Contact dermatitis is a common inflammatory skin condition characterized by erythematous and pruritic skin lesions that occur after contact with a foreign substance. There are two forms of contact dermatitis: irritant and allergic. Irritant contact dermatitis is caused by the non-immune-modulated irritation of the skin by a substance, leading to skin changes. Allergic contact dermatitis is a delayed hypersensitivity reaction in which a foreign substance comes into contact with the skin; skin changes occur after reexposure to the substance. The most common substances that cause contact dermatitis include poison ivy, nickel, and fragrances. Contact dermatitis usually leads to erythema and scaling with visible borders. Itching and discomfort may also occur. Acute cases may involve a dramatic flare with erythema, vesicles, and bullae; chronic cases may involve lichen with cracks and fissures. When a possible causative substance is known, the first step in confirming the diagnosis is determining whether the problem resolves with avoidance of the substance. Localized acute allergic contact dermatitis lesions are successfully treated with mid- or high-potency topical steroids, such as triamcinolone 0.1% or clobetasol 0.05%. If allergic contact dermatitis involves an extensive area of skin (greater than 20 percent), systemic steroid therapy is often required and offers relief within 12 to 24 hours. In patients with severe rhus dermatitis, oral prednisone should be tapered over two to three weeks because rapid discontinuation of steroids can cause rebound dermatitis. If treatment fails and the diagnosis or specific allergen remains unknown, patch testing should be performed.
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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 most common form of contact dermatitis, and yet is often overlooked. Recent progress in understanding the pathogenesis has reignited the interest of clinicians in this area of dermatology. Irritant contact dermatitis is not a homogenous entity, but rather a number of subtypes contributing to different clinical presentations. The diagnosis of irritant contact dermatitis is often clinical, and may only be possible after the exclusion of allergic contact dermatitis with patch testing. There is no readily available diagnostic test. There is an incomplete understanding of the factors which lead to the development of cumulative irritant contact dermatitis and persistent postoccupational dermatitis. We have used the experience from our tertiary referral occupational dermatology clinic to illustrate various aspects of irritant contact dermatitis, and to highlight the difficulty sometimes encountered in making this diagnosis. We believe that increased awareness of the often pivotal role of irritant contact dermatitis, as well as all the other factors contributing to occupational dermatitis, will lead to improvement in outcomes for patients.
PURPOSE OF REVIEW: The following paper reviews the recent literature pertaining to allergic contact dermatitis in the pediatric population. RECENT FINDINGS: Allergic contact dermatitis may affect as many as 20% of the pediatric population. Recent studies implicate the following chemicals as the most common causes: nickel, topical antibiotics, preservative chemicals, fragrances and rubber accelerators. Several less common, but emerging, allergens have also been reported recently, including para-phenylenediamine in henna tattoos, cocamidopropyl betaine in 'no tears' shampoos and cleansers, and disperse dyes in clothing materials. Allergic contact dermatitis occurs less frequently in the first few months of life and increases in prevalence with increasing age. In the adolescent age group, females have significantly higher rates of allergic contact dermatitis on the face. This is likely explained by increased exposures to nickel in piercings and to preservative and fragrance chemicals in cosmetic products. SUMMARY: The documented rates of allergic contact dermatitis in children are on the rise. This increased prevalence may be due to increased chemical exposures in this age group, better recognition by pediatricians and perhaps more widespread use of epicutaneous patch testing. This review outlines the basic pathophysiology, epidemiology and clinical manifestations of allergic contact dermatitis in children.
Contact allergies are complex diseases, and one of the important challenges for public health and immunology. The German 'Federal Institute for Risk Assessment' hosted an 'International Workshop on Contact Dermatitis'. The scope of the workshop was to discuss new discoveries and developments in the field of contact dermatitis. This included the epidemiology and molecular biology of contact allergy, as well as the development of new in vitro methods. Furthermore, it considered regulatory aspects aiming to reduce exposure to contact sensitisers. An estimated 15-20% of the general population suffers from contact allergy. Workplace exposure, age, sex, use of consumer products and genetic predispositions were identified as the most important risk factors. Research highlights included: advances in understanding of immune responses to contact sensitisers, the importance of autoxidation or enzyme-mediated oxidation for the activation of chemicals, the mechanisms through which hapten-protein conjugates are formed and the development of novel in vitro strategies for the identification of skin-sensitising chemicals. Dendritic cell cultures and structure-activity relationships are being developed to identify potential contact allergens. However, the local lymph node assay (LLNA) presently remains the validated method of choice for hazard identification and characterisation. At the workshop the use of the LLNA for regulatory purposes and for quantitative risk assessment was also discussed.
The preparation of food in restaurant kitchens carries a high risk of occupational dermatoses. Analysis of 33 cases revealed four different etiological types. Simple irritant dermatitis was rare (2 cases), plain contact dermatitis was more common (6 cases). Fifteen patients had relevant patch tests and scratch tests; ten had positive scratch tests only to explain the cause of their dermatitis. The last type was termed protein contact dermatitis. The major type IV allergens incriminated were metals, onion and garlic. The major proteinaceous allergens indicated by history and test results were fish and shell-fish. Open patch tests with the incriminated foods may cause erythema or oedema on normal skin after 20 minutes. Previously eczematous, now normal looking, skin often responds with a crop of dyshidrotic vesicles preceded by erythema and itching 30 minutes after the application of an open test. Examination for specific IgE is not always positive in such cases. Inhalant allergy was rare. The results indicate that food handlers are sensitized by the protein they touch, and then react to later contact with the proteins. Protein contact dermatitis is similarly common among veterinary surgeons, while the importance in other occupational groups remains to be studied.
Contact allergy is caused by a wide range of chemicals after skin contact. Its clinical manifestation, allergic contact dermatitis (ACD), is developed upon repeated contact with the allergen. This perspective focuses on two areas that have yielded new useful information during the last 20 years: (i) structure-activity relationship (SAR) studies of contact allergy based on the concept of hapten-protein binding and (ii) mechanistic investigations regarding activation of nonsensitizing compounds to contact allergens by air oxidation or skin metabolism. The second area is more thoroughly reviewed since the full picture has previously not been published. Prediction of the sensitizing capacity of a chemical is important to avoid outbreaks of ACD in the population. Much research has been devoted to the development of in vitro and in silico predictive testing methods. Today, no method exists that is sensitive enough to detect weak allergens and that is robust enough to be used for routine screening. To cause sensitization, a chemical must bind to macromolecules (proteins) in the skin. Expert systems containing information about the relationship between the chemical structure and the ability of chemicals to haptenate proteins are available. However, few designed SAR studies based on mechanistic investigations of prohaptens have been published. Many compounds are not allergenic themselves but are activated in the skin (e.g., metabolically) or before skin contact (e.g., via air oxidation) to form skin sensitizers. Thus, more basic research is needed on the chemical reactions involved in the antigen formation and the immunological mechanisms. The clinical importance of air oxidation to activate nonallergenic compounds has been demonstrated. Oxidized fragrance terpenes, in contrast to the pure terpenes, gave positive patch test reactions in consecutive dermatitis patients as frequently as the most common standard allergens. This shows the importance of using compounds to which people are exposed when screening for ACD in dermatology clinics.
Contact dermatitis is produced by external skin exposure to an allergen, but sometimes a systemically administered allergen may reach the skin and remain concentrated there with the aid of the circulatory system, leading to the production of systemic contact dermatitis (SCD). Metals such as nickel, cobalt, chromium, and zinc are ubiquitous in our environment. Metal allergy may result in allergic contact dermatitis and also SCD. Systemic reactions, such as hand dermatitis or generalized eczematous reactions, can occur due to dietary nickel or cobalt ingestion. Zinc-containing dental fillings can induce oral lichen planus, palmoplantar pustulosis, and maculopapular rash. A diagnosis of sensitivity to metal is established by epicutaneous patch testing and oral metal challenge with metals such as nickel, cobalt, chromium, and zinc. In vitro tests, such as the lymphocyte stimulating test (LST), have some advantages over patch testing to diagnose allergic contact dermatitis. Additionally, the determination of the production of several cytokines by primary peripheral blood mononuclear cell cultures is a potentially promising in vitro method for the discrimination of metal allergies, including SCD, as compared with the LST.
BACKGROUND: Patch testing is the most important diagnostic tool for the assessment of allergic contact dermatitis. OBJECTIVE: This study documents the North American Contact Dermatitis Group (NACDG) patch testing results from January 1, 2013, to December 31, 2014. METHODS: At 13 centers in North America, patients were tested in a standardized manner with a screening series of 70 allergens. Data were manually verified and entered into a central database. Descriptive frequencies were calculated, and trends were analyzed using χ test. RESULTS: A total of 4871 patients were tested. There were 3255 patients (66.8%) who had at least 1 positive reaction and 2412 patients (49.5%) who were ultimately determined to have a primary diagnosis of allergic contact dermatitis. A total of 434 patients (8.9%) had occupationally related skin disease. There were 9726 positive allergic reactions. Compared with the previous reporting periods (2011-2012 and 2001-2012, including at least three 2-year cycles), positive reaction rates for the top 25 screening allergens statistically increased for 2 allergens: methylchloroisothiazolinone/methylisothiazolinone (6.4%; risk ratios, 1.26 [1.07-1.50] and 2.08 [1.84-2.37]) and hydroxyethyl methacrylate (2.6%; risk ratios, 1.34 [1.02-1.76] and 1.23 [1.00-1.51]). Methylisothiazolinone, which was added to the screening series for this 2013-2014 cycle, had the third highest positive reaction rate of allergens tested (10.9%). Four other newly added allergen preparations-formaldehyde 2% (7%), diphenylguanidine (3.8%), propylene glycol 100% (2.8%), and benzophenone-4 (2.1%)-all had reaction rates greater than 2%. Twenty-one percent of tested patients had at least 1 relevant allergic reaction to an allergen not on the NACDG series; 14.6% of these were occupationally related. The T.R.U.E. TEST (SmartPractice Denmark, Hillerød, Denmark) would have hypothetically missed one quarter to one third of reactions detected by the NACDG screening series. CONCLUSIONS: These results confirm that the epidemic of sensitivity to methylisothiazolinone previously documented in Europe is also occurring in North America. Patch testing with allergens beyond a standard screening tray is necessary for the complete evaluation of occupational and nonoccupational allergic contact dermatitis.
Irritant and allergic contact dermatitis are common inflammatory skin diseases induced by repeated skin contact with low molecular weight chemicals, called xenobiotics or haptens. Although both diseases may have similar clinical presentations, they can be differentiated on pathophysiological grounds. Irritant contact dermatitis (ICD) is a non-specific inflammatory dermatitis brought about by activation of the innate immune system by the pro-inflammatory properties of chemicals. Allergic contact dermatitis (ACD) corresponds to a delayed-type hypersensitivity response with a skin inflammation mediated by hapten-specific T cells. Recent progress in the pathophysiology of chemical-induced skin inflammation has shown that ICD and ACD are closely associated and that the best way to prevent ACD is to develop strategies to avoid ICD. The immunological diagnosis of ICD or ACD requires investigation of the presence (ACD) or absence (ICD) of antigen-specific T cells. The detection of T cells can be performed in the skin (collected from ACD lesions or positive patch tests) and/or in the blood, particularly by using the enzyme-linked immunospot assay (ELISPOT). This method, recently developed in ACD to metals, offers a new biological tool enabling the immunobiological diagnosis of ACD.
An attempt is made to formulate some kind of working hypothesis concerning the pathophysiology, clinical appearance and treatment of irritant contact dermatitis. Acute irritant dermatitis may be caused by one single overwhelming external exposure of comparatively short duration. It is usually accidental and therefore recognized early as cause and effect. Chronic irritant dermatitis may be the result of a too early repetition of one impairing factor (chronic irritant dermatitis "traumiteration' type), but is more commonly the result of the influence of a variety of stimuli, each starting to be active before recovery from the foregoing stimuli has been completed (chronic irritant dermatitis 'summation' type.) By repetition of the same stimulus, or by a combination of varying stimuli, the degree of impairment surpasses a critical level, in consequence of which a clinical disease (irritant contact dermatitis) ensues. This clinical disease, however, is only 'the tip of the iceberg'. Such stimuli may be chemical, mechanical and/or climatic. To find out which are the harmful factors requires a detailed case history about the patient's work, habits and hobbies, thus enabling him to avoid as many damaging exposures as is practical, and hence reducing the sum of causative factors. A number of causative factors are enumerated. The article is intended to be a catalyst to promote discussion on this subject.
Irritant contact dermatitis is a result of activated innate immune response to various external stimuli and consists of complex interplay which involves skin barrier disruption, cellular changes, and release of proinflammatory mediators. In this review, we will focus on key cytokines and chemokines involved in the pathogenesis of irritant contact dermatitis and also contrast the differences between allergic contact dermatitis and irritant contact dermatitis.
The dermatologist should be aware of the many facets of occupational skin diseases, which can be caused by physical, chemical, and biological insults. The most common manifestation of occupational skin diseases is contact dermatitis (both irritant and allergic). Three factors point out the importance of occupational skin diseases as diseases that have a public health impact: 1) occupational skin diseases are common; 2) they often have a poor prognosis; and 3) they result in a noteworthy economic impact for society and for an individual. They are also diseases amenable to public health interventions. Specific industries and exposures may put a worker at risk of occupational contact dermatitis. The accuracy of the diagnosis of occupational contact dermatitis is related to the skill level, experience, and knowledge of the medical professional who makes the diagnosis and confirms the relationship with a workplace exposure. Prevention of occupational contact dermatitis is important, and a variety of prevention strategies are available.
To cite this article: Martin SF, Esser PR, Weber FC, Jakob T, Freudenberg MA, Schmidt M, Goebeler M. Invited review for the journal allergy mechanisms of chemical-induced innate immunity in allergic contact dermatitis. Allergy 2011; 66: 1152–1163. Abstract Allergic contact dermatitis (ACD) is one of the most prevalent occupational skin diseases and causes severe and long-lasting health problems in the case of chronification. It is initiated by an innate inflammatory immune response to skin contact with low molecular weight chemicals that results in the priming of chemical-specific, skin-homing CD8+ Tc1/Tc17 and CD4+ Th1/Th17 cells. Following this sensitization step, T lymphocytes infiltrate the inflamed skin upon challenge with the same chemical. The T cells then exert cytotoxic function and secrete inflammatory mediators to produce an eczematous skin reaction. The recent characterization of the mechanisms underlying the innate inflammatory response has revealed that contact allergens activate innate effector mechanisms and signalling pathways that are also involved in anti-infectious immunity. This emerging analogy implies infection as a potential trigger or amplifier of the sensitization to contact allergens. Moreover, new mechanistic insights into the induction of ACD identify potential targets for preventive and therapeutic intervention. We summarize here the latest findings in this area of research.
Allergic contact dermatitis is a common skin disease associated with inflammation and persistent pruritus. Transient receptor potential (TRP) ion channels in skin‐innervating sensory neurons mediate acute inflammatory and pruritic responses following exogenous stimulation and may contribute to allergic responses. Genetic ablation or pharmacological inhibition of TRPA1, but not TRPV1, inhibited skin edema, keratinocyte hyperplasia, nerve growth, leukocyte infiltration, and antihistamine‐resistant scratching behavior in mice exposed to the haptens, oxazolone and urushiol, the contact allergen of poison ivy. Hapten‐challenged skin of TRPA1‐deficient mice contained diminished levels of inflammatory cytokines, nerve growth factor, and endogenous pruritogens, such as substance P (SP) and serotonin. TRPA1‐deficient sensory neurons were defective in SP signaling, and SP‐induced scratching behavior was abolished in Trpa1 –/– mice. SP receptor antagonists, such as aprepitant inhibited both hapten‐induced cutaneous inflammation and scratching behavior. These findings support a central role for TRPA1 and SP in the integration of immune and neuronal mechanisms leading to chronic inflammatory responses and pruritus associated with contact dermatitis.—Liu, B., Escalera, J., Balakrishna, S., Fan, L., Caceres, A. I., Robinson, E., Sui, A., McKay, M. C., McAlexander, M. A., Herrick, C. A., Jordt, S. E., TRPA1 controls inflammation and pruritogen responses in allergic contact dermatitis. FASEB J. 27, 3549–3563 (2013). www.fasebj.org
Metals are in close contact with skin and mucous membranes on a repeated, if not constant, basis. Nickel and mercury, well-recognized causes of contact dermatitis; gold and palladium, recently gaining acceptance as patch test allergens on standard screening trays; and cobalt are reviewed in this article. Sensitization to nickel, the most frequently identified allergen on patch testing, is associated with ear piercing. Contact with this potential allergen is ubiquitous. Mercury may be encountered as organic mercury in thimerosal, used as an antiseptic and a preservative in topical medications and vaccines, and metallic mercury found in dental amalgam and thermometers. Both forms may cause contact dermatitis. Gold, recognized as a frequent sensitizer, has been implicated in some cases of eyelid, patchy diffuse and oral lichenoid dermatitis. Cobalt allergy, found frequently in patients who are nickel allergic, also has been associated with ear piercing. Palladium sensitivity is often associated with nickel allergy. However, the incidence of clinical relevance is yet to be established.
Rietschel, R L & Fowler, J F . Fisher’s contact dermatitis , 5th edition . Philadelphia : Lippincott, Williams and Wilkins , 2000 . 880 pp. $119 . ISBN 0-7817-2252-7 . It is always inspiring to contact dermatologists to see that a further edition of ‘Fisher’ has appeared. When I started my training in patch testing, it was the 2nd edition (1973) that guided me: a generation later, we have the 5th. The original 324 pages of the 1st edition (1967) have by now expanded to an encyclopaedic 862. Rietschel & Fowler have industriously updated and expanded the text, including the individual instructions for patients with common contact allergens, and the specifics of treatment of contact dermatitis. The familiar boxed summaries have sensibly been retained, as has the useful appendix listing patch-test allergens with their concentration and vehicle, sources of exposure, cross-reactions and comments. In spite of its size, its current authors have managed to keep it user-friendly. I can recommend this new edition strongly as an essential reference text to all those involved in this ever-fascinating area of dermatology. Richard J. G. Rycroft
Allergic contact dermatitis (ACD), one of the commonest occupational diseases, is a T-cell-mediated skin inflammation caused by repeated skin exposure to contact allergens, i.e. nonprotein chemicals called haptens. Allergic contact dermatitis, also referred to as contact hypersensitivity, is mediated by CD8+ T cells, which are primed in lymphoid organs during the sensitization phase and are recruited in the skin upon re-exposure to the hapten. Subsets of CD4+ T cells endowed with suppressive activity are responsible for both the down-regulation of eczema in allergic patients and the prevention of priming to haptens in nonallergic individuals. Therefore, ACD should be considered as a breakdown of the skin immune tolerance to haptens. Recent advances in the pathophysiology of ACD have demonstrated the important role of skin innate immunity in the sensitization process and have revisited the dogma that Langerhans cells are mandatory for CD8+ T-cell priming. They have also introduced mast cells as a pivotal actor in the magnitude of the inflammatory reaction. Finally, the most recent studies address the nature, the mode and the site of action of the regulatory T cells that control the skin inflammation with the aim of developing new strategies of tolerance induction in allergic patients.
The term 'baboon syndrome' (BS) was introduced 20 years ago to classify patients in whom a specific skin eruption resembling the red gluteal area of baboons occurred after systemic exposure to contact allergens. Thereafter, similar eruptions have been reported after systemic exposure to beta-lactam antibiotics and other drugs. In addition to the presentation of 2 of our own cases, we have reviewed and characterized the main clinical and histological aspects of published reports of drug-related baboon syndrome (DRBS) and compared the primary clinical signs from such cases to those found in other distinct drug eruptions. Of approximately 100 published baboon syndrome cases, 50 were identified as drug-induced. Of these, 8 were representatives of systemically induced contact dermatitis (SCD), and 42 were examples of drug eruptions elicited by systemic administration of either oral or intravenous drugs. The main clinical findings included a sharply defined symmetrical erythema of the gluteal area and in the flexural or intertriginous folds without any systemic symptoms and signs. 14 of 42 cases were elicited by amoxicillin, 30 of the 42 patients were male, and latency periods were between a few hours and a few days after exposure. DRBS is a rare, prognostically benign and often underdiagnosed drug eruption with distinct clinical features. The term baboon syndrome, however, does not reflect the complete range of symptoms and signs and is ethically and culturally problematic. Moreover, baboon syndrome is historically often equated with a mercury-induced exanthem in patients with previous contact sensitization. Symmetrical drug-related intertriginous and flexural exanthema, or SDRIFE, specifically refers to the distinctive clinical pattern of this drug eruption, and the following diagnostic criteria are proposed: 1) exposure to a systemically administered drug either at the first or repeated dose (excluding contact allergens); 2) sharply demarcated erythema of the gluteal/perianal area and/or V-shaped erythema of the inguinal/perigenital area; 3) involvement of at least one other intertriginous/flexural localization; 4) symmetry of affected areas; and 5) absence of systemic symptoms and signs.