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IN ATOPIC DERMATITIS,
CONTROL THE CORE OF THE DISEASE BY CONTROLLING INFLAMMATION

PATIENTS NEED STRATEGIES THAT MANAGE THE OVERALL DISEASE COURSE, BEYOND THE EPISODIC SIGNS AND SYMPTOMS1

Atopic dermatitis is an inflammatory disease that has been shown to be associated with a multitude of comorbid allergic diseases.2 Patients’ skin, including nonlesional skin, suffers from hidden signs of persistent inflammation, even after the itch has subsided.3-5 This underlying, chronic inflammation is a significant source of lesions and itch, the primary signs and symptoms of the disease.3-5 In fact, this inflammation is significantly greater in atopic dermatitis than in psoriasis.6 The Th2 inflammatory response that manifests as disease activity overtly during exacerbations persists subclinically even after the flare has subsided.3,4 Addressing the source of underlying, persistent inflammation may be key to keeping current and future disease signs and symptoms, including itch, at bay.4,5

THE MANAGEMENT OF ATOPIC DERMATITIS
SHOULD CONSIDER PROACTIVE DISEASE CONTROL1,7-9

In general, there is a reactive and episodic approach to the management of atopic dermatitis in which physicians often rely on superficial measures of symptoms and control.1 These therapeutic approaches for treating atopic dermatitis can be effective in some patients; however, these options may not be adequate in patients whose disease is not adequately controlled because of persistent, underlying inflammation.1

Unfortunately, patients with atopic dermatitis are often trapped in an endless cycle of frequent, unpredictable flares that last days, weeks or even longer, along with persistent itching and lesions.8,9 Disease management should consider a proactive approach to control, including a reduction in the number and severity of exacerbations and an increase in duration between exacerbations.1,7-9

A proactive approach is warranted for management of the persistent inflammatory process, which, even if subclinical, is always present.10

References: 1. Bieber T. Mechanisms of disease: atopic dermatitis. N Engl J Med. 2008:358(14):1483-1494. 2. Schneider L, Tilles S, Lio P, et al. Atopic dermatitis: a practice parameter update 2012. J Allergy Clin Immunol. 2013;131:295-299. 3. Gittler JK, Shemer A, Suárez-Fariñas M, et al. Progressive activation of TH2/TH22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis. J Allergy Clin Immunol. 2012;130(6):1344-1354. 4. Leung DYM, Boguniewicz M, Howell MD, Nomura I, Hamid QA. New insights into atopic dermatitis. J Clin Invest. 2004;113(5):651-657. 5. Suárez-Fariñas M, Tintle SJ, Shemer A, et al. Nonlesional atopic dermatitis skin is characterized by broad terminal differentiation defects and variable immune abnormalities. J Allergy Clin Immunol. 2011;127(4):954-964. 6. Czarnowicki T, Malajian D, Shemer A, et al. Skin-homing and systemic T-cell subsets show higher activation in atopic dermatitis versus psoriasis. J Allergy Clin Immunol. 2015;136(1):208-211. 7. Torrelo A, Ortiz J, Alomar A, et al. Health-related quality of life, patient satisfaction, and adherence to treatment in patients with moderate or severe atopic dermatitis on maintenance therapy: the CONDA-SAT study. Actas Dermo. 2013;104(5):409-417. 8. Gelmetti C, Wollenberg A. Atopic dermatitis—all you can do from the outside. Br J Dermatol. 2014;170(suppl 1):19-24. 9. Guttman-Yassky E, Dhingra N, Leung DYM. New era of biological therapeutics in atopic dermatitis. Expert Opin Biol Ther. 2013;13(4):1-23. 10. Wollenberg A, Frank R, Julia K, Ruzicka T. Proactive therapy of atopic eczema—an evidence-based concept with a behavioral background. J Dtsch Dermatol Ges. 2009;7(2):117-121.