Quick Guide to Contact Dermatitis. Jeanne Duus Johansen Jean-Pierre Lepoittevin Jacob P. Thyssen Editors

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1 Quick Guide to Contact Dermatitis Jeanne Duus Johansen Jean-Pierre Lepoittevin Jacob P. Thyssen Editors 123

2 Quick Guide to Contact Dermatitis

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4 Jeanne Duus Johansen Jean-Pierre Lepoittevin Jacob P. Thyssen Editors Quick Guide to Contact Dermatitis

5 Editors Jeanne Duus Johansen Gentofte Hospital National Allergy Research Centre Hellerup, Denmark Jacob P. Thyssen Department of Dermato-Allergology Gentofte Hospital Hellerup, Denmark Jean-Pierre Lepoittevin Laboratoire de Dermatochimie University of Strasbourg Strasbourg cedex, France ISBN DOI / ISBN (ebook) Library of Congress Control Number: Springer Heidelberg New York Dordrecht London Springer-Verlag Berlin Heidelberg 2016 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. Printed on acid-free paper Springer-Verlag GmbH Berlin Heidelberg is part of Springer Science+Business Media (

6 Contents Part I General Aspects 1 Immunological Background of Allergic Contact Dermatitis Thomas Rustemeyer 2 Clinical Features of Contact Dermatitis Niels K. Veien Part II Patch Testing Basics 3 Patch Testing Essentials Cecilia Svedman and Bruze Magnus 4 Testing with the Patient s Own Products An Goossens 5 Basics in Diagnostic Work Up and Assessment of Clinical Relevance Jeanne D. Johansen, Ulrik Fischer Friis, and Jacob P. Thyssen Part III Special Groups 6 Irritant Contact Dermatitis: Diagnosis and Risk Factors Marie-Louise Anna Schuttelaar 7 Photoreactions and Testing Margarida Gonçalo 8 Protein Contact Dermatitis and Testing Ana Gimenez-Arnau 9 Occupational Contact Dermatitis Anja Thielitz and Swen Malte John 10 Contact Dermatitis in Children Anne Birgitte Simonsen and Mette Sommerlund v

7 vi Contents Part IV Main Allergen Groups 11 Metals Anneli Julander 12 Fragrances Wolfgang Uter 13 Preservatives Klaus Ejner Andersen and Kristian Fredløv Mose 14 Rubber Vera Mahler Part V Allergens in Various Products 15 Textiles Laura Malinauskiene and Kristina Morgardt-Ryberg 16 Hair Dyes John McFadden 17 Dental Materials Marléne Isaksson 18 Shoes Sherry H. Yu, Apra Sood, and James S. Taylor 19 Gloves Kristiina Aalto-Korte 20 Glues Suchismita Paul and Peter C. Schalock 21 Metalworking Fluids Johannes Geier 22 Plants Christopher Lovell 23 Cosmetics Vanessa Smith and S. Mark Wilkinson 24 Worker s Protection: Gloves and Creams Britta Wulfhorst, Swen Malte John, and Meike Strunk 25 Overview of Allergens Present in the European, North American, and Chinese Baseline Series Jean-Pierre Lepoittevin and Christophe J. Le Coz

8 Contributors Kristiina Aalto-Korte, MD, PhD Health and Word Ability, Finnish Institute of Occupational Health, Helsinki, Finland Anne Birgitte Simonsen, MD Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark Klaus Ejner Andersen, MD, DMsc Department of Dermatology and Allergy Centre, Odense University Hospital, University of Southern Denmark, Odense, Denmark Ulrik Fischer-Friis, PhD Department of Derma-Allergology, National Allergy Research Centre, Copenhagen University Hospital Gentofte, Hellerup, Denmark Kristian Fredløv Mose, MD Department of Dermatology and Allergy Centre, Odense University Hospital, University of Southern Denmark, Odense, Denmark Johannes Geier, MD IVDK, University of Göttingen, Göttingen, Germany Ana Gimenez-Arnau, MD, PhD Department of Dermatology, Hospital del Mar. Universitat Autònoma de Barcelona, Barcelona, Spain Margarida Gonçalo, MD Clinic of Dermatology, University Hospital and Faculty of Medicine, University of Coimbra, Coimbra, Portugal An Goossens, RParm, PhD Contact Allergy Unit, Department of Dermatology, University Hospital K.U.Leuven, Leuven, Belgium Marléne Isaksson, MD, PhD Department of Occupational and Environmental Dermatology, Skåne University Hospital, Malmö, Skåne, Sweden Jeanne Duus Johansen, MD DMsc Department of Dermato-allergology, National Allergy Research Centre, Copenhagen University Hospital Gentofte, Hellerup, Denmark Anneli Julander, PhD Unit of Occupational and Environmental Dermatology, Karolinska Institutet, Institute of Environmental Medicine, Stockholm, Sweden Christophe J. Le Coz, MD Laboratoire de Dermatochimie, University of Strasbourg, ILB, Strasbourg, France vii

9 viii Contributors Jean-Pierre Lepoittevin, DSc Laboratoire de Dermatochimie, University of Strasbourg, ILB, Strasbourg, France Christopher Lovell, MB, ChB, MD, FRCP Department of Dermatology, Royal United Hospital, Bath NHS Trust RD1, Bath, UK Bruze Magnus, MD, PhD Department of Occupational and Environmental Dermatology, University Hospital, University of Lund, Malmö, Sweden Vera Mahler, MD Department of Dermatology, University Hospital of Erlangen, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Bavaria, Germany Laura Malinauskiene, MD, PhD Department of Occupational and Environmental Dermatology, Lund University, Skåne University Hospital, Malmö, Sweden Department of Pulmonology and Allergology, Vilnius University Hospital Santariskiu Clinics, Vilnius, Lithuania Swen Malte John, MD, PhD Department of Dermatology, Environmental Medicine and Health Theory, Lower Saxonian Institute of Occupational Dermatology (NIB), University of Osnabrueck, Osnabrück, Germany John McFadden, BM, DM, FRCP Department of Cutaneous Allergy, St John s Institute of Dermatology, St Thomas Hospital, King s College, London, UK Kristina Morgardt-Ryberg, MD, PhD Department of Occupational and Environmental Dermatology, Lund University, Skåne University Hospital, Malmö, Sweden Department of Dermatology, Uddevalla Hospital, Uddevalla, Sweden Suchismita Paul, BA Harvard Medical School, Boston, MA, USA Thomas Rustemeyer, MD, PhD Department of Dermatology and Allergology, VU university medical center, Amsterdam, The Netherlands Peter C. Schalock, MD Department of Dermatology, Massachusetts General Hospital, Harvard Medical School/Dermatology, Boston, MA, USA Marie-Louise Anna Schuttelaar, MD, PhD Department of Dermatology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands Vanessa Smith, MRCP Department of Dermatology, Leeds Teaching Hospitals NHS Trust, Leeds, UK Mette Sommerlund, MD, PhD Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark Apra Sood, MD Department of Dermatology and Plastic Surgery, Cleveland Clinic, Cleveland, OH, USA

10 Contributors ix Meike Strunk Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabrueck, Osnabrueck, Germany Cecilia Svedman, MD, PhD Department of Occupational and Environmental Dermatology, Skane University Hospital, University of Lund, Malmö, Sweden James S. Taylor, MD Dermatology-Plastic Surgery Institute, Cleveland Clinic, Cleveland, OH, USA Anja Thielitz, MD Department of Dermatology, Institute for Interdisciplinary Dermatologic Prevention and Rehabilitation (iderm) of the University of Osnabrück, Dermatologic Centre, Trauma Hospital, Hamburg, Germany Jacob P. Thyssen, MD, PhD Department of Dermato-Allergology, Allergy Research Centre, Copenhagen University Hospital Gentofte, Hellerup, Denmark Wolfgang Uter, MD, PhD Department of Medical Informatics, Biometry and Epidemiology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Erlangen, Germany Niels K. Veien, MD, PhD Honorary professor of Dermatology, University of Aarhus, Aarhus, Denmark S. Mark Wilkinson, MD, FRCP Department of Dermatology, Leeds Teaching Hospitals NHS Trust, Leeds, UK Britta Wulfhorst Faculty of Human Sciences, Medical School Hamburg, Hamburg, Germany Sherry H. Yu, BS, BA School of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USA

11 Part I General Aspects

12 Immunological Background of Allergic Contact Dermatitis 1 Thomas Rustemeyer Contents 1.1 Introduction Allergens Antigen-Presenting Cells Priming of Allergen-Specific T Cells Elicitation Reaction Immunological Tolerance Further Reading Abbreviations APC CCL CCR CD IFN-γ IL MHC TGF-β Th Antigen-presenting cells C-C chemokine ligand C-C chemokine receptor Classification determinant Interferon-γ Interleukin Major histocompatibility complex Transforming growth factor-β T-helper cell T. Rustemeyer, MD, PhD Department of Dermatology and Allergology, VU University Medical Center, De Boelelaan 1117, Amsterdam 1081 HV, The Netherlands t.rustemeyer@vumc.nl Springer-Verlag Berlin Heidelberg 2016 J.D. Johansen et al. (eds.), Quick Guide to Contact Dermatitis, DOI / _1 3

13 4 T. Rustemeyer 1.1 Introduction Allergic contact dermatitis is an acquired immunological inflammation in response to contact with specific allergens which are recognized by pro-inflammatory T cells. The majority of contact allergens are small molecules which can penetrate the epidermal barrier. In the skin, dendritic cells can pick up the allergen and present it on their cellular surface in the context of MHC class I and/or class II molecules. The release of unspecific danger signals facilitates the activation of dendritic cells. This allows for the maturation of allergen-presenting dendritic cells in the epidermis and dermis. The activated and fully matured dendritic cells migrate to the draining lymph nodes and present the allergen to T cells. They start to proliferate and form effector cells, which can get activated upon contact to their specific allergen. From now on, allergen contacts can induce allergen-specific T-cell-mediated immune responses with the clinical picture of allergic contact dermatitis. In the following sections, all major immunological events will be discussed (Fig. 1.1 ). 1.2 Allergens Most of the contact allergens are small and chemically reactive molecules not exceeding a molecular weight of 800 Dalton. Due to their size, they can penetrate through the epidermal barrier. In the epidermis and dermis, they can react with endogenous peptides and form immunologically relevant allergen-carrier complex. For some allergens, an enzymatic of metabolic activation step is needed to generate the actual allergen. In principal, all contact allergens have to a certain extent irritant properties. This irritancy can add to the allergenic potency by triggering the release of innate danger signals from immune cells. 1.3 Antigen-Presenting Cells In the epidermis and dermis are different types of professional antigen-presenting dendritic cells. Their common feature is the capacity to pick up and present antigens to other cells of the immune system. The epidermal antigen-presenting cells are called Langerhans cells, and the dermal types are summarized as dermal dendritic cells. Upon contact with contact allergens, dendritic cells get activated. The release of pro-inflammatory danger signals from surrounding cells or directly from the dendritic cells amplifies this activation. Under the inflammatory pressure, dendritic cells get fully matured and start to emigrate from (epi)dermal structures via the lymphatic vessels toward the draining lymph nodes. Here, they get attracted by chemokines binding to the chemokine receptor CCR7, which is expressed on the cellular surface of matured dendritic cells. This allows antigen-presenting cells to settle in the subcapsular compartments of the draining lymph nodes.

14 1 Immunological Background of Allergic Contact Dermatitis 5 sensitization elicitation hapten epidermis LC KC dermis migration & maturation inflammatory cytokines afferent lymphatic vessel draining lymph node efferent lymphatic vessels thoracic duct blood circulation Fig. 1.1 Major immunological events in allergic contact dermatitis. In the induction phase of allergic contact dermatitis ( left side of the drawing), skin contact with a contact allergen triggers migration and maturation of antigen-presenting cells ( APC ). These cells reach via the afferent lymphatic vessels the regional skin-draining lymph node. Allergen-presenting dendritic cells home into the T-cell-rich paracortical areas. Here, local conditions are optimal for encountering naive T cells that recognize allergen MHC molecule complexes. During T-cell priming, hapten-specific T cells strongly proliferate and generate effector and memory cells, which are partly released into the circulation. Renewed allergen contact leads to the elicitation reaction (shown at the right side ). Allergen- specific effector T cells are triggered to produce pro-inflammatory cytokines. Thereby, more inflammatory cells are recruited to the allergen contact site which results in strong local inflammatory mediator release. This leads to a gradually increasing inflammatory reaction, reaching a maximum within one to few days, after which reactivity successively declines ( Kanerva s Occupational Dermatology, 2012 Editors: Thomas Rustemeyer, Peter Elsner, Swen-Malte John, Howard I. Maibach et al. Springer-Verlag Berlin Heidelberg 2012, with Permission of Springer Science+Business Media) 1.4 Priming of Allergen-Specific T Cells In the draining lymph nodes, naive T cells can extravasate from capillaries and patrol in the subcapsular compartments. If they encounter properly presented antigen which fits in the groves of their specific T-cell receptors, they get the first signal for getting activated ( antigen-specific signal ). If the antigen is presented in the context of MHC class I molecules on the surface of the dendritic cell, then CD8 + T cells do recognize it. In analogy, presentation of antigen by MHC class II molecules results in the recognition by CD4 + T cells. The second signal consists of sufficient interaction of co-stimulatory cell membrane-bound signals of both matured

15 6 T. Rustemeyer dendritic cells and naive T cells ( receptor-mediated co-stimulatory signal ). These two signals stimulate the priming of allergen-specific T cells from the naive state into the antigen-experienced state. The primed T cells start to proliferate, which can result in swelling of the lymph node. The presence of soluble immunological mediators in the microenvironment of the T cells can skew developing T cells toward distinct effector subtypes (third signal: cytokine-driven T-cell skewing ). These local cytokines are generated by antigen-matured dendritic cells and by resident stromal cells of the lymph node. As a consequence, the generating allergen-specific T cells can either become pro-inflammatory cells or immunoregulatory T cells. The first T-cell types can be subdivided into Th1 cells, characterized by the production of IFN-γ in particular; Th2 with a predominant production of IL-4, IL-5, and IL-13; and Th17 with high IL-17 and IL-23 production. The latter T cells have immunoregulatory properties and can either actively suppress pro-inflammatory reactions, then they are called suppressor T cells or cause antigen-specific tolerance. These cells are characterized by the release of immunosuppressive/-regulatory cytokines such as IL-10 and TGF-β. Furthermore, a subset of primed T cells keep homing receptors to settle in the draining lymph node. These cells express CCR7 and bind their ligand CCL19 expressed in the subcapsular compartment. They form the longterm immunological memory and are called central memory T cells. In contrast, CCR7 - T cells have to leave the lymph node and become peripheral effector/memory T cells. These T cells recirculate in the blood and control peripheral tissues. In summary, during the priming of allergen-specific T cells, functionally different subsets can develop. These subsets determine the immunological outcome and clinical appearance of the elicitation reaction in allergic contact dermatitis. 1.5 Elicitation Reaction In case of repeated contact with the specific allergen, an elicitation reaction can occur. Hereto, less allergen suffices to stimulate the immunological reaction. As during the sensitization reaction, allergen binds to endogenous peptides and proteins and gets presented by antigen-presenting cells. In contrast to the sensitization reaction, also nonprofessional antigen-presenting cells such as keratinocytes and endothelial cells can present the allergen in a sufficient manner to stimulate allergenspecific T cells since these primed T cells are not longer dependent on the allergen presentation by professional antigen-presenting cells. When the allergen gets detected by randomly bypassing allergen-specific T cells, they start to produce and to secrete their specific cytokines. In case of a developing allergic contact dermatitis reaction, pro-inflammatory effector T cells belonging to Th1, Th2, or Th17 subsets secrete pro-inflammatory cytokines. This drives the attraction and subsequent activation of infiltrated immunological cells and resident tissue cells. The massive release of inflammatory mediators causes vasodilatation, edema, spongiosis, and vesiculation. The development of this delayed immunological response can take several days. In later phases of acute allergic contact dermatitis reactions, the allergen is eliminated by either metabolization or taken away by phagocytes. As a