Quick Guide To Contact Dermatitis Optimized EPUB Download
Uploaded by
gh.uyn.hghoangroongnamQuick Guide To Contact Dermatitis Optimized EPUB Download
Uploaded by
gh.uyn.hghoangroongnamQuick Guide to Contact Dermatitis
Visit the link below to download the full version of this book:
https://medipdf.com/product/quick-guide-to-contact-dermatitis/
Click Download Now
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
Contributors
Kristiina Aalto-Korte
Health and Word Ability, Finnish Institute of Occupational Health, Helsinki,
Finland
Anne Birgitte Simonsen
Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark
Klaus Ejner Andersen
Department of Dermatology and Allergy Centre, Odense University
Hospital, University of Southern Denmark, Odense, Denmark
Ulrik Fischer-Friis
Department of Derma-Allergology, National Allergy Research Centre,
Copenhagen University Hospital Gentofte, Hellerup, Denmark
Kristian Fredløv Mose
Department of Dermatology and Allergy Centre, Odense University
Hospital, University of Southern Denmark, Odense, Denmark
Johannes Geier
IVDK, University of Göttingen, Göttingen, Germany
Ana Gimenez-Arnau
Department of Dermatology, Hospital del Mar. Universitat Autònoma de
Barcelona, Barcelona, Spain
Margarida Gonçalo
Clinic of Dermatology, University Hospital and Faculty of Medicine,
University of Coimbra, Coimbra, Portugal
An Goossens
Contact Allergy Unit, Department of Dermatology, University Hospital
K.U.Leuven, Leuven, Belgium
Marléne Isaksson
Department of Occupational and Environmental Dermatology, Skåne
University Hospital, Malmö, Skåne, Sweden
Jeanne Duus Johansen
Department of Dermato-allergology, National Allergy Research Centre,
Copenhagen University Hospital Gentofte, Hellerup, Denmark
Anneli Julander
Unit of Occupational and Environmental Dermatology, Karolinska
Institutet, Institute of Environmental Medicine, Stockholm, Sweden
Christophe J. Le Coz
Laboratoire de Dermatochimie, University of Strasbourg, ILB, Strasbourg,
France
Jean-Pierre Lepoittevin
Laboratoire de Dermatochimie, University of Strasbourg, ILB, Strasbourg,
France
Christopher Lovell
Department of Dermatology, Royal United Hospital, Bath NHS Trust –
RD1, Bath, UK
Bruze Magnus
Department of Occupational and Environmental Dermatology, University
Hospital, University of Lund, Malmö, Sweden
Vera Mahler
Department of Dermatology, University Hospital of Erlangen, Friedrich-
Alexander-University of Erlangen-Nuremberg, Erlangen, Bavaria, Germany
Laura Malinauskiene
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
Department of Dermatology, Environmental Medicine and Health Theory,
Lower Saxonian Institute of Occupational Dermatology (NIB), University
of Osnabrueck, Osnabrück, Germany
John McFadden
Department of Cutaneous Allergy, St John’s Institute of Dermatology, St
Thomas’ Hospital, King’s College, London, UK
Kristina Morgardt-Ryberg
Department of Occupational and Environmental Dermatology, Lund
University, Skåne University Hospital, Malmö, Sweden
Department of Dermatology, Uddevalla Hospital, Uddevalla, Sweden
Suchismita Paul
Harvard Medical School, Boston, MA, USA
Thomas Rustemeyer
Department of Dermatology and Allergology, VU university medical center,
Amsterdam, The Netherlands
Peter C. Schalock
Department of Dermatology, Massachusetts General Hospital, Harvard
Medical School/Dermatology, Boston, MA, USA
Marie-Louise Anna Schuttelaar
Department of Dermatology, University Medical Center Groningen,
University of Groningen, Groningen, The Netherlands
Vanessa Smith
Department of Dermatology, Leeds Teaching Hospitals NHS Trust, Leeds,
UK
Mette Sommerlund
Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark
Apra Sood
Department of Dermatology and Plastic Surgery, Cleveland Clinic,
Cleveland, OH, USA
Meike Strunk
Department of Dermatology, Environmental Medicine and Health Theory,
University of Osnabrueck, Osnabrueck, Germany
Cecilia Svedman
Department of Occupational and Environmental Dermatology, Skane
University Hospital, University of Lund, Malmö, Sweden
James S. Taylor
Dermatology-Plastic Surgery Institute, Cleveland Clinic, Cleveland, OH,
USA
Anja Thielitz
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
Department of Dermato-Allergology, Allergy Research Centre, Copenhagen
University Hospital Gentofte, Hellerup, Denmark
Wolfgang Uter
Department of Medical Informatics, Biometry and Epidemiology, Friedrich-
Alexander University Erlangen-Nürnberg, Erlangen, Erlangen, Germany
Niels K. Veien
Honorary professor of Dermatology, University of Aarhus, Aarhus,
Denmark
S. Mark Wilkinson
Department of Dermatology, Leeds Teaching Hospitals NHS Trust, Leeds,
UK
Britta Wulfhorst
Faculty of Human Sciences, Medical School Hamburg, Hamburg, Germany
Sherry H. Yu
School of Medicine, Case Western Reserve University School of Medicine,
Cleveland, OH, USA
Part I
General Aspects
© Springer-Verlag Berlin Heidelberg 2016
Jeanne Duus Johansen, Jean-Pierre Lepoittevin and Jacob P. Thyssen (eds.), Quick Guide to Contact
Dermatitis, DOI 10.1007/978-3-662-47714-4_1
1. Immunological Background of
Allergic Contact Dermatitis
Thomas Rustemeyer1
(1) Department of Dermatology and Allergology, VU University Medical
Center, De Boelelaan 1117, Amsterdam, 1081 HV, The Netherlands
Thomas Rustemeyer
Email: [email protected]
1.1 Introduction
1.2 Allergens
1.3 Antigen-Presenting Cells
1.4 Priming of Allergen-Specific T Cells
1.5 Elicitation Reaction
1.6 Immunological Tolerance
Further Reading
Keywords Immunology – T cell – Dendritic cell – Langerhans cell –
Irritancy – Contact allergen – Skin barrier – Cytokine – Local skin memory
– Immunological tolerance
Abbreviations
APC Antigen-presenting cells
CCL C-C chemokine ligand
CCR C-C chemokine receptor
CD Classification determinant
IFN-γ Interferon-γ
IL Interleukin
MHC Major histocompatibility complex
TGF-β Transforming growth factor-β
Th T-helper cell
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).
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)
1.2 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.
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 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 long-term
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 allergen-specific 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 consequence, the
inflammatory reaction starts to silence and fades away. In case of longer-
lasting allergen exposures, epidermal changes can occur with acanthosis
and hyperkeratosis and desquamation of the keratinocytes. Although
complete clinical healing can occur, few allergen-specific T cells can reside
at sites of former allergen exposure. These T cells form a local skin
memory. Upon repeated local allergen exposure, these cells get more easily
activated and can already show clinical reactions within several hours. The
residing allergen-specific cells cause a local lower activation threshold of
allergic contact dermatitis reactions.
1.6 Immunological Tolerance
Under certain conditions, the priming of allergen-specific T cells can result
in anti-inflammatory T cells. These T cells are rather immunosuppressive
and tolerogenic. In particular, primary allergen contacts via oral mucosa
seem to stimulate the generation of tolerogenic allergen-specific T cells.
Individuals who are tolerized in this way are protected from developing
sensitization and getting allergic contact dermatitis reactions at later
allergen contacts.
Further Reading
Rustemeyer T, Ingrid MW, van Hoogstraten B, von Blomberg ME, Gibbs S, Scheper, RJ.
Mechanisms of irritant and allergic contact dermatitis. In: Johansen JD, Frosch, PJ, Lepoittevin, J-P,
editors. Contact dermatitis. 5th ed; 2011. p. 43–91.
© Springer-Verlag Berlin Heidelberg 2016
Jeanne Duus Johansen, Jean-Pierre Lepoittevin and Jacob P. Thyssen (eds.), Quick Guide to Contact
Dermatitis, DOI 10.1007/978-3-662-47714-4_2
2. Clinical Features of Contact
Dermatitis
Niels K. Veien1
(1) Dermatology, University of Aarhus, Aarhus, Denmark
Niels K. Veien (Honorary professor)
Email: [email protected]
2.1 Introduction
2.2 Clinical Features
2.3 Regional Contact Dermatitis
2.3.1 Irritant Contact Dermatitis of the Scalp
2.3.2 Allergic Contact Dermatitis of the Scalp
2.3.3 Irritant Contact Dermatitis of the Face
2.3.4 Allergic Contact Dermatitis of the Face
2.3.5 Irritant Contact Dermatitis of the Trunk
2.3.6 Allergic Contact Dermatitis of the Trunk
2.3.7 Irritant Contact Dermatitis of the Hands
2.3.8 Allergic Contact Dermatitis of the Hands
2.3.9 Irritant Contact Dermatitis of the Feet
2.3.10 Allergic Contact Dermatitis of the Feet
2.3.11 Systemic Allergic Contact Dermatitis
2.4 Differential Diagnoses
References
