scholarly journals Atopic dermatitis in children: up to date insight on development and trends in therapy

2020 ◽  
Vol 23 (4) ◽  
pp. 265-270
Author(s):  
Ivan I. Balabolkin
Keyword(s):  
Atopic Dermatitis ◽  
Environmental Factors ◽  
Allergen Immunotherapy ◽  
Calcineurin Inhibitors ◽  
Barrier Dysfunction ◽  
Innate And Adaptive Immunity ◽  
Pathogenetic Therapy ◽  
Ige Mediated ◽  
Genetic And Environmental Factors ◽  
The Impact

The development of atopic dermatitis (AD) in children is determined by the impact of genetic and environmental factors, epidermal barrier dysfunction, and changes in the system of innate and adaptive immunity. 76.3% of patients have IgE-mediated atopic dermatitis. The article elucidates questions of the pathogenesis and treatment of atopic dermatitis using topical corticosteroids, calcineurin inhibitors, emollients, antihistamines, allergen immunotherapy, omalizumab, probiotics. Conducting individualized pathogenetic therapy in ATD allows you to achieve control throughout the disease.

scholarly journals Approach to the Assessment and Management of Pediatric Patients with Atopic Dermatitis: A Consensus Document. Section II: Comorbid Disease in Pediatric Atopic Dermatitis

2019 ◽  
Vol 23 (5_suppl) ◽  
pp. 12S-18S ◽  
Author(s):  
Chih-ho Hong ◽  
Marissa Joseph ◽  
Vy HD Kim ◽  
Perla Lansang ◽  
Irene Lara-Corrales
Keyword(s):  
Atopic Dermatitis ◽  
Health Care Providers ◽  
Pediatric Patients ◽  
Allergic Diseases ◽  
Care Providers ◽  
Barrier Dysfunction ◽  
Consensus Document ◽  
Common Skin ◽  
Genetic And Environmental Factors ◽  
Skin Conditions

Pediatric atopic dermatitis (AD) is one of the most common skin conditions encountered by health-care providers caring for infants, children, and adolescents. Pediatric patients with AD may present with other allergic and nonallergic comorbidities that require appropriate treatment and referral. They may also experience a trajectory of allergic diseases known as the atopic march, which depends on a complex interaction between genetic and environmental factors and likely involves early epidermal barrier dysfunction. Here we provide a review and clinical recommendations on the assessment and referral of comorbidities in pediatric AD.

Clinical Insights About Topical Treatment of Mild-to-Moderate Pediatric and Adult Atopic Dermatitis

2019 ◽  
Vol 23 (3_suppl) ◽  
pp. 3S-13S ◽  
Author(s):  
Charles W. Lynde ◽  
James Bergman ◽  
Loretta Fiorillo ◽  
Lyn Guenther ◽  
Jill Keddy-Grant ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Calcineurin Inhibitors ◽  
Skin Condition ◽  
Future Research ◽  
Barrier Dysfunction ◽  
Psychosocial Burden ◽  
Epidermal Barrier ◽  
Topical Corticosteroids ◽  
Topical Calcineurin Inhibitors ◽  
Inflammatory Conditions

Atopic dermatitis (AD) is a chronic inflammatory skin condition, also referred to as atopic eczema, that is identified by itching and recurrent eczematous lesions. It often starts in infancy where it affects up to 20% of children but is also highly prevalent in adults. AD inflicts a significant psychosocial burden on patients and their families and increases the risk of other immune-mediated inflammatory conditions, such as asthma and allergic rhinitis, food allergy, and mental health disorders. It is a lifelong condition associated with epidermal barrier dysfunction and altered immune function. Through the use of emollients and anti-inflammatory agents, current prevention and treatment therapies attempt to restore epidermal barrier function. Acute flares are treated with topical corticosteroids. Topical calcineurin inhibitors (TCIs) and topical corticosteroids (TCSs) are used for proactive treatment to prevent remission. There remains a need and opportunity to improve AD care through future research directed toward an improved understanding of the heterogeneity of the disease and its subtypes, the role of autoimmunity in its pathogenesis, the mechanisms behind disease-associated itch and response to specific allergens, and the comparative effectiveness and safety of therapies.

scholarly journals Impact of Genetic and Environmental Factors on hsCRP Concentrations and Response to Therapeutic Agents

2009 ◽  
Vol 55 (2) ◽  
pp. 256-264 ◽  
Author(s):  
Jian Shen ◽  
Jose M Ordovas
Keyword(s):  
Environmental Factors ◽  
Genetic Polymorphisms ◽  
Genetic Variants ◽  
Inflammatory Marker ◽  
Lipid Lowering ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Fenofibrate Treatment ◽  
Genetic And Environmental Factors ◽  
The Impact

Abstract Background: Inflammation plays an instrumental role in all stages of atherosclerosis. High-sensitivity C-reactive protein (hsCRP), a systemic inflammatory marker, has been gaining recognition as an independent risk factor for cardiovascular disease (CVD). Both baseline hsCRP concentrations and drug-induced hsCRP changes are highly variable and potentially subject to genetic regulation. Content: This review summarizes the current studies examining the effect of genetic and environmental factors on baseline plasma hsCRP concentrations, with a main focus on C-reactive protein, pentraxin-related (CRP) genetic polymorphisms and various dietary components that affect hsCRP concentrations. We also address the association of CRP genetic variations with CVD risk, a relationship that may support or refute the causality of CRP in the atherosclerotic process. Moreover, we discuss the impact of CRP genetic polymorphisms on hsCRP changes in response to 3-week fenofibrate treatment in the genetic intervention of the Genetics of Lipid Lowering Drugs and Diet Network study. Summary: Genetic variants on the CRP locus and other loci and dietary and lifestyle factors are responsible for the interindividual variability of plasma hsCRP concentrations. CRP genetic variants further influence differing plasma hsCRP response after 3-week fenofibrate treatment in patients with metabolic syndrome. Future studies focusing on the influence and interaction of genetic variation on the hsCRP response to dietary and other behavior modification as well as drug treatment could have important implications for the development of more personalized preventive and therapeutic approaches to reduce CVD.

scholarly journals Atopic Dermatitis: From Etiology and History to Treatment

2021 ◽  
Vol 48 (3) ◽  
pp. 68-76
Author(s):  
L. Dourmishev ◽  
N. Mironova
Keyword(s):  
Atopic Dermatitis ◽  
Environmental Factors ◽  
Immunoglobulin E ◽  
Clinical Course ◽  
Inflammatory Skin Disease ◽  
Comprehensive Overview ◽  
Common Skin ◽  
Morphological Variants ◽  
Genetic And Environmental Factors ◽  
Developed World

Abstract Atopic dermatitis (AD) is a chronic recurrent inflammatory skin disease in patients with atopy. Atopy itself, is defined as a predisposition to develop immune response with overproduction of immunoglobulin E to low doses of allergens. AD is one of the most common skin disorders in the developed world, affecting up to 20% of children and about 3% of adults. The pathogenesis of the disease is complex, with both genetic and environmental factors playing a significant role in it. Clinically, hallmarks of atopic dermatitis include dry, itchy skin and various cutaneous efflorescence, compatible to dermatitis or eczema. Atopic dermatitis subdivides into three morphological variants manifesting during infancy, childhood and adulthood. Various environmental factors and associated diseases may have serious influence on the clinical course or may trigger disease relapses. The aim of this review article is to serve as a comprehensive overview of the etiology, pathogenesis, clinical course and diagnosis, as well as potential challenges facing the successful treatment of atopic dermatitis.

Skin microbiomein adult atopic dermatitis

2018 ◽  
pp. 209-214
Author(s):  
О.В. Кандалова ◽  
И.В. Елистратова ◽  
О.Б. Иванченко ◽  
А.В. Гречко ◽  
С.Г. Морозов
Keyword(s):  
Atopic Dermatitis ◽  
Environmental Factors ◽  
Bacterial Infection ◽  
Adaptive Immunity ◽  
Bacterial Contamination ◽  
Proteolytic Enzymes ◽  
Regulatory Proteins ◽  
Skin Microbiome ◽  
Innate And Adaptive Immunity

Данный миниобзор посвящен изучению роли микробиома кожи и, в частности, роли стафилококков в обострении атопического дерматита у взрослых людей. Были проанализированы предпосылки бактериальной контаминации кожи и роль факторов внешней среды. Представлены данные по влиянию S. aureaus на разные звенья природного и адаптивного иммунитета за счет синтеза специфических регуляторных белков, протеолитических ферментов и гидролаз. Обозначены некоторые направления борьбы с бактериальной инфекцией для предупреждения обострения атопического дерматита у взрослых. In this mini review we have analyzed the role of skin microbiome in the atopic dermatitis relapse in adults, in particular, a role of S. aureaus in this process. The background for the skin bacterial contamination under the influence of environmental factors has been analyzed. We reviewed some S. aureaus effects on the components of innate and adaptive immunity due to the secretion of specific regulatory proteins, a number of proteolytic enzymes, and some hydrolases. There were indicated some ways to eliminate the bacterial infection to prevent the atopic dermatitis relapse in adults

scholarly journals Regulation of Skin Barrier Function via Competition between AHR Axis versus IL-13/IL-4‒JAK‒STAT6/STAT3 Axis: Pathogenic and Therapeutic Implications in Atopic Dermatitis

2020 ◽  
Vol 9 (11) ◽  
pp. 3741
Author(s):  
Masutaka Furue
Keyword(s):  
Atopic Dermatitis ◽  
Barrier Function ◽  
Coal Tar ◽  
Calcineurin Inhibitors ◽  
Skin Barrier ◽  
Skin Inflammation ◽  
Interleukin 4 ◽  
Skin Barrier Function ◽  
Barrier Dysfunction ◽  
Therapeutic Implications

Atopic dermatitis (AD) is characterized by skin inflammation, barrier dysfunction, and chronic pruritus. As the anti-interleukin-4 (IL-4) receptor α antibody dupilumab improves all three cardinal features of AD, the type 2 cytokines IL-4 and especially IL-13 have been indicated to have pathogenic significance in AD. Accumulating evidence has shown that the skin barrier function is regulated via competition between the aryl hydrocarbon receptor (AHR) axis (up-regulation of barrier) and the IL-13/IL-4‒JAK‒STAT6/STAT3 axis (down-regulation of barrier). This latter axis also induces oxidative stress, which exacerbates inflammation. Conventional and recently developed agents for treating AD such as steroid, calcineurin inhibitors, cyclosporine, dupilumab, and JAK inhibitors inhibit the IL-13/IL-4‒JAK‒STAT6/STAT3 axis, while older remedies such as coal tar and glyteer are antioxidative AHR agonists. In this article, I summarize the pathogenic and therapeutic implications of the IL-13/IL-4‒JAK‒STAT6/STAT3 axis and the AHR axis in AD.

scholarly journals Combat exposure severity as a moderator of genetic and environmental liability to post-traumatic stress disorder

2013 ◽  
Vol 44 (7) ◽  
pp. 1499-1509 ◽  
Author(s):  
E. J. Wolf ◽  
K. S. Mitchell ◽  
K. C. Koenen ◽  
M. W. Miller
Keyword(s):  
Environmental Factors ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Combat Exposure ◽  
Shared Environment ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Genetic And Environmental Factors ◽  
The Impact

BackgroundTwin studies of veterans and adults suggest that approximately 30–46% of the variance in post-traumatic stress disorder (PTSD) is attributable to genetic factors. The remaining variance is attributable to the non-shared environment, which, by definition, includes combat exposure. This study used a gene by measured environment twin design to determine whether the effects of genetic and environmental factors that contribute to the etiology of PTSD are dependent on the level of combat exposure.MethodThe sample was drawn from the Vietnam Era Twin Registry (VETR) and included 620 male–male twin pairs who served in the US Military in South East Asia during the Vietnam War era. Analyses were based on data from a clinical diagnostic interview of lifetime PTSD symptoms and a self-report measure of combat exposure.ResultsBiometric modeling revealed that the effects of genetic and non-shared environment factors on PTSD varied as a function of level of combat exposure such that the association between these factors and PTSD was stronger at higher levels of combat exposure.ConclusionsCombat exposure may act as a catalyst that augments the impact of hereditary and environmental contributions to PTSD. Individuals with the greatest exposure to combat trauma were at increased risk for PTSD as a function of both genetic and environmental factors. Additional work is needed to determine the biological and environmental mechanisms driving these associations.

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