening – will only suggest food sensitization 1. Eichenfield LF, et al. J Am Acad Dermatol. 2014;70:338-351. 2. Ott H, et al. Acta Derm Venereol. 2009;89(3):257-261. 3. Folster-Holst, et al. Allergy. 2006;61(5):629-632. 4. Thijs J, et al. Curr Opin Allergy Clin Immunol. 2015;15(5):453-460. 5. Mansouri Y, et al. J Clin Med. 2015;4:858-87.
Slide 26-

Medical Management: Overview Video 4
Slide 27-

Case Scenario: Wynonna Wynonna is a 7-year-old female diagnosed at age 9 months with AD primarily involving her forearms and lower legs Current meds: emollients 1-2 x/day + low-potency TCS Upon questioning, Wynonna reports that her pruritus has not improved, and is sometimes unbearable when she plays soccer. She also says it is sometimes difficult to fall asleep PE: moderate erythema with numerous excoriations noted on trunk, arms and legs but no sign of infection
Slide 28-

Goals of Therapy Reduce the number and severity of flares Reduce pruritus and improve quality of life Maintain normal activities of daily living Maximize disease-free periods Prevent infectious complications Avoid/Minimize side effects of therapy Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. Lyons JJ, et al. Immunol Allergy Clin North Am. 2015;35(1):161-183.
Slide 29-

Overview of Atopic Dermatitis Management TCI, topical calcineurin inhibitor; TCS, topical corticosteroid Modified from Eichenfield LF, et al. Pediatrics. 2015;136(3):554-565. Basic Management  Skin Care -Moisturizers -Warm bath/shower  Trigger Avoidance Mild Disease Acute Treatment Low-potency TCS 2x/d applied to inflamed skin
Slide 30-

Overview of Atopic Dermatitis Management (cont) TCI, topical calcineurin inhibitor; TCS, topical corticosteroid Modified from Eichenfield LF, et al. Pediatrics. 2015;136(3):554-565. Basic Management  Skin Care -Moisturizers -Warm bath/shower  Trigger Avoidance Maintenance TCI Maintenance TCS Mild Disease Moderate-to-Severe Disease For relapsing course (frequent/persistent flares despite treatment) TCS applied at first signs/symptoms or to flare-prone areas Acute Treatment Low-potency TCS 2x/d applied to inflamed skin Acute Treatment  Medium-potency TCS applied to inflamed skin  Consider 2° infection; treat with antibiotic if present -Introduce dilute bleach baths 2-7x/wk as maintenance Consider  Nonadherence  Misdiagnosis  Referral Flare not resolved within 7 days
Slide 31-

Medical Management I Video 5
Slide 32-

Skin Hydration Bathing followed by immediate application of emollient Emollient Use generously - no danger from “excess use” Lotions vs creams vs oils vs ointments Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 33-

Skin Hydration (cont) Bathing followed by immediate application of emollient Emollient Use generously - no danger from “excess use” Lotions vs creams vs oils vs ointments General recommendations are: Warm (not hot) water Bath better than shower 5-10 minutes Neutral/low pH, hypoallergenic, fragrance-free non-soap cleansers preferred Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 34-

Skin Hydration (cont) Bathing followed by immediate application of emollient Emollient Use generously - no danger from “excess use” Lotions vs creams vs oils vs ointments General recommendations are: Warm (not hot) water Bath better than shower 5-10 minutes Neutral/low pH, hypoallergenic, fragrance-free non-soap cleansers preferred Bleach baths now standard of maintenance care for pediatric moderate-to-severe AD Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 35-

Topical Corticosteroids (TCS) Recommended if symptoms are not controlled by moisturizers alone Low-potency Maintenance therapy to prevent exacerbations Intermediate- and high-potency (halogenated) Exacerbations for short period or proactive therapy Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 36-

Topical Corticosteroids (TCS) (cont) Recommended if symptoms are not controlled by moisturizers alone Low-potency Maintenance therapy to prevent exacerbations Intermediate- and high-potency (halogenated) Exacerbations for short period or proactive therapy Ultra-high-potency No more than 1-2 weeks Non-facial, non-skinfold areas Potent, fluorinated corticosteroids should not be used on mucous membranes, face, eyelids, genitalia, and intertriginous areas or in young infants beyond a few days Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 37-

Topical Corticosteroids (TCS) (cont) Twice-daily application needed for most until signs and symptoms improve For frequent, repeated outbreaks at the same site, maintenance “proactive” therapy with intermediate-potency TCS 2-3x/wk may be beneficial Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 38-

Topical Corticosteroids (TCS) (cont) Twice-daily application needed for most until signs and symptoms improve For frequent, repeated outbreaks at the same site, maintenance “proactive” therapy with intermediate-potency TCS 2-3x/wk may be beneficial Adverse effects of TCS Local- striae, skin atrophy, periorbital dermatitis, rosacea, allergic contact dermatitis Systemic Dependent on skin surface area involved, skin thickness, use of occlusive dressing, duration of use, potency Risk of adrenal suppression greatest in infants and small children Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 39-

Topical Calcineurin Inhibitors (TCI) Pimecrolimus cream 1%; tacrolimus 0.03% and 0.1% ointment Block production of proinflammatory cytokines and other inflammatory mediators1,2 Advantages vs. TCS2 For face, anogenital, skin folds, or other sensitive areas No atrophogenic properties; can reverse steroid-induced atrophy Steroid-sparing: reduce overall TCS when used for maintenance 1. Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. 2. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 40-

Topical Calcineurin Inhibitors (TCI) (cont) 2-3x/wk “proactive” application effective in preventing recurrence1,2 Local adverse effects such as stinging and burning are most common1,2 and primarily occur when applied to acutely inflamed lesions Increased risk of malignancy not observed3, but black box warning for theoretical risk persists and requires reassurance when prescribed 1. Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. 2. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132. 3. Siegfried EC, et al. BMC Pediatr. 2016;16:75.
Slide 41-

Other Topical Options Crisaborole: Topical phosphodiesterase-4 (PDE4) inhibitor approved in December 2016 for mild-to-moderate AD in children age ≥2 y
Slide 42-

Other Topical Options (cont) Crisaborole: Topical phosphodiesterase-4 (PDE4) inhibitor approved in December 2016 for mild-to-moderate AD in children age ≥2 y Tar preparations1,2 No randomized trials have demonstrated efficacy Should not be used on acutely inflamed skin Tar shampoo may be beneficial 1. Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. 2. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 43-

Other Topical Options (cont) Crisaborole: Topical phosphodiesterase-4 (PDE4) inhibitor approved in December 2016 for mild-to-moderate AD in children age ≥2 y Tar preparations1,2 No randomized trials have demonstrated efficacy Should not be used on acutely inflamed skin Tar shampoo may be beneficial Topical antihistamines1,2 Not recommended because of lack of evidence supporting efficacy, risk of absorption and of contact dermatitis Even oral anthistamines are only used in AD for their soporific effects or for associated allergic disorders (nonsedating antihistamines) 1. Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. 2. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132.
Slide 44-

Other Topical Options (cont) Crisaborole: Topical phosphodiesterase-4 (PDE4) inhibitor approved in December 2016 for mild-to-moderate AD in children age ≥2 y Tar preparations1,2 No randomized trials have demonstrated efficacy Should not be used on acutely inflamed skin Tar shampoo may be beneficial Topical antihistamines1,2 Not recommended because of lack of evidence supporting efficacy, risk of absorption and of contact dermatitis Even oral anthistamines are only used in AD for their soporific effects or for associated allergic disorders (nonsedating antihistamines) Topical antimicrobials2 Not recommended because of lack of efficacy, risk of contact dermatitis Exception: antiseptic dilute bleach baths3-5 1. Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. 2. Eichenfield LF, et al. J Am Acad Dermatol. 2014;71(1):116-132. 3. Hon KL, et al. J Dermatolog Treat. 2016;27(2):156-162. 4. Wong SM, et al. J Dermatol. 2013;40(11):874-880. 5. Huang JT, et al. Pediatrics. 2009;123:e808-e814.
Slide 45-

Additional Considerations Identify and eliminate triggering factors Avoidance of common irritants – soaps/detergents/wool/occlusive fabrics Potential contact allergens, such as fragrance, preservatives, botanicals Recommend control of temperature and humidity Consider possible allergy triggers (other than foods) with skin tests, although skin tests (and allergy patch tests) are poorly predictive of triggering factors Allergen immunotherapy Selected patients with aeroallergen sensitivity – may worsen AD Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299.
Slide 46-

Additional Considerations (cont) Identify and eliminate triggering factors Avoidance of common irritants – soaps/detergents/wool/occlusive fabrics Potential contact allergens, such as fragrance, preservatives, botanicals Recommend control of temperature and humidity Consider possible allergy triggers (other than foods) with skin tests, although skin tests (and allergy patch tests) are poorly predictive of triggering factors Allergen immunotherapy Selected patients with aeroallergen sensitivity – may worsen AD Limited data regarding the benefits of leukotriene inhibitors (shown to be ineffective for AD) Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299.
Slide 47-

Additional Considerations (cont) Patient and family education Chronic nature of disease, exacerbating factors, efficacy and safety of treatments Demonstrate skin care techniques Provide written treatment plan Refer to other healthcare providers as needed Advise of patient support organizations Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299.
Slide 48-

Additional Considerations (cont) Patient and family education Chronic nature of disease, exacerbating factors, efficacy and safety of treatments Demonstrate skin care techniques Provide written treatment plan Refer to other healthcare providers as needed Advise of patient support organizations Patient and family quality of life often impaired Additional treatment may be needed for itching, behavioral disorders, and sleep disturbances Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299.
Slide 49-

Medical Management II Video 6
Slide 50-

Difficult-to-Treat Patients with Atopic Dermatitis Phototherapy Narrowband UVB most commonly used due to low risk profile, relative efficacy, availability, clinician experience Incidence of adverse events considered to be low Most common are actinic damage, local erythema/tenderness, pruritus, burning, stinging Rarely used because of poor accessibility and often poorly tolerated, especially for acute AD Home phototherapy a consideration for patients with poor adherence Sidbury R, et al. J Am Acad Dermatol. 2014;71(2):327-349. Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299.
Slide 51-

Difficult-to-Treat Patients with Atopic Dermatitis (cont) Systemic agents Lack of comparative trial data makes it difficult to determine the relative efficacy and safety of available options Most commonly used in US are Cyclosporine, methotrexate, mycophenolate mofetil Corticosteroids Should be avoided if possible due to side effects, risk for abuse Reserved for acute, severe exacerbations as a short-term bridge to other systemic, non-steroid therapy in adults; no role in children Sidbury R, et al. J Am Acad Dermatol. 2014;71(2):327-349. Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299.
Slide 52-

Difficult-to-Treat Patients with Atopic Dermatitis (cont) Systemic agents (cont) Antimicrobials1 Recommended only in patients with clinical evidence of bacterial evidence Antihistamines1 Sedating ones may be beneficial in the setting of sleep loss secondary to pruritus 1. Sidbury R, et al. J Am Acad Dermatol. 2014;71(2):327-349.
Slide 53-

Difficult-to-Treat Patients with Atopic Dermatitis (cont) Systemic agents (cont) Antimicrobials1 Recommended only in patients with clinical evidence of bacterial evidence Antihistamines1 Sedating ones may be beneficial in the setting of sleep loss secondary to pruritus Other interventions that have not been proven to work and are not supported in treatment guidelines Primrose oil, omega-3, vitamin D, aromatherapy Probiotics/Synbiotics2,3 Limited data suggest benefit of synbiotics (combination of prebiotics and probiotics) but not probiotics Highly dependent on strains, doses 1. Sidbury R, et al. J Am Acad Dermatol. 2014;71(2):327-349. 2. Rather IA, et al. Front Microbiol. 2016;7:507. 3. Chang YS, et al. JAMA Pediatr. 2016;170(3):236-242.
Slide 54-

Prevention of Flares Video 7
Slide 55-

Case Scenario: Juan Juan is a child seen for continuing care of atopic dermatitis History Diagnosed 3 years ago with atopic dermatitis at age 11 months Achieves good symptom relief with basic measures (bathing, moisturizers, control of triggers) However, experiences frequent flares which cause him to scratch intensely  developed secondary skin infection
Slide 56-

Prevention of Flares Preventing or at least increasing the time interval between flares is a critical goal of management Important to act quickly in treating a flare1 1. Wollenberg A, et al. JEADV. 2016;30:729-747. TCI, topical calcineurin inhibitor; TCS, topical corticosteroid
Slide 57-

Prevention of Flares (cont) Preventing or at least increasing the time interval between flares is a critical goal of management Important to act quickly in treating a flare1 Two approaches (with continued basic management)2,3, 4 1. Wollenberg A, et al. JEADV. 2016;30:729-747. 2. Sidbury R, et al. J Am Acad Dermatol. 2014;71(2):327-349. 3. Eichenfield LF, et al. Pediatrics. 2015;136(3):554-565. 4. Schmitt J, et al. Br J Dermatol. 2011;164(2):415-428. TCI, topical calcineurin inhibitor; TCS, topical corticosteroid
Slide 58-

Prevention of Flares (cont) Preventing or at least increasing the time interval between flares is a critical goal of management Important to act quickly in treating a flare1 Two approaches (with continued basic management)2,3, 4 Antiseptic/Antibiotic therapy Topical- dilute bleach bath (minimally twice-weekly; severe may require daily) Systemic- S. aureus most common pathogen; MSSA >> MRSA Oral cephalosporin; amoxicillin/clavulanate 1. Wollenberg A, et al. JEADV. 2016;30:729-747. 2. Sidbury R, et al. J Am Acad Dermatol. 2014;71(2):327-349. 3. Eichenfield LF, et al. Pediatrics. 2015;136(3):554-565. 4. Schmitt J, et al. Br J Dermatol. 2011;164(2):415-428. TCI, topical calcineurin inhibitor; TCS, topical corticosteroid
Slide 59-

Prevention of Flares (cont) Patient/Family education1,2 Promote adherence to maintenance therapy Written action plan Multidisciplinary teaching3 Dermatological, nutritional, psychological components Psychological support is particularly important in those with emotional triggers or experiencing significant distress Nutritional education particularly important in children with food allergies 1. Sidbury R, et al. J Am Acad Dermatol. 2014;71(2):327-349. 2. Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299. 3. Spielman SC, et al. J Clin Med. 2015;4:1156-1170.
Slide 60-

Prevention of Flares (cont) Control trigger factors: more important for associated allergic disorders1,2 Hard to demonstrate that allergic triggers play a role in AD Young children- food allergies (probably <10% and especially in severely affected children with AD) Older children and adults- environmental aeroallergens 1. Sidbury R, et al. J Am Acad Dermatol. 2014;71(2):327-349. 2. Schneider L, et al. J Allergy Clin Immunol. 2013;131(2):295-299.
Slide 61-

Emerging Therapies Video 8
Slide 62-

Crisaborole: New Topical for Mild-to-Moderate AD Overview Phosphodiesterase-4 inhibitor  ↑ cAMP  ↓ release of pro-inflammatory cytokines Approved by FDA December 2016 Phase 3 trials 2 randomized, double-blind, vehicle-controlled trials Patients Age ≥2 years with diagnosed atopic dermatitis, ≥5% treatable body surface area, IGSA score of 2 or 3 Excluded: biologic therapy or systemic corticosteroids within 28 days, TCS/TCI within 14 days Treatment Ointment applied twice daily to each lesion (except scalp) for 28 days Paller AS, et al. J Am Acad Dermatol. 2016;75(3):494-503. IGSA, Investigator’s Static Global Assessment score; TCI, topical calcineurin inhibitor; TCS, topical corticosteroid
Slide 63-

Crisaborole: Results of 2 Phase 3 Trials Paller AS, et al. J Am Acad Dermatol. 2016;75(3):494-503. P=.005 Trial AD-301: Crisaborole (n=503), vehicle (n=256); Trial AD-302: crisaborole (n=513), vehicle (n=250) P<.001 % of Patients with ISGA of Clear (0) or Almost Clear (1) at Day 29
Slide 64-

Crisaborole: Results of 2 Phase 3 Trials (cont) Paller AS, et al. J Am Acad Dermatol. 2016;75(3):494-503. P<.001 P<.001 P<.001 P<.001 P=.008 Trial AD-301: Crisaborole (n=503), vehicle (n=256); Trial AD-302: crisaborole (n=513), vehicle (n=250) % of Patients with Improvement in AD Signs at Day 29
Slide 65-

Case Scenario: Tamika Tamika is a 32-year-old female diagnosed with severe AD at age 23 years She has been treated with intensive topical therapy as well as systemic medications, and has either developed adverse effects or not responded (cyclosporine; mycophenolate mofetil; methotrexate) Preventive therapy with twice-weekly topical corticosteroid therapy has yielded limited benefit She continues to experience impaired quality of life, including poor sleep, which has made it difficult for her as a school teacher
Slide 66-

Dupilumab Fully human monoclonal antibody that blocks IL-4-receptor-  blocks actions of the Th-2 cytokines IL-4 and IL-13 Subcutaneous injection Peng W, et al. Clin Exper Allergy. 2015;45:566-574.
Slide 67-

Patients: Adults with moderate-to-severe AD with inadequate response to topical treatment Randomized (1:1:1:1:1:1) to 16 weeks of treatment with: Dupilumab 300 mg every week Dupilumab 300 mg every 2 weeks Dupilumab 200 mg every 2 weeks Dupilumab 300 mg every 4 weeks Dupilumab 100 mg every 4 weeks or Placebo every week Thaci D, et al. Lancet. 2016;387(10013):40-52. Dupilumab: Phase 2b Trial
Slide 68-

Dupilumab: Phase 2b Trial Results Thaci D, et al. Lancet. 2016;387(10013):40-52. N=379 P<0.0001 dupilumab (all doses) vs placebo
Slide 69-

Results: Improvements in EASI score were significantly greater at all doses of dupilumab vs placebo Treatment-emergent adverse event in 81% (dupilumab) and 80% (placebo) Nasopharyngitis: 28% (dupilumab) vs 26% (placebo) Thaci D, et al. Lancet. 2016;387(10013):40-52. Dupilumab: Phase 2b Trial Results (cont)
Slide 70-

Dupilumab: Phase 3 Trials (SOLO 1 and SOLO 2) 2 Separate phase 3, double-blind, parallel-group clinical trials SOLO 1 and SOLO 2 Adults with chronic moderate-to-severe AD inadequately controlled by topical treatment or for whom topical treatment was inadvisable Investigator Global Assessment score 3 or 4 IGA determines severity of AD and clinical response to treatment [range 0 (clear) to 4 (severe)] Simpson EL, et al. N Engl J Med. 2016;doi:10.1056/NEJMoa1610020.
Slide 71-

Dupilumab: Phase 3 Trials (cont) Randomized to: Dupilumab 300 mg every week Dupilumab 300 mg every other week or Placebo Moisturizers bid for ≥7 d before randomization, then throughout trial Topical or systemic rescue treatment allowed If systemic rescue treatment  patient discontinued (categorized as no response) Simpson EL, et al. N Engl J Med. 2016;doi:10.1056/NEJMoa1610020.
Slide 72-

Dupilumab: Phase 3 Trials Results Simpson EL, et al. N Engl J Med. 2016;doi:10.1056/NEJMoa1610020. *Reduction from baseline of ≥2 points on the IGA at week 16. P<.001 for all comparisons between dupilumab and placebo
Slide 73-

Dupilumab: Phase 3 Trials Results (cont) Simpson EL, et al. N Engl J Med. 2016;doi:10.1056/NEJMoa1610020. *Improvement from baseline of at least 75% on the Eczema Area and Severity Index (EASI) at week 16. P<.001 for all comparisons between dupilumab and placebo
Slide 74-

Dupilumab: Phase 3 Trials Results (cont) Significantly greater improvement with dupilumab vs placebo regarding Pruritus Sleep Symptoms of anxiety or depression Quality of life Fewer patients treated with dupilumab used rescue medication (19% vs 52%) Simpson EL, et al. N Engl J Med. 2016;doi:10.1056/NEJMoa1610020.
Slide 75-

Dupilumab: Phase 3 Trials Results (cont) Simpson EL, et al. N Engl J Med. 2016;doi:10.1056/NEJMoa1610020.
Slide 76-

Pro-inflammatory Targets Interleukins IL-4 receptor- IL-5 IL-12/IL-23 p40 IL-13 IL-22 IL-31 IL-31 receptor Janus kinase inhibitor Thymic stromal lymphopoietin H4-receptor blocker Liver X receptor agonist