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J. Marie Lachapelle - Patch Testing and Prick Testing: A Practical Guide Official Publication of the ICDRG

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J. Marie Lachapelle Patch Testing and Prick Testing: A Practical Guide Official Publication of the ICDRG

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Knowledge in the field of allergic contact dermatitis continues to expand rapidly owing to progress in the chemical, immunological, and clinical fields, including improved techniques of patch testing and prick testing. The third edition of this important book, which includes additional color illustrations, has been extensively revised, updated, and expanded to reflect the most recent developments. These include advances in patch testing methodology, in particular the new chambers that are appearing on the market, revision of the baseline series of patch tests to reflect the latest evidence-based work, and additional testing procedures. The result is a superb guide to the current management of positive and negative patch test and prick test reactions that will be invaluable for all practicing dermatologists, from the beginner to the well-trained expert.

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Part 1
Patch Testing
Jean-Marie Lachapelle and Howard I. Maibach Patch Testing and Prick Testing 3rd ed. 2012 A Practical Guide Official Publication of the ICDRG 10.1007/978-3-642-25492-5_1 Springer-Verlag Berlin Heidelberg 2012
1. Pathophysiology of Allergic and Irritant Contact Dermatitis
Audrey Nosbaum 1, Jean-Franois Nicolas 1 and Jean-Marie Lachapelle 2
(1)
Department of Allergy and Clinical Immunology, University Hospital Lyon-Sud, Pierre-Bnite, Cedex, France
(2)
Department of Dermatology, Catholic, University of Louvain, Brussels, Belgium
Abstract
Contact dermatitis comprises two main groups: irritant (ICD) and allergic (ACD) contact dermatitis. It presents as acute, subacute, or chronic eczema. Although it is possible to differentiate ICD from ACD on clinical ground, both diseases can have very similar clinical, histological, and molecular presentations.
The mechanisms at the origin of the eczema are different in the two types of dermatitis, at least as far as the initiation stages of the skin inflammation are concerned. ICD is a nonspecific inflammatory dermatosis, mainly due to the toxicity of chemicals on the skin cells which triggers inflammation by activation of the skin innate immune system.
1.1 Introduction
Contact dermatitis comprises two main groups: irritant (ICD) and allergic (ACD) contact dermatitis. It presents as acute, subacute, or chronic eczema. Although it is possible to differentiate ICD from ACD on clinical ground, both diseases can have very similar clinical, histological, and molecular presentations.
The mechanisms at the origin of the eczema are different in the two types of dermatitis, at least as far as the initiation stages of the skin inflammation are concerned (Fig. ].
Fig 11 Mechanisms of irritant and allergic contact dermatitis ICD and ACD - photo 1
Fig. 1.1
Mechanisms of irritant and allergic contact dermatitis.
ICD and ACD are induced by skin contact with chemicals. The early stages are different as the chemical is pro-inflammatory by its direct toxicity on the skin cells in ICD while the active chemical triggers an inflammatory reaction mediated by specific T cells in ACD. The later stages giving rise to an eczema lesion are, on the other hand, very similar and involve cytokines, chemokines, phenomena of apoptosis, cellular necrosis, and the recruitment of a polymorphic inflammatory infiltrate. This explains why ACD and ICD lesions can be confused clinically and histologically
1.2 Pathophysiology of Irritant and Allergic Skin Inflammation
ICD has long been considered as a nonimmunological inflammation, whereas ACD as an immunological inflammation. In fact, both types of eczema implicate the immune cells, but ICD follows the activation of innate immunity, while ACD is the result of acquired immunity and the induction of specific proinflammatory T cell effectors []. It should be noted that the development of ACD initially requires the activation of innate immune cells which permit maturation of the cutaneous dendritic cells. The dendritic cells are then required for the presentation of allergens to T cells in the lymph nodes and thus to the induction of an acquired immune response.
1.2.1 Irritant and/or Allergic Chemicals
All chemicals, whether they are responsible for ICD or ACD, can be considered as irritants with very important differences in the concentrations necessary to induce irritation []. For example, dinitrofluorobenzene (DNFB) is an irritant at 0.05%, while geraniol is an irritant at 50%. On the other hand, only those chemicals which behave as haptens are allergens. Indeed, they interact in a covalent manner or not, with amino acids, and thus are able to modify the proteins giving rise to neoantigens. Contact allergens are thus only a minority of chemicals.
Skin contact with an irritant may only induce an ICD. However, contact with a hapten can induce ICD or ACD, the latter occurring only if the individual has been immunized during the previous skin exposures to the same chemical.
1.2.2 Skin Irritation: Activation of Innate Immunity
1.2.2.1 Innate Immunity
Innate immunity refers to all the cells and molecules capable of distinguishing danger signals of an infectious, physical, or chemical nature and of inducing an inflammatory reaction. The inflammation enables the individual to eliminate the infection and repair the damage caused by the physical and/or chemical agents (wound healing). Innate immunity is therefore synonymous with inflammation. In the blood, the innate immune cells are the hematopoietic cells, with the exception of T and B lymphocytes, which form the acquired arm of the immune response. In the skin, the totality of the epidermal and dermal cells participates to the skin innate immunity. The recognition of chemicals as dangerous molecules for the body (i.e., xenobiotics) is very similar to that of microorganisms which deliver danger signals through interaction with a set of membranous and intercellular receptors, e.g., Toll-like (TLR) and NOD-like receptors (NLR) []. This leads to the activation of the inflammasome and the NF-B pathways, resulting in the production of inflammatory cytokines and chemokines, among which are IL-1, IL-3, IL-6, IL-8, and TNF-. Molecules of innate immunity also include the complement, the plasmatic enzyme systems of coagulation and fibrinolysis, interferons, etc.
1.2.2.2 Skin Irritation: Mechanisms of Action
The penetration of a chemical through the different layers of the skin, notably the epidermis and the dermis, is responsible for the release of a large number of cytokines and chemokines by different cell types whose respective roles in the induction of inflammation are not yet well understood [].
The profile of cytokine expression during ICD varies over time and also depends on the nature, environment, and dose of the chemical. The most frequently found mediators of ICD are IL-1 (interleukin-1), IL-1, IL-6, IL-8, TNF- ( tumor necrosis factor -), GM-CSF ( granulocyte/macrophage colony-stimulating factor ), and IL-10, which is an anti-inflammatory cytokine []. However, initiation of the inflammation seems to be mainly linked to IL-1, TNF-, and derivatives of arachidonic acid. Indeed, IL-1 and TNF- are two primary cytokines capable of inducing secondary mediators (including numerous cytokines, chemokines, adhesion molecules, growth factors) which are essential for the recruitment of leukocytes to the altered skin site. Thus, a multistep cascade in the production of inflammatory mediators takes place, finally inducing histological modifications followed by the clinical expression of eczema.
1.2.2.3 Direct Responsibility of the Chemical in ICD
In ICD, the chemical is directly responsible for the cutaneous inflammation by its toxic physicochemical properties, which are proinflammatory. The analysis of the inflammation of the ICD finds all the characteristics of a nonspecific inflammatory reaction, i.e., a hyperproduction of cytokines and chemokines, the presence of a polymorphic inflammatory infiltrate, and lesions of apoptosis/necrosis of the epidermal cells with a compensatory proliferation of keratinocytes. There is no argument for an involvement of T cells.
1.3 Skin Allergy: The Role of Specific Immunity
1.3.1 Antigen-Specific Immunity
Specific immunity involves B cells (humoral immunity) and T cells (cellular immunity). Specific immunity takes care of the immune memory which protects us from reinfection but which is also responsible for the chronicity of eczema in allergic patients.
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