New insights into the role of T cells in atopic dermatitis and allergic contact dermatitis.
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Allergic contact dermatitis (ACD) in children is underrecognized. It is often confused with antibody-mediated allergies such as urticaria or allergic rhinitis, but the mechanism in ACD involves T lymphocytes and not antibody. Surprisingly, sensitization to common allergens is likely to occur in infancy. All contact allergens are weak allergens requiring repeated exposure over long periods of time. Detection of specific allergens is by epicutaneous (patch) testing and will provide the basis for allergen avoidance therapeutic strategies.
Contact dermatitis is a common condition that can be categorized as irritant dermatitis and allergic contact dermatitis. Although each of these conditions may have a similar presentation, allergic contact dermatitis is immunologically mediated, whereas irritant contact dermatitis is not. Contact dermatitis can be acute, subacute, or chronic, and each of these phases may progress into the next. Almost any substance may induce a cutaneous reaction, depending on its concentration, the duration of contact, and the condition of the contacted skin. It is estimated that there are more than 6 million chemicals in the environment; approximately 3000 are potential sensitizers. A careful history may identify the responsible agent. If the contactant is identified and eliminated, the contact dermatitis can be a self-limited, mild condition. If the exposure is not discontinued, a cycle of itching, scratching, and skin disruption occurs, which leads to chronic changes in the skin. The history of presentation, including occupational exposures, and distribution of the rash are important in identifying the offending agent. More severe cases may require more extensive evaluation, possibly including patch testing, to determine the offending agent. This article reviews treatment, including antihistamines, topical and oral steroids, physical measures such as cold water compresses, and the treatment of secondary infection.
Allergic contact dermatitis (ACD) to haptens can serve as a valuable paradigm for understanding the physiopathology of T cell mediated immune responses. In sensitized individuals, exposure to the relevant hapten initiates clinical expression of ACD, which depends on the rapid activation of specific T cells. Mechanisms of tissue damage include direct cytotoxicity against keratinocytes, mostly mediated by CD8+ T cells, and T cell release of cytokines, which amplify the inflammatory response by targeting resident skin cells. The expression of ACD is actively regulated by specialized subsets of T lymphocytes with suppressive functions. In particular, T regulatory cells producing high levels of IL-10 suppress ACD by blocking the functions of dendritic cells. In contrast CD4+CD25+ regulatory T cells prevent immunopathological reactions and maintain peripheral tolerance to haptens by acting via a cell-to-cell contact mechanism. Understanding the role of suppressor T cells and the requirements for their in vivo and in vitro expansion are critical steps for the development of specific desensitization protocols in hapten-allergic individuals. This information may also provide the basis for novel interventions in other immune-mediated diseases.
According to the National Center for Health Statistics Survey, a large proportion of patients with contact dermatitis, atopic dermatitis, or eczema visit nondermatologists, and only approximately 40% visit dermatologists. Therefore, the prompt, proper diagnosis of the cause and prescription of precise treatment can be delayed. We wanted to create a clear understanding of the nuances of the allergic contact dermatitis and its effect on the economics and life quality of the patients for not only the dermatologists but also the primary care physicians. In an observational multicenter study planned for a span of 1 year with approximately 570 patients suspected of allergic contact dermatitis, data were collected at enrollment on their history, physical characteristics, and quality of life and were analyzed using routine statistical procedures. The "quality of life" data on these patients, most of whom have a history of long-standing disease, show a high correlation between the clinical factors such as symptom activity and frequency of episodes and the subscales of quality of life. These patients had a lesser score on mental and vital subscales (SF-36) than US population norms, showing a moderate impact of the disease on their mental health and vitality. There is an urgent need for a simpler and quicker method that could lead to an earlier and more precise diagnosis so the causal substance can be identified and avoided and the disease treated in a timely and cost-effective manner.
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A case of the hands and face dermatitis in a patient employed in a store with motor-car spare parts is presented. Both the patient and her doctor were convinced that skin lesions were caused by the contact with metals, oils and greases. After detecting allergy to primine (after 48 and 96 h, + +), the patient recalled that two months earlier she had started to grow primrose (Primula obconica) at home. Patch tests with the primrose leaf and flower were also positive (+ +). The presented case provides evidence that routine primine testing is essential in all patients with suspected contact allergy dermatitis. In Poland like in the majority of countries, primina is not included in the standard kit.
Irritant contact dermatitis is the most frequent cause of occupational skin disease. Here, the author describes a host of common irritants and lists, by occupation, the irritants to which workers are most likely to be exposed. Diagnosis, prevention, therapy, and prognosis also are reviewed.
In the IInd Department of Dermatology, Vienna University, 200 patients (143 female, 57 male) suffering from leg ulcers due to chronic venous insufficiency underwent patch testing with routine allergens, vehicles and their ingredients, as well as topical antibiotics. 114 patients (57%) had contact allergy. Balsam of Peru heads the list of allergens with postive reactions in 22%, closely followed by oil/water emulsions such as Drointin (21%), Ultrasicc (20%) and Ung. emulsificans aqu. (15,5%). The causative agents in these preparations were emulsifiers on the one hand (Lanette O, E, N) and preservatives (parabens) on the other hand. In comparison, allergic reactions to water/oil emulsions were less common. The low index of sensitivity to local antibiotics was also surprising. The results of the present study, in accordance with other reports in the literature, underline the need (1) for full label diclosure of cosmetics and topically-applied drugs and (2) for patch-testing every patient suffering from leg ulcers of long duration.
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Contact dermatitis is the most frequent occupational dermatosis and non-specific irritants in addition to specific Type IV sensitization are involved. We reviewed our database for data from 1994 to 1998 and selected 360 consecutive patients working in healthcare environments and experiencing contact dermatitis at their hands, wrists and forearms. We found that allergic contact dermatitis and irritant contact dermatitis were considered to be work-related in 16.5% (72/436) and 44.4% (194/436) of diagnoses, respectively. Occupational irritant contact dermatitis is due to exposure to a wide range of irritants in the workplace, such as soaps, solvents, cleansers and protective gloves, which conspire to remove the surface lipid layer and/or produce cellular damage. In this study the major relevant aetiological agents that induced occupational allergic contact dermatitis were: nickel sulphate (41 patch positivities), components of disinfectants [glutaraldehyde (5) and benzalkonium chloride (7)] and rubber chemicals [thiuram mix (15), carba mix (9) and tetramethylthiuram monosulphide (6)]. The best treatment for allergic contact dermatitis is to avoid those allergens causing the rash. Whenever this is not possible, contact with them needs to be reduced using properly selected protective gloves. Finally, subjects with atopic dermatitis should avoid 'wet work' and contact with irritants, because atopic dermatitis is significantly associated with irritant contact dermatitis.
All contact dermatitis patients are told to avoid their specific allergens. As regards topical pharmaceutical agents, however, it is almost impossible for these patients to identify the products that contain their allergens. In order to provide reliable information for these patients, we have designed a computer assisted data system. The CODEX (COntact DErmatitis indeX) system consists of three computer readable files: a Product File containing the complete composition of the pharmaceutical products on the Belgian market that are applied on the skin and the mucous membranes, a Patient File with the patient's anamnesis, and a Literature File with cross-referenced material on contact dermatitis. Each patient is given a list of the products that contain his/her allergen(s). The data bases are analyzed statistically and updated periodically. Cosmetics in general are excluded.
BACKGROUND: Atopic diseases are common in children and adolescents. However, epidemiological knowledge is sparse for hand eczema and allergic contact dermatitis in this age group. Furthermore, no population-based studies have evaluated the prevalence of atopic diseases and hand and contact dermatitis in the same group of adolescents. OBJECTIVES: To assess prevalence measures of atopic dermatitis (AD), asthma, allergic rhinitis and hand and contact dermatitis in adolescents in Odense municipality, Denmark. METHODS: The study was carried out as a cross-sectional study among 1501 eighth grade school children (age 12-16 years) and included questionnaire, interview, clinical examination and patch testing. RESULTS: The lifetime prevalence of AD was 21.3% (girls 25.7% vs. boys 17.0%, P < 0.001) using predefined questionnaire criteria. The 1-year period prevalence of AD was 6.7% and the point prevalence 3.6% (Hanifin and Rajka criteria). In the interview the lifetime prevalence of inhalant allergy was estimated as 17.7% (6.9% allergic asthma, 15.7% allergic rhinitis). The lifetime prevalence of hand eczema based on the questionnaire was 9.2%, the 1-year period prevalence was 7.3% and the point prevalence 3.2%, with a significant predominance in girls. A significant association was found both between AD and inhalant allergy, and between AD and hand eczema using lifetime prevalence measures. The point prevalence of contact allergy was 15.2% (girls 19.4% vs. boys 10.3%, P < 0.001), and present or past allergic contact dermatitis was found in 7.2% (girls 11.3% vs. boys 2.5%). Contact allergy was most common to nickel (8.6%) and fragrance mix (1.8%). CONCLUSIONS: High prevalence figures were found for atopic diseases, hand eczema and allergic contact dermatitis, and the diseases were closely associated. A considerable number of adolescents still suffers from AD, and a considerable sex difference was noted for hand eczema and allergic contact dermatitis. Nickel allergy and perfume allergy were the major contact allergies. In the future this cohort of eighth grade school children will be followed up with regard to the course and development of atopic diseases, hand eczema and contact dermatitis.
Irritant contact dermatitis is the clinical result of sufficient inflammation arising from release of pro-inflammatory cytokines from skin cells (principally keratinocytes) in response to (usually) chemical stimuli. Different clinical forms may arise. The three main pathophysiological changes seen are skin barrier disruption, epidermal cellular changes and cytokine release. An important role of irritancy in allergic contact dermatitis (ACD) comes from earlier animal and human studies. Evidence is outlined which is consistent with a "danger model" of ACD rather than one based on a traditional "self-nonself" immune model. In such a model an antigenic signal will produce sensitization only in the presence of a danger signal; in the absence of a danger signal tolerance will occur. We propose that the danger signal in ACD is cytokine release from nonimmune skin cells (principally keratinocytes) and that both the antigenic and "danger" signals arises from the hapten.
Between 1995 and 1998, 174 dental personnel were referred as patients to the Department of Occupational and Environmental Dermatology, Stockholm. After clinical examination, 131 were patch tested with the Swedish standard series and 109 with a dental screening series. Furthermore, 137 were tested for IgE-mediated allergy to natural rubber latex (NRL). Hand eczema was diagnosed in 109/174 (63%), 73 (67%) being classified as irritant contact dermatitis and 36 (33%) as allergic. Further diagnoses included other eczemas, urticaria, rosacea, psoriasis, tinea pedis, bullous pemphigoid or no skin disease. 77/131 (59%) had positive reactions to substances in the standard series and 44/109 (40%) to substances exclusive to the dental series. 24/109 (22%) patients had positive reactions to (meth)acrylates, the majority with reactions to several test preparations. Reactions to HEMA (2-hydroxyethyl methacrylate), EGDMA (ethyleneglycol dimethacrylate) and MMA (methyl methacrylate) were most frequent. 9 of the 24 were positive only to (meth)acrylates, the remaining 15 also had reactions to allergens in the standard series. 23 of these had hand eczema and 1 facial eczema. In 17 of the 24 allergic to (meth)acrylates, the dermatitis had started in 1995 or later, in 15 within the previous 12 months. Of 8 who had been sick-listed, 7 also had a history of atopy and 6 were allergic to nickel. The most frequent allergens besides (meth)acrylates were nickel, cobalt, palladium, fragrance mix, colophonium and thiuram mix. Allergy to natural rubber latex was diagnosed in 14/137 (10%). In conclusion, irritant hand dermatitis was the dominant diagnosis. Contact allergy to (meth)acrylate was seen in 22% of the patch tested patients, with reactions to 3 predominant test substances. 1/3 of the patients with allergy to (meth)acrylates had been sick-listed for dermatitis, but in all these cases the (meth)acrylate allergy was seen together with atopy and/or further contact allergies.
Contact dermatitis of the lower extremity is reviewed in regard to symptoms, clinical manifestations, etiologic agents, and treatment. Examples of some of the clinical manifestations are presented pictorially.