The Role of Biologics and Precision-Based Medicine in Treating Atopic Diseases in Children
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Pediatric Dermatology and Allergy (J Lee, Section Editor)
The Role of Biologics and Precision-Based Medicine in Treating Atopic Diseases in Children Rita Kachru, MD* Kellie Lim, MD Lorraine Anderson, MD Address * 1245 16th Street, Suite 303, Santa Monica, CA, 90404, USA
Published online: 17 August 2020 * Springer Nature Switzerland AG 2020
This article is part of the Topical Collection on Pediatric Dermatology and Allergy Keywords Allergic asthma I Atopic dermatitis I Biologics I Chronic Spontaneous Urticaria I Precision based medicine
Abstract Purpose of Review Children with atopic diseases such as asthma and atopic dermatitis often have poorly controlled disease, which can occur as a result of noncompliance from the concern of side effects from prolonged use of medications. This fear is not unfounded as often increasing doses of inhaled, topical, or oral steroids are required for control and carry a cumulative risk burden for growth and development in this population. The availability of biologics in this patient population has been pivotal in expanding options to reduce disease burden and unfavorable side effects. Recent Findings In addition to biologics expanding treatment options for children, their use has added insight into mechanisms of disease. In doing so, there is a better understanding of current biomarkers in tailoring treatment approaches. As novel biomarkers are studied, we are gaining more insight into targeted treatment options. Summary This review discusses biologics currently available for children for the treatment of atopic diseases, with a focus on certain phenotypic and endotypic biomarkers that may help guide therapy.
The Role of Biologics and Precision-Based Medicine in Treating
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Introduction A central pathophysiologic mechanism of atopic disorders is the cross-linking of antigen to immunoglobulin E (IgE) located on the surface of effector cells, such as mast cells and eosinophils, causing the release of pro-inflammatory mediators including histamine, leukotrienes, and cytokines [1, 2]. This phenomenon, called a type 1 hypersensitivity reaction, elicits symptoms familiar to atopic disease such as the wheal and flare eruptions of the skin (urticaria), intermittent wheeze (asthma), or anaphylaxis (hypotension, multiple organ involvement). The antigen and surrounding milieu are important factors in influencing the direction of the immune response. Intercellular pathogens, such as Mycobacterium tuberculosis, stimulate TH1 cells that secrete cytokines such as IL-2 and IFN- gamma, which suppress IgE synthesis through direct effects on B cells [3]. Extracellular pathogens such as Helminths or allergens stimulate TH2 cells that secrete a functionally distinct group of cytokines, IL-4, IL-5, IL-9, and IL-13, which are important mediators of IgE synthesis [4]. A complex interaction between the microbiome and a TH2-skewed inflammatory environment can redirect regulatory T cells towards a pro-inflammatory phenotype [5].
Until recently, therapy for atopic diseases such as severe
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