Atopic Dermatitis Progression: Evaluating Intervention Strategies
Several risk factors have been identified that appear to be consistently and strongly associated with the development of atopic dermatitis (AD): a family history of atopy, an inherited genetic predisposition, and active and passive exposure to tobacco smoke. Recent studies also have demonstrated that a simple intervention from birth—the daily application of an emollient moisturizer—seems to protect susceptible infants from the development of AD. Semin Cutan Med Surg 36(supp2):S39-S41 © 2017 published by Frontline Medical Communications
Atopic dermatitis; eczema; emollients; filaggrin; food allergy; inflammatory cytokines; interleukin; T helper cells
A fundamental question concerning atopic dermatitis (AD) has been the topic of many recent studies: What are the relative contributions of genetics and environment in disease susceptibility and expression?
Genetic Predisposition and Family History
Evidence for a genetic predisposition in AD comes from a variety of studies. Most recently, a study comparing AD in identical and fraternal twins demonstrated concordance rates of up to 0.86 in monozygotic and 0.41 in dizygotic pairs, providing clear evidence for a genetic predisposition to AD.1
In addition, Wen and colleagues2 reported that about 70% of patients with AD have a positive family history for atopic diseases. Previous studies had demonstrated that the chances of a patient having AD are 2- to 3-fold if one parent has AD, and 3- to 5-fold if both parents are atopic.3,4 Interestingly, Ruiz and colleagues5 demonstrated more than 2 decades ago that a maternal history of AD may be more predictive than a paternal history.
Method of Participation
Participants should read the activity information, review the activity in its entirety, and complete the online post-test and evaluation. Upon completing this activity as designed and achieving a passing score on the post-test, you will be directed to a Web page that will allow you to receive your certificate of credit via e-mail or you may print it out at that time. The online post-test and evaluation can be accessed at http://tinyurl.com/meetingthechallengeofatopic. Inquiries about CME accreditation may be directed to the University of Louisville Office of Continuing Medical Education & Professional Development (CME & PD) at email@example.com or (502) 852-5329.
This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of the University of Louisville and Global Academy for Medical Education, LLC. The University of Louisville is accredited by the ACCME to provide continuing medical education for physicians.
The University of Louisville Office of Continuing Medical Education & Professional Development designates this enduring material for a maximum of 2.0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Continuing Nursing Education
Postgraduate Institute for Medicine is accredited with distinction as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. This educational activity for 2.0 contact hour(s) is provided by the Postgraduate Institute for Medicine. Designated for 0.5 contact hours of pharmacotherapy credit for Advance Practice Registered Nurses.
The diagnosis of atopic dermatitis can be challenging because the type and appearance of skin lesions can vary and some common cutaneous conditions—such as seborrheic dermatitis (“cradle cap”) in infants—may coexist. In most cases, attention to characteristic features of AD leads to the correct diagnosis. Awareness of clinical circumstances that should lead to consideration of some rare conditions in the differential diagnosis also is important.
Recently published studies that have furthered the understanding of the role of filaggrin, filaggrin gene mutations, and transepidermal water loss have demonstrated that daily, full-body emollient applications, beginning at birth, may prevent the expression of AD in susceptible children. For all patients with AD, the use of adequate skin hydration combined with the prompt application of ointment or cream moisturizers (“soak and seal”) remains the cornerstone of AD therapy.
Recent advances in understanding the complex pathophysiology of AD have led to the development of new and emerging topical and systemic medications that may effectively manage the signs and symptoms of AD in patients who do not respond adequately to standard treatment regimens. These include the topical phosphodiesterase-4 inhibitor crisaborole, recently approved for use in AD by the US Food and Drug Administration (FDA), and the subcutaneously administered interleukin-4 receptor α subunit inhibitor dupilumab, for which phase III pivotal study data are now available.
Clinicians must remain up-to-date on the findings from clinical studies on the diagnosis and management of AD, as well as the benefits and risks of all treatment options available, to make the appropriate choices for management of their individual patients.
By reading and studying this supplement, participants should be better able to:
- Discuss the features of AD that should allow a clinical diagnosis of the condition in most patients, and list the factors in children and adults that should lead to the consideration of alternative diagnoses or identification of comorbid conditions.
- Explain how the current understanding of the role of the epidermal skin barrier and transepidermal water loss should affect—and continue to improve— the day-to-day care of patients with AD.
- More effectively individualize patient treatment strategies by considering the full range of current and emerging therapeutic options.
- Consider the evidence-based recommendations in the current guidelines for the diagnosis and treatment of AD published by the American Academy of Dermatology.
- Describe the rationales and mechanisms of action of the new and emerging therapies for AD, particularly the recently approved topical agent crisaborole and the systemic medication dupilumab (phase III study results under FDA review at the time of publication of this supplement).
Individuals in a position to control the content of this educational activity are required to disclose: 1) the existence of any relevant financial relationship with any entity producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients with the exemption of non-profit or government organizations and non-health care related companies, within the past 12 months; and 2) the identification of a commercial product/device that is unlabeled for use or an investigational use of a product/device not yet approved.
Lawrence F. Eichenfield, MD, Advisory Board/Speaker: Valeant Pharmaceuticals North America LLC. Consultant: Anacor Pharmaceuticals, Inc./Pfizer Inc., Eli Lilly and Company, Genentech, Inc., Otsuka America Pharmaceutical, Inc./Medimetriks Pharmaceuticals, Inc., Sanofi Genzyme/Regeneron Pharmaceuticals, TopMD, Valeant. Investigator: Sanofi Genzyme/Regeneron.
Linda F. Stein Gold, MD, Consultant: Anacor. Grant/Research: Anacor, GlaxoSmithKline. Data Monitoring Committee: Otsuka.
Staff and Advisory Board Disclosures: The CME & PD staff pediatricians, family practitioners, and Advisory Board have nothing to disclose.
CME/CE Reviewers: Cindy England Owen, MD, Assistant Professor, Division of Dermatology, University of Louisville School of Medicine, has no relevant financial relationships to disclose. The PIM planners and managers, Trace Hutchison, PharmD; Samantha Mattiucci, PharmD, CHCP; Judi Smelker- Mitchek, MBA, MSN, RN; and Jan Schultz, MSN, RN, CHCP, have nothing to disclose.
Global Academy for Medical Education Staff: Sylvia H. Reitman, MBA, DipEd; Jenny Campano; Tristan Nelsen, MNM, CMP, HMCC; and Joanne Still have no relevant financial relationships to disclose.
Off-Label/Investigational Use Disclosure
This CME/CE activity discusses the off-label use of certain approved medications as well as data from clinical trials on investigational agents. Any such material is identified within the text of the articles.
Contact Information for Technical Questions
Please technical questions or concerns to Global Academy for Medical Education at 973-290-8225 or email firstname.lastname@example.org.
Copyright © 2017 by Global Academy for Medical Education, LLC, Frontline Medical Communications Inc., and its Licensors. All rights reserved. No part of this publication may be reproduced or transmitted in any form, by any means, without prior written permission of the Publisher. Global Academy for Medical Education, LLC, Global Education Group, and Frontline Medical Communications will not assume responsibility for damages, loss, or claims of any kind arising from or related to the information contained in this publication, including any claims related to the products, drugs, or services mentioned herein.
1. Elmose C, Thomsen SF. Twin studies of atopic dermatitis: Interpretations and applications in the filaggrin era. J Allergy (Cairo). 2015;2015:902359.
2. Wen HJ, Chen PC, Chiang TL, Lin SJ, Chuang YL, Guo YL. Predicting risk for early infantile atopic dermatitis by hereditary and environmental factors. Br J Dermatol. 2009;161:1166-1172.
3. Wadonda-Kabondo N, Sterne JA, Golding J, et al. Association of parental eczema, hayfever, and asthma with atopic dermatitis in infancy: Birth cohort study. Arch Dis Child. 2004;89:917-921.
4. Küster W, Petersen M, Christophers E, Goos M, Sterry W. A family study of atopic dermatitis. Clinical and genetic characteristics of 188 patients and 2,151 family members. Arch Dermatol Res. 1990;282:98-102.
5. Ruiz RG, Kemeny DM, Price JF. Higher risk of infantile atopic dermatitis from maternal atopy than from paternal atopy. Clin Exp Allergy. 1992;22:762-766.
6. Kantor R, Kim A, Thyssen JP, Silverberg JI. Association of atopic dermatitis with smoking: A systematic review and meta-analysis. J Am Acad Dermatol. 2016;75:1119-1125.e1. J Invest Dermatol. 2011;131:67-73.
7. Irvine AD, McLean WHI. Breaking the (un)sound barrier: Filaggrin is a major gene for atopic dermatitis. J Invest Dermatol. 2006;126:1200-1202.
8. Eichenfield LF, Tom WL, Chamlin SL, et al. Guidelines of care for the management of atopic dermatitis: Section 1. Diagnosis and assessment of atopic dermatitis. J Am Acad Dermatol. 2014;70:338-351.
9. Howell MD, Kim BE, Gao P, et al. Cytokine modulation of atopic dermatitis filaggrin skin expression. J Allergy Clin Immunol. 2009;124(3 suppl 2):R7-R12.
10. Kelleher M, Dunn-Galvin A, Hourihane JO, et al. Skin barrier dysfunction measured by transepidermal water loss at 2 days and 2 months predates and predicts atopic dermatitis at 1 year. J Allergy Clin Immunol. 2015;135:930-935.e1.
11. Simpson EL, Chalmers JR, Hanifin JM, et al. Emollient enhancement of the skin barrier from birth offers effective atopic dermatitis prevention. J Allergy Clin Immunol. 2014;134:818-823.
12. Mason JM, Carr J, Buckley C, et al. Improved emollient use reduces atopic eczema symptoms and is cost neutral in infants: Before-and-after evaluation of a multifaceted educational support programme. BMC Dermatol. 2013;13:7.
13. Horimukai K, Morita K, Narita M, et al. Application of moisturizer to neonates prevents development of atopic dermatitis. J Allergy Clin Immunol. 2014;134: 824-830.e6.
14. Kim JP, Chao LX, Simpson EL, Silverberg JI. Persistence of atopic dermatitis (AD): A systematic review and meta-analysis. J Am Acad Dermatol. 2016;75:681- 687.e11.
15. Spergel JM, Boguniewicz M, Schneider L, Hanifin JM, Paller AS, Eichenfield LF. Food allergy in infants with atopic dermatitis: Limitations of food-specific IgE measurements. Pediatrics. 2015;136:e1530-e1538.
16. Tsakok T, Marrs T, Mohsin M, et al. Does atopic dermatitis cause food allergy? A systematic review. J Allergy Clin Immunol. 2016;137:1071-1078.
17. Gdalevich M, Mimouni D, David M, Mimouni M. Breast-feeding and the onset of atopic dermatitis in childhood: A systematic review and meta-analysis of prospective studies. J Am Acad Dermatol. 2001;45:520-527.
18. Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372:803-813.
This continuing medical education (CME/CE) supplement was developed from a satellite symposium held at the Skin Disease Education Foundation’s 17th Annual Las Vegas Dermatology Seminar, November 11, 2016, in Las Vegas, Nevada. The Guest Editors acknowledge the editorial assistance of Global Academy for Medical Education and Joanne Still, medical writer, in the development of this supplement. The manuscript was reviewed and approved by the Guest Editors as well as the Editors of Seminars in Cutaneous Medicine and Surgery. The ideas and opinions expressed in this supplement are those of the Guest Editors and do not necessarily reflect the views of the supporter, Global Academy for Medical Education, the University of Louisville, Postgraduate Institute for Medicine, or the Publisher.
* Director of Dermatology Research, Henry Ford Health System, Detroit, Michigan
† Chief, Pediatric and Adolescent Dermatology, Professor of Dermatology and Pediatrics, Rady Children’s Hospital, University of California, San Diego School of Medicine, San Diego, California
Publication of this CME/CE article was jointly provided by University of Louisville, Postgraduate Institute for Medicine, and Global Academy for Medical Education, LLC, and is supported by an educational grant from Anacor Pharmaceuticals, Inc. The authors have received an honorarium for their participation in this activity. They acknowledge the editorial assistance of Joanne Still, medical writer, and Global Academy for Medical Education in the development of this continuing medical education journal article.
Linda F. Stein Gold, MD, Consultant: Anacor. Grant/Research: Anacor, GlaxoSmithKline. Data Monitoring Committee: Otsuka America Pharmaceutical, Inc.
Lawrence F. Eichenfield, MD, Advisory Board/Speaker: Valeant Pharmaceuticals North America LLC. Consultant: Anacor/Pfizer Inc., Eli Lilly and Company, Genentech, Inc., Otsuka/Medimetriks Pharmaceuticals, Inc., Sanofi Genzyme/Regeneron Pharmaceuticals, TopMD, Valeant. Investigator: Sanofi Genzyme/Regeneron. Address reprint requests to: Linda F. Stein Gold, MD, 2360 Heronwood Drive, Bloomfield Hills, MI 48302; email@example.com
1085-5629/13/$-see front matter © 2017 Frontline Medical Communications doi:10.12788/j.sder.2017.010