po scorad - La Fondation pour la Dermatite Atopique
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po scorad - La Fondation pour la Dermatite Atopique
Fondation pour la Dermatite Atopique Recherche et Education Une fondation pour les professionnels de santé Une fondation pour les patients atteints de dermatite atopique Les missions La Fondation pour la Dermatite Atopique est une fondation d’entreprise Pierre Fabre exclusivement dédiée à l’eczéma atopique Une fondation pour la recherche Les projets de recherche fondamentale ou clinique peuvent faire l’objet d’un soutien financier après validation par le Conseil Scientifique de la Fondation. Une fondation pour l’éducation thérapeutique Comme toutes les maladies chroniques, la dermatite atopique est difficile à prendre en charge. Le découragement gagne souvent enfants et parents qui ne comprennent pas toujours comment tirer le meilleur parti des traitements disponibles. L’éducation thérapeutique met en œuvre des moyens adaptés pour apporter les connaissances nécessaires, un savoir-faire et un savoir-être précieux. La Fondation pour la Dermatite Atopique aide le développement des centres d’éducation thérapeutique. Les membres fondateurs Pierre Fabre Dermocosmétique Laboratoires A-Derma Laboratoires Dermatologiques Avène Pierre Fabre Dermatologie Laboratoires Dermatologiques Ducray Laboratoires Klorane Pierre Fabre Médicament Le Conseil d’Administration Collège de Professeurs Professeur Yves De Prost (Paris) Professeur François Bernard Michel (Montpellier) Professeur Jean Revuz (Paris) Conseil Scientifique Professeur Carle Paul (Hôpital Larrey - Toulouse) Professeur Jean-François Nicolas (Centre Hospitalier - Lyon Sud) Professeur Jean-François Stalder (Hôtel Dieu - Nantes) Aider la recherche dans le domaine de la dermatite atopique Etude sur les récepteurs à l’histamine PO SCORAD Experimental dermatology • Original article Allergy ORIGINAL ARTICLE SKIN AND EYE DISEASES Patient-Oriented SCORAD (PO-SCORAD): a new selfassessment scale in atopic dermatitis validated in Europe Association between copy-number variations of the human histamine H4 receptor gene and atopic dermatitis in a Chinese population J.-F. Stalder1, S. Barbarot1, A. Wollenberg2, E. A. Holm3, L. De Raeve4, S. Seidenari5, A. Oranje6, M. Deleuran7, F. Cambazard8, A. Svensson9, D. Simon10, E. Benfeldt11, T. Reunala12, J. Mazereeuv13, F. Boralevi14, B. Kunz15, L. Misery16, C. G. Mortz17, U. Darsow18, C. Gelmetti19, T. Diepgen20, J. Ring18,21, M. Moehrenschlager21, U. Gieler22 & A. Taı̈eb14, for the PO-SCORAD Investigators Group* B. Chen,1 T. Ye,1,2,3 Y. Shao,1,2,3 J. Zhang,1,2,3 Q. Zhong,1,2,3 X. Hu,1,2,3 W. Zhang4 and B. Yu1,2,3 Dermatology Department and Shenzhen Key Discipline of Dermatology, Peking University Shenzhen Hospital, Shenzhen, China; Shenzhen Key Laboratory for Translational Medicine of Dermatology and Biomedical Research Institute, Shenzhen PKU-HKUST Medical Center, Shenzhen, China Department of Dermatology, Nantes University Hospital, Nantes, France; Department of Dermatology and Allergy, Ludwig-Maximilian University, Munich, Germany; Skin Clinic in Ballerup, ‘‘Helsehuset’’, Ballerup, Denmark; Department of Dermatology UZ Brussels, Vrije Universiteit Brussel, Brussel, Belgium; Department of Dermatology, University of Modena and Reggio Emilia, Modena, Italy; University Hospital Rotterdam and Erasmus University, Rotterdam, the Netherlands; Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark; Jean Monet Faculty, Saint-Etienne, France; Department of Dermatology, Skane University Hospital, Malmö, Sweden; Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland; Department of Dermato-allergology, Copenhagen University Hospital Gentofte, Hellerup, Denmark; Medical School, Tampere University, Tampere, Finland; Department of Dermatology and André Hospital, Paul Sabatier University, Larrey Hospital, Toulouse, France; Department of Dermatology and Pediatric Dermatology, St Andre Bordeaux, France; Dermatologikum Hamburg, Hamburg, Germany; Department of Dermatology, Brest University Hospital, Brest, France; Department of Dermatology and Allergy centre, Odense University Hospital, Odense, Denmark; Deptartment of Dermatology and Allergy nchen and Division of Environmental Dermatology and Allergy, Helmholtz Center/Tum, Munich, GerBiederstein, Technische Universität München many; Department of Anesthesia, Intensive care and Dermatologic Sciences, Fondazione Ca’ Granda ‘‘Ospedale Maggiore Policlinico’’, Milan, Italy; University Hospital Heidelberg, Department of Social Medicine, Center of Occupational & Environmental Dermatology, Heidelberg, Germany; Hochgebirgsklinik Davos-Wolfgang, Christine-Kuehne Centre for Allergy Research and Education (CK-CARE), Davos, Switzerland; Department of Psychosomatic Medicine-Psychodermatology, University of Giessen, Giessen, Germany doi:10.1111/ced.12117 Summary To cite this article:: Stalder J-F, Barbarot S, Wollenberg A, Holm EA, De Raeve L, Seidenari S, Oranje A, Deleuran M, Cambazard F, Svensson A, Simon D, Benfeldt E, Reunala T, Mazereeuv J, Boralevi F, Kunz B, Misery L, Mortz CG, Darsow U, Gelmetti C, Diepgen T, Ring J, Moehrenschlager M, Gieler U, Taıeb Taı̈ Taı̈eb A, for the PO-SCORAD Investigators Group. Patient-Oriented SCORAD (PO-SCORAD): a new self-assessment scale in atopic dermatitis validated in Europe. Allergy 2011; 66: 1114–1121. Keywords atopic dermatitis (MesH); eczema score; patient-oriented; SCORing of Atopic Dermatitis index; self-assessment score. Correspondence Pr. Jean-François Stalder, Service de Dermatologie, CHU de Nantes, Hôtel Dieu, 44035 Nantes, France. Tel.: +33-2-40-08-31-15 Fax: +33-2-40-08-31-17 E-mail: [email protected] *The PO-SCORAD investigator group is listed in the Acknowledgments section Accepted for publication 12 February 2011 DOI:10.1111/j.1398-9995.2011.02577.x Edited by: Hans-Uwe Simon Abstract Background: Patient-oriented medicine is an emerging concept, encouraged by the World Health Organization, to greater involvement of the patient in the management of chronic diseases. The Patient-Oriented SCORing Atopic Dermatitis (PO-SCORAD) index is a self-assessment score allowing the patient to comprehensively evaluate the actual course of atopic dermatitis (AD), using subjective and objective criteria derived mainly from the SCORAD, a validated AD severity clinical assessment tool. Objectives: To validate the PO-SCORAD index in a large European population of patients exhibiting all forms of AD severity by assessing its correlation with the SCORAD index. Patients/methods: Four hundred and seventy-one patients (185 adults, 286 children) consulting for AD in hospitals from 9 European countries were recruited. The investigators and the patients used the SCORAD and PO-SCORAD scales, respectively, to assess AD severity at inclusion (D0) and 28 ± 7 days later (D28). Results: Patient-Oriented SCORing Atopic Dermatitis and SCORAD scores were significantly correlated at D0 [r = 0.67 (95% CI: 0.62; 0.72), P < 0.0001]. Consistency was confirmed at D28, with a stronger linear correlation between both scales [r = 0.79 (95% CI: 0.75; 0.83), P < 0.0001]. Absolute changes from baseline in SCORAD and PO-SCORAD scores were also significantly correlated [r= 0.71 (95% CI: 0.64; 0.76), P < 0.0001]. Although no specific intervention was investigated, AD improved over the study, with a decrease of PO-SCORAD and SCORAD scores from D0 to D28 by )19.19% and )24.39%, respectively. The consistency of the correlations was similar in the adult and children groups. Conclusions: This study validated the use of PO-SCORAD to self-assess AD severity and demonstrated its good correlation with SCORAD. Background. Atopic dermatitis (AD) is a chronic, relapsing allergic skin disease. The histamine H4 receptor (HRH4) has been shown to be associated with a number of autoimmune disorders, including AD. Aim. To explore a possible association between copy-number variations (CNVs) of the HRH4 gene and the risk of AD in a Chinese population. Methods. Genomic DNA and RNA were collected from 541 patients with AD and 613 healthy controls, and the CNVs and mRNA levels of HRH4 were examined. ELISA was used to measure the levels of IgE in all participants. Results. Amplifications of HRH4 copy numbers were associated with the risk of developing AD (P < 0.05, OR = 1.85, 95% CI 1.30–2.63), whereas deletions of HRH4 copy numbers were not associated with disease risk for AD (P = 0.30, OR = 0.82, 95% CI 0.57–1.19). HRH4 mRNA levels were much higher in samples with HRH4 copy-number amplifications than in those without such amplifications (P < 0.05). IgE levels were associated with amplifications (P < 0.05, OR = 1.96, 95% CI 1.19–3.25), but not with deletions (P = 0.63, OR = 0.87, 95% CI 0.49–1.54) of HRH4 copy numbers. Conclusions. CNVs of the HRH4 gene are associated with AD in a Chinese population. Introduction Atopic dermatitis (AD) is a chronic relapsing allergic skin disease characterized by typically distributed eczematous skin lesions and intense pruritus. AD affects 15–20% of children and 2–10% 2 of adults.1,2 The Correspondence: Dr Bo Yu, Dermatology Department, Peking University Shenzhen Hospital, no. 1120, Lianhua Road, Futian District, Shenzhen Guangdong 518036, China E-mail: [email protected] Conflict of interest: none declared. The first two authors have contributed equally to this study, and should be considered joint first authors. Accepted for publication 4 November 2012 aetiology of AD remains unclear, but it is recognized to be a complex genetic disorder. Family and twin studies also support a significant genetic predisposition to AD.3 Up to now, genetic studies have indicated that AD is associated with the Nod-like receptor (NLR) family genes, such as C3 and CD14.4–6 Histamine plays an important role in allergic and autoimmune diseases. Four histamine receptor subtypes, HRH1–4, have been identified. Of these, HRH1 and HRH2 are recognized as the main histamine receptor subtypes affecting inflammation and other immune responses, and have been used for treatment of AD and other immune and inflammatory diseases.7,8 HRH4 is the most recently described histamine receptor, which was independently cloned and characterized by several ª The Author(s) CED ª 2013 British Association of Dermatologists Clinical and Experimental Dermatology, 38, 295–301 Allergy 66 (2011) 1114–1121 ª 2011 John Wiley & Sons A/S 1114 CED Clinical and Experimental Dermatology CPD 295 NS ATORY INVESTIGATIO CLINICAL AND LABOR Pediatric Dermatology International Guidelines Etude sur la corticophobie 1–6, 2013 tion in Atopic Therapeutic Patient Educa Experiences Dermatitis: Worldwide M.D.,† Linda De Raeve, M.D., M.D.,* Alan Ball, B.A.,* M.D.,* Claire Bernier, Marcoux, M.D.,¶ Jean-Francois Stalder, Deleuran, M.D.,§ Danielle Uwe Gieler, M.D.,‡ Mette Sue Lewis-Jones, M.D.,‡‡ , M.D.,** Peter Lio, M.D.,†† Lawrence F. Eichenfield Christine Chiaverini, M.D.,*** ucation Roberto Takaoka, M.D.,¶¶ Carlo Gelmetti, M.D.,§§ and for the Oriented Patient-Ed M.D.,* Barbarot, bastien Sébastien (OPENED) Laurent Misery, M.D.,††† Network in Dermatology UZ Department of Dermatology Nantes, France, †Department ic Medicine, Nantes University Hospital, ‡Department Department of Psychosomat *Department of Dermatology , Aarhus University Brussel, Brussels, Belgium, Department of Dermatology §Department Brussels, Vrije Universiteit of Giessen, Giessen, Germany, Justine University Hospital, Montreal, Canada, , St. , Psychodermatology, University Department of Dermatology ¶Department Departmentt of Dermatology ††Departmen San Diego, California, Hospital, Aarhus, Denmark, Medical , Rady Children’s Hospital, , Ninewells Hospital and Departmentt of Dermatology **Departmen Departmentt of Dermatology Fondazione Chicago, Illinois, ‡‡Departmen and Dermatological Sciences, Care Intensive Children’s Memorial Hospital, , University of Sao Paulo Departmentt of Anesthesia, §§Departmen Departmentt of Dermatology ¶¶Departmen ent School, Dundee, Scotland, Department †††Departm Policlinico, Milan, Italy, Hospital, Nice, France, Ca’ Granda Ospedale Maggiore ***Departm ent of Dermatology, Archet Department Brazil, Hospital, Brest, France Medical School, Sao Paulo, of Dermatology, University has proven effective in patient education (TPE) of life (QoL) for Abstract: Therapeutic and improving quality adherence atopic dermatitis increasing treatment chronic diseases, especially TPE experiences patients with numerous worldwide undertaken to identify (AD). This study was located in 11 countries, from 23 hospitals, in TPE programs in AD treatment. Experts e on 10 major items. Patients AD or responded to a questionnair moderate to severe and adolescents with were used. were mainly children and collective approaches Individual QoL. varied from one to six markedly affected the number of sessions were Depending on the center, and 20 to 200 patients 12 hours of education), (corresponding to 2 to team comprised multidisciEach center’s education followed each year. psychologists). Evaluations nurses, doctors, (e.g., s some plinary professional satisfaction index, or assessment, QoL, a from were based on clinical was obtained, it came three. When funding companies (Germany), combination of the (France), insurance role regional health authorities pharmaceutical firms (Japan, Italy). The or in donations (United States), but their involvement was always highlighted, Despite of patient associations country to another. varied from one the increasing the TPE process our findings demonstrate the nonexhaustive approach, BJD British Journal of Dermatology C L I N I C A L A N D L A B O R A T O R Y I N V E S TI G A T I O N S Topical corticosteroid phobia in atopic dermatitis: a study of its nature, origins and frequency H. Aubert-Wastiaux, L. Moret,* A. Le Rhun,* A.M. Fontenoy,* J.M. Nguyen,* C. Leux,* L. Misery,� P. Young,� M. Chastaing,� N. Danou,§ P. Lombrail,* F. Boralevi,– J.P. Lacour,** J. Mazereeuw-Hautier,�� J.-F. Stalder and S. Barbarot The FASEB Journal article fj.10-168658. Published online January 31, 2011. Department of Dermatology, CHU Hôtel-Dieu, 1 place Alexis Ricordeau, 44035 Nantes Cedex 1, France *PIMESP (Pôle d’Information Médicale et de Santé Publique), CHU Hôtel-Dieu, Nantes, France �Department of Dermatology, CHU Morvan, Brest, France �Dermatologist, Rouen, France §Dermatologist, Paris, France –Pediatric Dermatology Unit, Hôpital Pellegrin-Enfants, CHU Bordeaux, Bordeaux, France **Department of Dermatology, CHU Archet, Nice, France ��Department of Dermatology, CHU Larrey, Toulouse, France The FASEB Journal • Research Communication Hélène Hele Hé lèlene Aubert-Wastiaux. E-mail: [email protected] Accepted for publication 28 May 2011 Funding sources This study was sponsored by the Foundation for Atopic Dermatitis, Pierre Fabre Laboratoire (Toulouse, France), which provided funds to cover logistic expenses (e.g. printing the questionnaires), but had no access to the data collected and played no role in their analysis, the writing of the manuscript or the decision to submit it for publication. Conflicts of interest None declared. DOI 10.1111/j.1365-2133.2011.10449.x Background Topical corticosteroids remain the mainstay of atopic dermatitis therapy. Many atopic dermatitis therapeutic failures appear to be attributable to poor adherence to treatment due to topical corticosteroid phobia. Objectives To assess the facets, origins and frequency of fear of topical corticosteroid use among patients with atopic dermatitis. Methods A questionnaire comprising 69 items, generated from information gathered during interviews with 21 patients and 15 health professionals, was given to consecutive patients consulting at the outpatient dermatology departments of five regional university hospitals or with 53 dermatologists in private practice. Results A total of 208 questionnaires were analysed (including 144 from parents 80Æ7% of the and 87 from adult patients, 27 of whom were also parents); 80 respondents reported having fears about topical corticosteroids and 36% admitted nonadherence to treatment. A correlation was found between topical corticosteroid phobia and the need for reassurance, the belief that topical corticosteroids pass through the skin into the bloodstream, a prior adverse event, inconsistent information about the quantity of cream to apply, a desire to self-treat for the shortest time possible or poor treatment adherence. Topical corticosteroid phobia was not correlated with atopic dermatitis severity. Conclusion Topical corticosteroid phobia is a genuine and complex phenomenon, common among French patients with atopic dermatitis, that has an important impact on treatment compliance. As defined by the U.K. Working Party’s diagnostic criteria,1 atopic dermatitis (AD) is a relapsing, chronic, inflammatory, cutaneous disorder that occurs mainly in childhood and sometimes persists into adulthood. AD currently affects 10–20% of children worldwide.2,3 It is a public health concern because of its prevalence, cost and impact on quality of life.4,5 Thus, the broad impact of AD warrants optimization of relevant support services. Topical corticosteroids (TCS), the mainstay of AD treatment, are often required for months or years to control the disease. Although they have long been known to have side-effects, their efficacy and safety, when used appropriately, are well established.6–10 Why some patients with AD do not respond to TCS remains unexplained, but poor adherence to the prescribed regimen may underlie treatment failure. Indeed, adherence by patients with AD is known to be poor, at ~30%,11 as it is for other chronic diseases.12 What is usually called corticosteroid phobia is frequent. Corticosteroid phobia is certainly a misnomer because the term ‘phobia’ defines an irrational fear.13 In fact, corticosteroid phobia is the dedicated term to describe all types of fear about steroid use. In routine clinical practice, it is not unusual for patients to express fear or anxiety about using TCS and TCS phobia appears to be common (60–73% of patients),14,15 potentially leading to poor adherence and lack of response to � 2011 The Authors 808 DOI: 10.1111/pde.12024 1 Julie Henry,* Chiung-Yueh Hsu,* Marek Haftek,† Rachida Nachat,* Heleen D. de Koning,‡ Isabelle Gardinal-Galera,*,§ Kiyotaka Hitomi,� Stéfana Balica,§ Catherine Jean-Decoster,¶ Anne-Marie Schmitt,¶ Carle Paul,*,§ Guy Serre,* and Michel Simon*,1 Summary Correspondence M.D., Service to Jean Francois Stalder, Address correspondence 44035 Nantes, de Nantes–Hôtel Dieu, de Dermatologie, CHU com. France, or e-mail: jfstalder@mac. Hornerin is a component of the epidermal cornified cell envelopes BJD � 2011 British Association of Dermatologists 2011 165, pp808–814 Inc. © 2013 Wiley Periodicals, *Centre National de la Recherche Scientifique (CNRS)-Toulouse III University UMR5165, Institut Fédératif de Recherche 150 (INSERM-CNRS-Université Paul Sabatier-Centre Hospitalier Universitaire), Toulouse, France; †Lyon I University EA4169, Lyon, France; ‡Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; § Department of Dermatology, Toulouse University Hospital, Toulouse, France; �Graduate School of Bioagricultural Sciences, Nagoya University, Naboya, Japan; and ¶Centre Européen de Recherche sur la Peau et les Epithéliums de Revêtement, Pierre Fabre Dermo-Cosmétique, Toulouse, France A single-nucleotide polymorphism within the gene encoding hornerin (HRNR) has recently been linked with atopic dermatitis (AD) susceptibility. HRNR shares features with filaggrin, a key protein for keratinocyte differentiation, but conflicting reports have been published concerning its expression in the epidermis, and its role is still unknown. To analyze HRNR expression and function in the epidermis, anti-HRNR antibodies were produced and used in Western blot analysis and immunohistochemical, confocal, and immunoelectron microscopy analyses of human skin and of cornified cell envelopes purified from plantar stratum corneum. We also tested whether HRNR was a substrate of transglutaminases. In the epidermis, HRNR was detected at the periphery of keratohyalin granules in the upper granular layer and at the corneocyte periphery in the whole cornified layer. Detected in Western blot analysis as numerous bands, HRNR was relatively insoluble and only extracted from epidermis with urea and/or reducing agents. The presence of HRNR in the purified envelopes was confirmed by immunoelectron microscopy and by Western blot analysis after V8-protease digestion. HRNR was shown to be a substrate of transglutaminase 3. These data demonstrate that HRNR is a component of cornified cell envelopes of human epidermis. Its reduced expression in AD may contribute to the epidermal barrier defect observed in the disease.—Henry, J., Hsu, C.-Y., Haftek, M., Nachat, R., de Koning, H. D., Gardinal-Galera, I., Hitomi, K., Balica, S., Jean-Decoster, C., Schmitt, A.-M., Paul, C., Serre, G., Simon, M. Hornerin is a component of the epidermal cornified cell envelopes. FASEB J. 25, 000– 000 (2011). www.fasebj.org ABSTRACT Etude sur la filaggrine Key Words: atopic dermatitis � skin � keratinocytes � transglutaminase � terminal differentiation � corneocytes Differentiation of the epidermis is an oriented process during which keratinocytes of the basal layer undergo a series of metabolic and structural changes 0892-6638/11/0025-0001 © FASEB throughout their migration to the surface of the skin. Cornification, the later stages of the process, is a real programmed cell death, and results in the formation of corneocytes. It is the stacking up of these anucleate cells, forming the outermost layer or stratum corneum (also called cornified layer), that enables the epidermis to fulfill one of its main functions: it provides a multiple barrier between the body and its environment by opposing water loss and the penetration of exogenous molecules, UV radiation, and pathogens, and by protecting the body, because of its great mechanical resistance. Alterations in keratinocyte differentiation are involved in the pathophysiology of many skin diseases, e.g.,, atopic dermatitis (AD; OMIM%603635). AD is a common chronic inflammatory skin disease affecting 15–20% of children and 1–3% of adults in industrialized countries. It is often linked with other atopic conditions, such as asthma and allergic rhinitis. AD results from complex interactions between genetic and environmental factors. The pathogenesis of the disease is still poorly understood, although immune system dysfunctions, as well as defects in the epidermal barrier, have long been suspected (1– 4). A major breakthrough was the discovery (5) that loss-of-function mutations in the gene encoding filaggrin (FLG) on chromosome 1q21 are a major risk factor for AD, with an estimated odds ratio �3 (for a review, see ref. 6). This strengthens the hypothesis of a stratum corneum failure as a primary event, potentially leading to increased penetration of allergens and skin inflammation (1, 2, 7). Indeed, FLG is an essential component of the stratum corneum. Correspondence: CNRS-UPS UMR5165, CHU Purpan, Pl. du Dr Baylac TSA40031, 31059 Toulouse cedex 9, France. E-mail: [email protected] doi: 10.1096/fj.10-168658 This article includes supplemental data. Please visit http:// www.fasebj.org to obtain this information. 1 Développer l’éducation thérapeutique dans la dermatite atopique Collaboration avec plus de 35 centres dans le monde Les outils d’éducation thérapeutique Vous ou votre enfant avez un eczéma atopique pique c’est... L’eczéma ato N L’ecz c fair q ue e ? ScoRaD po- t... ’es ém a atopique Poussée Poussée Une évolution é par poussées po atopique c ’ L’ecz ma D -ScoRaD Accalmie qu e faire ? Accalmie s Le conseils ... e st Des dossiers de formation res s et inflammatoi Des plaques rouge Une peau sèche Un chevalet pédagogique sur la dermatite atopique Le jeu de l’oie d e La Fondation pour la Dermatite Atopique remercie le Professeur Carlo Gelmetti pour sa collaboration dans la conception et la réalisation de ce document. l ’ a t o p i e Poster et BD : «Comment appliquer ta crème en images» 11 12 2 11 6 12 5 2 8 6 12 Les cartes PO SCORAD l ’ h o r l o g e 7 6 12 4 8 2 10 5 11 6 12 5 2 3 8 4 7 6 5 3 6 12 5 1 2 3 9 8 4 7 de l’atopie 1 10 9 5 1 4 7 4 7 6 12 2 11 3 8 3 4 7 11 9 1 9 2 10 3 10 5 1 8 5 1 2 11 11 6 12 9 4 7 11 10 9 3 4 7 10 3 9 2 8 L’horlo ge 1 10 1 9 4 7 12 10 3 8 8 FONDATION POUR LA DERMATITE ATOPIQUE : RECHERCHE ET EDUCATION Siège social : Hôtel-Dieu Saint Jacques - 2, rue Viguerie - 31000 TOULOUSE Tel. : 33 (5) 63 58 88 95 11 1 10 9 11 6 12 5 1 10 2 Pour les parents et le corps enseignant Mon enfant a de l’eczéma ? 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