What is the meaning of atopic allergy
Dr. Nicole Chadha received her B.A. in psychology from the University of Kansas, then returned to her southern roots in Georgia to pursue her career in medicine. She graduated with her medical degree from the Medical College of Georgia in Augusta, GA. She subsequently completed her pediatric residency at Palmetto Health Richland Children’s Hospital associated with the University of South Carolina and fellowship in Allergy/Immunology at Vanderbilt University.
Upon completion of her fellowship, Dr. Chadha remained on faculty at Vanderbilt as an Assistant Professor within the Division of Pediatric Allergy, Immunology, and Pulmonary Medicine. Dr.
Chadha is board certified in Pediatrics and Allergy and Immunology. She is a member of the American Academy of Allergy, Asthma, and Immunology, and the American College of Asthma Allergy and Immunology.
Dr. Chadha chose to specialize in Allergy in specific because she enjoys studying the intricacies of the immune system and likes that the specialty allows her to treat both children and adults. The chronic nature of allergic disease affords her the chance to build lasting relationships with her patients. She finds grand reward in providing care and education that results in an improved quality of life for her patients.
Dr. Chadha has numerous interests in a variety of allergic and immunologic conditions, including food allergy, asthma, urticaria, allergic rhinitis, primary immunodeficiency and eosinophilic esophagitis.
She has contributed to research on eosinophilic esophagitis in children and has presented her work both locally and nationally.
Dr. Chadha lives in Charlotte with her husband, Ashley, a pediatric pulmonologist, 2 young sons, and 2 dogs. In her free time, she enjoys traveling, reading, cooking, interior design, volunteering and taking part in community events.
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LOS ANGELES – Evidence is building for the hypothesis that impairments in the skin’s microbiome promote Staphylococcus aureus colonization and drive atopic dermatitis, Dr.
Donald Y.M. Leung said at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.
The link between the bacteria and atopic dermatitis has endless been discussed, but its role in pathogenesis still needs definition, he said.
“We’ve never been capable to glance at the entire bacterial composition of the skin, but now with next-generation sequencing it’s finally possible to glance at every the phylla and species. Other investigators own shown that during flares of atopic dermatitis there’s a reduction in bacterial diversity and an increase in staph, with S.
aureus being particularly abundant. Then, post-flare, you see see a drop in S. aureus; this clearly suggests (it’s) important,” according to Dr. Leung, head of the division of pediatric allergy and immunology at National Jewish Health in Denver and professor of pediatrics at the University of Colorado.
Staphylococcus aureus is known to secrete virulence factors including cytotoxins, superantigens, lipases, and proteases that activate inflammatory cells and can cause significant skin barrier dysfunction.
The discovery that filaggrin mutations result in structural abnormalities in the skin barrier and are associated with sharply increased rates of atopic dermatitis and peanut allergy own strengthened the association, but filaggrin can’t be the whole tale.
Mutations in filaggrin are largely confined to individuals of Northern European ancestry; African Americans don’t own filaggrin mutations.
Yet atopic dermatitis is a global phenomenon. Further, a skin barrier defect is not enough to cause atopic dermatitis, Dr. Leung said. But such a defect, whether caused by a filaggrin mutation or something else, allows S. aureus to attach to and colonize the skin. Staph overgrowth or infection then activates an inflammatory cell cascade involving natural killer T cells, mast cells, cytokines, and Langerhans cells. That’s why the most effective treatments for atopic dermatitis address both the need to rebuild the skin barrier as well as the counterproductive immune response, he added.
Elsewhere at the AAAAI meeting, Dr. Andrea L. Jones, of National Jewish Health, presented an analysis of 718 children and adolescents with atopic dermatitis, every of whom had been cultured for S. aureus, in that institution’s database. Methicillin-resistant S. aureus (MRSA) was found in 19%; 57% were positive for methicillin-sensitive S. aureus (MSSA) and 23% lacked S. aureus. Of note, the prevalence of peanut allergy was highest at 78% in the group with MRSA; the prevalence was 39% in those with MSSA and 4% in those without S. aureus.
The prevalence of allergies to wheat, egg, milk, or soybeans in the youths with atopic dermatitis was unrelated to MRSA colonization.
“Our hypothesis – although we need to do a prospective study – is that staph colonization may lead to barrier dysfunction and thus permit environmental allergens to invade through the skin. Interestingly enough, people who weren’t colonized by staph had a extremely low level of sensitization to peanut,” said Dr.
Leung, who was the senior investigator in the study.
Dr. Leung was a coauthor on another study that points to a potential new avenue of treatment in atopic dermatitis. Presented by investigators at the University of California, San Diego, at a recent meeting of the Society for Investigative Dermatology, the study showed that atopic dermatitis is marked by a defect in the commensal skin bacteria which normally hold S. aureus in check.
In that study, the quantity of S. aureus growing on a defined area of lesional skin of atopic dermatitis patients was almost 10-fold greater than that on nonlesional skin and the skin of controls without atopic dermatitis.
Commensal bacteria on lesional skin may possess markedly reduced antimicrobial activity. The NIH-sponsored Atopic Dermatitis Research Network plans to conduct clinical trials to see if transplanting beneficial commensal bacteria will reduce staph colonization in atopic dermatitis patients and thereby result in therapeutic benefit, Dr. Leung noted.
He reported serving on scientific advisory boards for more than half a dozen pharmaceutical companies and receiving numerous research grants from the NIH.
Ahogo KC, Kouassi YI, Gbery IP, Azagoh KR, Yeboua KI, Kouassi KA, Allou AS.
Atopic dermatitis in children: Epidemiological andclinical aspects in Côte d'Ivoire. Our Dermatol Online. 2017;8(Suppl.1):25-27.
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- American Board of Allergy and Immunology
- American Board of Pediatrics
<p>This section provides information about the protein and gene name(s) and synonym(s) and about the organism that is the source of the protein sequence.<p><a href=’/help/names_and_taxonomy_section’ target=’_top’>More…</a></p>Names & Taxonomyi
|<p>This subsection of the <a href=»http://www.uniprot.org/help/names_and_taxonomy_section»>Names and taxonomy</a> section provides an exhaustive list of every names of the protein, from commonly used to obsolete, to permit unambiguous identification of a protein.<p><a href=’/help/protein_names’ target=’_top’>More…</a></p>Protein namesi||
sympodialis allergen Mala s 8
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Automatic assertion inferred from database entriesi
|<p>This subsection of the <a href=»http://www.uniprot.org/help/names_and_taxonomy_section»>Names and taxonomy</a> section provides information on the name(s) of the organism that is the source of the protein sequence.<p><a href=’/help/organism-name’ target=’_top’>More…</a></p>Organismi||Malassezia sympodialis (strain ATCC 42132) (Atopic eczema-associated yeast)
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|<p>This subsection of the <a href=»http://www.uniprot.org/help/names_and_taxonomy_section»>Names and taxonomy</a> section contains the taxonomic hierarchical classification lineage of the source organism. It lists the nodes as they appear top-down in the taxonomic tree, with the more general grouping listed first.<p><a href=’/help/taxonomic_lineage’ target=’_top’>More…</a></p>Taxonomic lineagei||cellular organisms › Eukaryota › Opisthokonta › Fungi › Dikarya › Basidiomycota › Ustilaginomycotina › Malasseziomycetes › Malasseziales › Malasseziaceae › Malassezia › Malassezia sympodialis|
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- Fellowship: Vanderbilt University, Allergy/Immunology
- Residency: University of South Carolina, Palmetto Health Richland Children’s Hospital
- Medical School: Medical College of Georgia
- College: University of Kansas, B.A., Psychology
Atopic dermatitis in children: Epidemiological and clinical aspects in Côte d’Ivoire
Kouadio Celestin Ahogo1, Yao Isidore Kouassi1, Ildevert Patrice Gbery1, Kouadio Richard Azagoh2, Kouame Issouf Yeboua1, Kouame Alexandre Kouassi1, Ange Sylvain Allou1
1Dermatology Service, Félix Houphouët Boigny University, CHU Treichville, Abidjan, Côte d’Ivoire, 2Pediatric service, Félix Houphouët Boigny University, CHU Treichville, Abidjan, Côte d’Ivoire
Corresponding author: Dr.
Kouadio Celestin Ahogo, E-mail: [email protected]
Submission: 04.08.2017; Acceptance: 27.10.2017
Few studies own been devoted to atopic dermatitis in children in sub-Saharan Africa. We therefore make this study in Côte d’Ivoire in order to contribute to a better knowledge of atopic dermatitis in children on black skin.
In our study the prevalence was 9.2%. The duration of the disease before the consultation ranged from 3-45 days. Atopic dermatitis occurs more frequently in children from2 to 5 years ancient. More than half of the patients had a history of atopy and the lesions generally were localized in the folds. 60% of the lesions were dry and were trigged by dust. The pruritus was often insomnia and the scratching leads to hyperpigmentation of the lower eyelid; a characteristic sign on black skin not often reported in the literature.
Key words: Atopic dermatitis, Children, Black skin, Cote d’Ivoire
MATERIALS AND METHODS
This was a prospective study, with descriptive and analytical sight over 12 months.
The target population waspatients seen in consultation over the period of our study. Boys and girls from 0 to 15 years with atopic dermatitis were included in the study. Data from the study were collected on an inquiry sheet that included socio-demographic and clinical data.
On epidemiologic stage, 70 cases of atopic dermatitis own been recorded out of a entire of 765 children seen in consultation. The prevalence of atopic dermatitis in children was 9.2%.
52.9% of the patients were male with a sex ratio (M/F)at 1.1. The age of the children’s ranged from 6 months to 13 years. Children from 2 to 5 years represented 42.9% of the patients, followed by the age group from 6 to 13 years (30%). The duration of the disease before the consultation ranged from 3-45 days. Outbreaks of the disease were more than 15 days in 72.4% of cases.
A triggering factor was found in 15.7% of our patients, it was mainly dust (17.1%)and perfumes (5.7%). The personal and family histories of atopy are represented in Table I.
Table 1: Personal and family histories of atopy
The types of eczema observed were: dry (60%), oozing (32.9%), and lichenification (07.1%).
These lesions were found in the folds (54.3%), the trunk (51.4%), the legs (31.4%), and the face (30%)with pigmentation of the lower eyelid (7.1%). The scalp (22.9%)and generalized (02.9%). Atopic dermatitis was minor in 57.1% of cases, moderate (40%), and severe (2.9%); the other signs of atopic dermatitis observed in children are represented in Table II. Complications were observed in 58.57% of children. These included insomnia pruritus (44.3%), bacterial (12.9%)and viral (1.4%)secondary infection.
Table 2: Other signs of atopic dermatitis
Atopic dermatitis or constitutional eczema generally occurs in children in a specific condition called atopy.
Its pathophysiological, epidemiological, clinical and therapeutic aspects own been the subject of several studies in Europe and in America [1,2]. However, few studies own beendevoted to atopic dermatitis in sub-Saharan Africa. Therefore, we proposed to make this study in order to contribute to a better knowledge of atopic dermatitis in children, on black skin in Africa.
Atopic dermatitis in Côte d’Ivoire occurs more frequently in children from 2 to 5 years ancient. More than half of the patients had a history of atopy and the lesions generally localized in the folds.
These were mainly dry lesions most often triggered by dust. The pruritus was often insomnia and the scratching lead to hyperpigmentation of the lower eyelid; a characteristic sign on black skin not often reported in the literature.
70 cases of atopic dermatitis was observed among 765 pediatric dermatoses, the prevalence was therefore 9.2%. In Western Europe, the prevalence of atopic dermatitis in children is between 10-20% [3,4]. The most affected age group in the study was 2 to 6 years. In fact, atopic dermatitis often begins duringthe first year of life (the new born)and decreases around the age of 5 years.
54.2% of the children had a history of atopic disease. These included allergic rhinitis (37.1%), asthma (25.7%)and allergic conjunctivitis (17.1%). Six (06)of our patients regularly developed a food allergy. The association of several atopic clinical signs in the same patient is classic but inconstant [5,6]. The duration of relapses was in 72.4% of cases longer than 15 days. This could be explained in our context by self-medication.
In one-quarter of the patients dust (17.1%)was the triggerfactor. Atopic dermatitis is a multifactorial disease modulated by genetic and environmental influences [7,8]. Concerning the clinical aspects, atopic dermatitis in our study was predominantly in folds (54.3%). This predominance in folds was mostly observed in children over 2 years of age. As for the nursling, they had mainly facial lesions. Dry lesions (60%)were the most frequent, followed by oozing lesions (32.9%). Seepage often represents an entry point for bacterial and viral complications of atopic dermatitis [9,10].
In fact, bacterial secondary infection occurred in 12.9% of cases. Lichenification was present in 7.1% of our patients. Chronic scratching is the main factor of thisLichenification. Insomnia pruritus was found in 44.3% of our patients. Pruritus leads to sleep disturbances, sometimes with children’s growth retardation . Instead, hyperpigmentation was observed on thelower eyelid (7.1%). This characteristic sign most visible on dark skin is due to chronic friction.
This article has been written by these authors, it has not been send or published by another journal.
Atopic dermatitis:current epidemiology and clinical data. French J Allergol Clin Immunol. 2002;42:373-7.
2.Schmitt J, Langan S, Deckert S, Svensson A, von Kobyletzki L, Thomas K, et al. Assessment of clinical Signs of atopic dermatitis:A systematic review and recommendation. J Allergy Clin Immunol. 2013;132:1337-47.
3.Taïeb A. Atopic dermatitis:definition, epidemiology, natural history, gravity and scores. Ann Dermatol Venereol. 2005132:35-43.
4.Akdis CA, Akdis M, Bieber T, Bindslev-Jensen C, Boguniewicz M, Eigenmann P, et al.
Diagnosis and treatment of atopic dermatitis in children and adults:European Academy of Allergology and Clinical Immunology/American Academy of Allergy, Asthma and Immunology/PRACTALL Consensus Report. J Allergy Clin Immunol. 2006;118:152-69.
5.Asher MI, Montefort S, Björkstén B, Lai CK, Strachan DP, Weiland SK, et al. Worldwide time trends In the prevalence of symptoms of asthma, allergic rhinitis conjunctivitis, and eczema in childhood:ISAAC Phases One and Three repeat multi-cross-sectional surveys. Lancet. 2006;368:733-43.
6.The prevalence of asthma, rhinitis and eczema in 13 to 14 years ancient children in Africa:The ISAAC Phase III.
7.Borralevi T, Hubiche T, Léauté-Labrèze C, Saubusse E, Fayon M, Roul S, et al. Epicutaneous aeroallergen sensitization in atopic dermatitis infants determine the role of epidermal barrier impairment. Allergy. 2008;63:205-10.
8.Dominguez-Bello MG, Costello EK, Contreras M, Magris M, Hidalgo G, Fierer N, et al. Delivery mode shapes the acquisition and structure of the initial microbiota across multiple body habitats in newborns. Proc Natl Acad Sci U S A. 2010;107:11971-5.
9.Sidbury R, Davis DM, Cohen DE, Cordoro KM, Berger TG, Bergman JN, et al. Guidelines for the management of atopic dermatitis:section 2.
Management and treatment of atopic dermatitis with topical therapies.
J Am Acad Dermatol. 2014;71:116-32.
10.Kong HH, Oh J, Deming C, Conlan S, Grice EA, Beatson MA, et al. Temporal shifts in the skin Atopic dermatitis. Genome Res. 2012;22:850-9.
11.Silverberg JI, Simpson EL. Association between severe eczema in children and multiple comorbid conditions and increased health care utilization. Pediatr Allergy Immunol. 2013;24:476-86.
Source of Support: Nil
Conflict of Interest: None declared.
M. sympodialis allergen Mala s 8
Malassezia sympodialis (strain ATCC 42132) (Atopic eczema-associated yeast)
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