Allergic contact dermatitis is the most frequent occupational disease in industrialized countries. It is caused by CD8+ T cell–mediated contact hypersensitivity (CHS) reactions triggered at the site of contact by a variety of chemicals, also known as weak haptens, present in fragrances, dyes, metals, preservatives, and drugs. Despite the myriad of potentially allergenic substances that can penetrate the skin, sensitization is relatively rare and immune tolerance to the substance is often induced by as yet poorly understood mechanisms. Here we show, using the innocuous chemical 2,4-dinitrothiocyanobenzene (DNTB), that cutaneous immune tolerance in mice critically depends on epidermal Langerhans cells (LCs), which capture DNTB and migrate to lymph nodes for direct presentation to CD8+ T cells. Depletion and adoptive transfer experiments revealed that LCs conferred protection from development of CHS by a mechanism involving both anergy and deletion of allergen-specific CD8+ T cells and activation of a population of T cells identified as ICOS+CD4+Foxp3+ Tregs. Our findings highlight the critical role of LCs in tolerance induction in mice to the prototype innocuous hapten DNTB and suggest that strategies targeting LCs might be valuable for prevention of cutaneous allergy.
The development of chronic allergic dermatitis in early life has been associated with increased onset and severity of allergic asthma later in life. However, the mechanisms linking these two diseases are poorly understood. Here, we report that the development of oxazolone-induced chronic allergic dermatitis, in a mouse model, caused enhanced ovalbumin-induced allergic asthma after resolution of the former disease. Our findings show that oxazolone-induced dermatitis caused a marked increase in tissue mast cells, which persisted long after the resolution of this disease. Subsequent ovalbumin sensitization and airway challenge of mice that had recovered from dermatitis resulted in increased allergic airway hyperreactivity. The findings demonstrate that the accumulation of mast cells during dermatitis has the detrimental effect of increasing allergic airway hypersensitivity. Importantly, our findings also show that exposure to a given allergen can modify the immune response to an unrelated allergen.
Allergy; Fc receptors; IgE; Mast cells/basophils; Skin; Rodent
Allergic contact dermatitis is a typical delayed-type hypersensitivity to sensitizing haptens mediated by T cells. Th1/Tc1 cells are currently considered to be the primary effectors in allergic contact dermatitis. There is little information concerning the role played in allergic contact dermatitis in humans by Th-17/Tc-17 cells, a recently defined subpopulation of effector T cells.
In the present report we attempted to characterize Th-17/Tc-17 cells in the infiltrates of the skin in elicitation phase of allergic contact dermatitis.
Th-17 as well as Th1/Th2 cytokine gene expression was examined by semi-quantitative real-time polymerase chain reaction in paired samples of positive patch test biopsies and normal skins from 11 patients allergic to 9 different allergens. The in situ characterization of IL-17-producing cells was carried out using anti-RORC and anti-T cell subset antibodies by double immunofluorescence.
Compared to normal paired skins, gene expression of transcription factor for human Th-17 cells, RORC, and Th-17-related cytokines IL-17A, IL-17F and IL-23, was significantly increased in positive patch test biopsies. The mRNA for IFN-γ and IL-4 was also increased. In the dermal infiltrates, about 20 % of the infiltrating cells were IL-17-producing cells as they expressed RORC, and such RORC expressing cells were detected in both CD4+ (~30%) and CD8+ (~20%) subsets.
This is the first demonstration of Th-17/Tc-17 cells in the elicitation phase of human allergic contact dermatitis, showing that they are a regular participant in the immunopathology of this common allergic reaction regardless of the nature of the triggering allergens.
Allergic contact dermatitis; IL-17; Th-17 lymphocytes; patch test; RORC
A variety of cell-mediated hypersensitivity reactions in experimental animals include a prominent infiltrate of basophilic leukocytes. This form of reactivity has been designated cutaneous basophil hypersensitivity and is favored when sensitization to several types of antigen is accomplished without the use of complete Freund's adjuvant. A similar type of hypersensitivity response was sought in man using morphologic techniques which permit identification of basophilic leukocytes. Eight individuals with allergic contact dermatitis to a variety of allergens were studied and six of these developed typical contact reactions with erythema, edema, and epidermal vesicles. The microscopic findings in 3-day biopsies from these individuals differed significantly from classic descriptions of tuberculin hypersensitivity and showed, in addition to mononuclear cells and the characteristic epidermal changes, a substantial infiltrate of basophilic leukocytes and evidence of altered vascular permeability with vascular compaction, dermal edema, and fibrin deposition. Serial biopsies from one individual permitted analysis of the microscopic pathology as it unfolded at successive intervals after patch test. The initial lesion consisted of perivascular accumulations of lymphocytes; this was followed by an influx of basophils and, subsequently, of eosinophils. These findings associate contact allergy in man with the parallel reactions of cutaneous basophil hypersensitivity in animals and provide further evidence for the heterogeneity of the cellular immune response. The data are consistent with the hypothesis that interaction between sensitized lymphocytes and antigen, at a local test site, is responsible for the attraction of basophils. They also directly implicate the clotting system in delayed-type reactions and suggest the possibility of a synergistic relationship between cellular immunity and reactions mediated by basophil-bound, homocytotrophic antibody.
Allergic contact dermatitis differs from most other immune reactions by its strict dose dependence during the elicitation phase. Moreover, almost all known contact allergens can also induce dose-dependent irritative dermatitis and in general only elicit allergic contact dermatitis in sensitized individuals when applied within a narrow dose range. Therefore, we hypothesized that elicitation of contact hypersensitivity (CHS) may require two signals, antigen-specific effector cell activation and a non-antigen-specific proinflammatory signal, both of which are provided by application of a sufficient dose of hapten. To dissociate these putative two signals, oxazolone-sensitized mice were ear challenged with a dose of the specific hapten which was too low to elicit CHS. At the same time, an unrelated hapten was applied in a conventional concentration to the same skin site. Whereas neither treatment alone elicited a significant CHS response, application of both compounds together resulted in a strong CHS response that was indistinguishable from that elicited by the full dose of the specific hapten. Upon coadministration of the irrelevant hapten, allergic contact dermatitis could be elicited even when the dose of the specific hapten was further reduced by a factor of 10(3). In contrast, a dose reduction of the irrelevant hapten by a factor of two resulted in the loss of the CRS response. These data indicate that non-antigen-specific effects of epicutaneously applied haptens significantly contribute to the elicitation of CHS responses and that the capacity of the hapten to evoke this proinflammatory stimulus rather than its antigenicity is responsible for the strict concentration dependence.
The cutaneous lymphocyte-associated antigen (CLA) is the major T cell ligand for the vascular adhesion molecule E-selectin, and it has been proposed to be involved in the selective targeting of memory T cells reactive with skin-associated Ag to cutaneous inflammatory sites. To further investigate the relation of CLA and cutaneous T cell responses, we analyzed the CLA phenotype of circulating memory T cells in patients with allergic contact dermatitis and atopic dermatitis (AD) alone vs in patients manifesting bronchopulmonary atopy (asthma with or without AD) and nonallergic individuals. Significant T cell proliferative responses to Ni, a contact allergen, and to the house dust mite (HDM), an allergen to which sensitization is often observed in AD and/or asthma, was noted only in allergic and atopic individuals, respectively. When the minor circulating CLA+CD3+CD45RO+ subset was separated from the major CLA-CD3+CD45RO+ subpopulation in Ni-sensitive subjects, the Ni- dependent memory T cell response was largely confined to the CLA+ subset. A similar restriction of the T cell proliferative response to the CLA+ memory subset was observed for HDM in patients with AD alone. In HDM-sensitive patients with asthma with or without AD, however, the CLA- subset exhibited a strong antigen-dependent proliferation, in contrast to patients with AD alone, whose CLA- subset proliferated very weakly to HDM. In asthma with or without AD, the HDM-dependent proliferation slightly predominated in the CLA- when compared to the CLA+ subset. The functional linkage between CLA expression and disease- associated T cell effector function in AD was also demonstrated by the finding that the circulating CLA+ T cell subset in AD patients, but not nonatopic controls, selectively showed both evidence of prior activation (human histocompatibility antigen-DR expression) and spontaneous production of interleukin 4 but not interferon-gamma. Taken together, these observations demonstrate the correlation of CLA expression on circulating memory T cells and disease-associated memory T cell responses in cutaneous hypersensitivity, and they suggest the existence of mechanisms capable of sorting particular T cell Ag specificities and lymphokine patterns into homing receptor-defined memory subsets.
Metal-working fluids contain complex mixtures of chemicals and metal workers constitute a potential risk group for the development of allergic contact dermatitis.
Two metal workers developed allergic contact dermatitis on the hands and lower arms from exposure to a neat oil used in metal processing. Patch testing revealed that the relevant contact allergen was a cycloaliphatic epoxy resin, 1,2-cyclohexanedicarboxylic acid, bis(oxiranylmethyl) ester, added to the oil as a stabilizer. None of the patients had positive reactions to the bisphenol A-based epoxy resin in the standard series.
These cases emphasize that well-known contact allergens may show up from unexpected sources of exposure. Further, it can be a long-lasting, laborious process to detect an occupational contact allergen and cooperation from the patient and the manufacturer of the sensitizing product is essential.
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.
Chromium (Cr) causes delayed-type hypersensitivity reactions possibly mediated by accumulating T cells into allergic inflamed skin, which are called irritants or allergic contact dermatitis. However, accumulating T cells during development of metal allergy are poorly characterized because a suitable animal model is not available. This study aimed to elucidate the skewing of T-cell receptor (TCR) repertoire and cytokine profiles in accumulated T cells in inflamed skin during elucidation of Cr allergy. A novel model of Cr allergy was induced by two sensitizations of Cr plus lipopolysaccharide solution into mouse groin followed by single Cr challenge into the footpad. TCR repertoires and nucleotide sequences of complementary determining region 3 were assessed in accumulated T cells from inflamed skin. Cytokine expression profiles and T-cell phenotypes were determined by qPCR. CD3+CD4+ T cells accumulated in allergic footpads and produced increased T helper 1 (Th1) type cytokines, Fas, and Fas ligand in the footpads after challenge, suggesting CD4+ Th1 cells locally expanded in response to Cr. Accumulated T cells included natural killer (NK) T cells and Cr-specific T cells with VA11-1/VB14-1 usage, suggesting metal-specific T cells driven by invariant NKT cells might contribute to the pathogenesis of Cr allergy.
Allergic Contact Dermatitis (ACD) is regarded as a T-cell-mediated delayed-type hypersensitivity reaction. We studied the kinetics of the expression of CS-1 fibronectin, thymus and activation-regulated chemokine (CCL17/ TARC) and different chemokine receptors (CR) in skin biopsies from individuals suffering from back problems, with the antigen responsible of their contact dermatitis and an irrelevant antigen.
Samples were taken at 2, 10, and 48 hours for histological and immunohistochemical studies using monoclonal antibodies against human CS-1 fibronectin, CCL17, CD3, CD68, CD49d, CXCR3, CCR5, and CCR3.
At positive antigen stimulated sites there was an early expression of CS-1 fibronectin (2 hours), followed by CCL17 and a later accumulation of alplha4/beta1+ (CD49d), CD3+, CD68+, CXCR3+ and CCR5+ mononuclear cells. At 48 hours, approximately 59 % of infiltrating cells were CXCR3+, 42% CCR5+, and only 14 % CCR3+.
These results showed for the first time a very early expression of CS-1 fibronectin which preceded production of CCL17 in blood endothelial cells (BCEs) from patients' skin with ACD. The role of these molecules in recruitment of monocytes and effector T cells in ACD is discussed.
Allergic contact dermatitis; CS-1 fibronectin; CCL17
Occupational and recreational plant exposure on the skin is fairly common. Plant products and extracts are commonly used and found extensively in the environment. Adverse reactions to plants and their products are also fairly common. However, making the diagnosis of contact dermatitis from plants and plant extracts is not always simple and straightforward. Phytodermatitis refers to inflammation of the skin caused by a plant. The clinical patterns may be allergic phytodermatitis, photophytodermatitis, irritant contact dermatitis, pharmacological injury, and mechanical injury. In this article, we will focus mainly on allergy contact dermatitis from plants or allergic phytodermatitis occurring in Asia.
Phytodermatitis; phytophotodermatitis; plant dermatitis
A female in her early 50s presented with a long-standing history of episodic urticaria and angioedema. She also reported urticarial reactions after ingestion of aspirin, prednisone and multiple antibiotics. These medications were all taken during upper respiratory tract infections. An elimination diet followed by a series of open challenges to food chemicals demonstrated an urticarial eruption following the ingestion of mints, which contain high levels of salicylates. A double-blinded placebo-controlled challenge to salicylate confirmed her sensitivity and explained her reaction to aspirin. The patient informed her treating physician of her copious ingestion of mints during upper respiratory tract infections. Drug hypersensitivity to antibiotics and prednisone was excluded on the basis of negative radioallergosorbent tests (RASTs) and/or absent skin-test responses and/or tolerance to oral challenges. This patient had a salicylate intolerance that caused her episodic urticaria and angioedema, and also masqueraded as a drug allergy due to the concurrent ingestion of mints.
Observation of 100 patients with atopic dermatitis due to hypersensitivity to pollen over a period of 12 years emphasized certain important diagnostic and therapeutic features. The incidence was higher in females than in males and higher in middle and old age than in the earlier years.
Pollen dermatitis may be the sole or major manifestation of allergy; 43 patients gave no history of other allergic symptoms. It may involve any or all areas of the body. The site or the distribution of lesions or the nature of the lesions gave no clue as to the diagnosis of pollen sensitivity.
The character of the eruption varied widely from patient to patient and in given patients from week to week at times.
Atopic dermatitis due to pollen sensitivity may be purely seasonal, perennial with seasonal exacerbations or perennial without seasonal variation.
Reactions to skin testing with pollens suspected as allergens may be positive, equivocal or negative. In 58 patients there were positive correlative skin reactions to pollens.
The diagnosis of atopic dermatitis due to pollen sensitivity, and the composition of the desensitizing antigen or antigens, must be based primarily on the clinical history and the area of residence.
Most patients could tolerate only very weak dilutions at the beginning of desensitization therapy. Strong dilutions caused exacerbation of the dermatitis.
Good or excellent results were obtained with perennial pollen desensitization therapy administered over long periods. In 13 patients good results took four to eight years of desensitization therapy. Fifty required less than two years. Tolerance of the patient for a given dose of antigen should determine the maximum dilution used in therapy.
The aim of this randomized controlled clinical trial was to investigate the effect of a new Iranian toothpaste and a commercially available toothpaste containing desensitizing agent (5% potassium nitrate) on dentine hypersensitivity in a 24-week study.
Materials and Methods:
Fifty healthy volunteers, who had at least two sensitive root surfaces, completed the study period. The participants were randomly given one of the two toothpastes; Iranian (antihypersensitive Pooneh) or commercially available (fresh mint Sensodyne) toothpaste. Visual analogue scales (VASs) indicating the intensity of tooth hypersensitivity responding to tactile, airblast and cold-water stimuli were examined at baseline and weeks 2, 4, 12 and 24.
Overall, VAS scores for tactile, airblast, and cold-water tests significantly reduced compared with the baseline in both groups (all P values <0.001).
However, there was no significant difference between the two groups regarding the measured parameters.
This study demonstrated that the Iranian dentifrice (antihypersensitive Pooneh) was as effective as the commercially available one (fresh mint Sensodyne) in reducing tooth hypersensitivity.
Clinical Trial; Potassium Nitrate; Dentin Hypersensitivity; Toothpaste
Atopic dermatitis (AD) is a chronic dermatosis bearing clinical, histological, and immunologic similarities to chronic allergic contact dermatitis (ACD). AD shows a Th2 cell-dominant inflammatory infiltrate, elevated serum IgE levels, a permeability barrier abnormality, and Staphylococcus aureas colonization. Repeated hapten challenges reportedly produce a Th2-like hypersensitivity reaction (Th2-like HR). Here, 9–10 challenges with oxazolone (Ox) to hairless mice also produced a chronic Th2-like HR. Permeability barrier function and expression of differentiation proteins, filaggrin, loricrin, and involucrin, became abnormal. CRTH-positive Th2-dominant inflammatory infiltrate, with increased IL-4 expression, and a large increase in serum IgE levels were observed. The barrier abnormality was associated with decreased stratum corneum (SC) ceramide content and impaired lamellar body secretion, resulting in abnormal lamellar membranes, as in human AD. Furthermore, as in human AD, epidermal serine protease activity in SC increased and expression of two lamellar body-derived antimicrobial peptides, CRAMP and mBD3, declined after Ox challenges, paralleling the decrease of their human homologues in AD. Thus, multiple Ox challenges to normal murine skin produce a chronic Th2-like HR, with multiple features of human AD. Because of its reproducibility, predictability, and low cost, this model could prove useful for evaluating both pathogenic mechanisms and potential therapies for AD.
Menthol is a widely-used cooling and flavoring agent derived from mint leaves. In the peripheral nervous system, menthol regulates sensory transduction by activating TRPM8 channels residing specifically in primary sensory neurons. Although behavioral studies have implicated menthol actions in the brain, no direct central target of menthol has been identified. Here we show that menthol reduces the excitation of rat hippocampal neurons in culture and suppresses the epileptic activity induced by pentylenetetrazole injection and electrical kindling in vivo. We found menthol not only enhanced the currents induced by low concentrations of GABA but also directly activated GABAA receptor (GABAAR) in hippocampal neurons in culture. Furthermore, in the CA1 region of rat hippocampal slices, menthol enhanced tonic GABAergic inhibition although phasic GABAergic inhibition was unaffected. Finally, the structure-effect relationship of menthol indicated that hydroxyl plays a critical role in menthol enhancement of tonic GABAAR. Our results thus reveal a novel cellular mechanism that may underlie the ambivalent perception and psychophysical effects of menthol and underscore the importance of tonic inhibition by GABAARs in regulating neuronal activity.
A delayed hypersensitivity type of allergic contact dermatitis was observed following exposure to certain brands of 50% cotton, 50% polyester coloured permanent-pressed sheets produced by a particular manufacturer. The dermatitis presented as an extremely pruritic follicular eczema of the body and vesicular edema of the ears and face. Patch testing excluded formalin as the allergen but suggested permanent-pressing chemicals as a possibility. Several washings of the sheets did not prevent the development of the dermatitis. The removal of sheets did not immediately result in improvement: the condition could persist for up to eight weeks after their discontinuance.
The initiation and maintenance of tobacco use are influenced by several factors, but of equal and often overlooked importance, until recently, is the palatability of the product. Because of the role that flavor may play in the initiation and maintenance of tobacco use, the Food and Drug Administration has decided to ban the use of flavorings, other than menthol, from cigarettes. To date, little attention has been paid to the impact of flavoring in smokeless tobacco (ST) products.
This study combined the data from 5 previously completed treatment or switching studies to examine the choice of brand flavor in the course of ST use, from initiation to regular use.
The analyses revealed that a majority of subjects’ first and current choice of product was flavored, specifically mint or wintergreen, and that a significant number of ST users switched to a flavored brand after already initiating ST use with a regular nonflavored product. In this population, however, flavored products did not appear to lead to greater dependence or increased exposure to nicotine or carcinogens.
More treatment seeking ST users began by using mint-flavored product and switched to and were current users of mint-flavored products. It is possible that mint products play a role in the initiation and maintenance of ST use.
Chromium is a transition metal and has been shown to elicit contact dermatitis. Although leather products have been known to be the most significant source of chromium exposure these days, the majority of reports have been related to exposure from shoe products. We herein report a professional golfer who became allergic to golf gloves made of chromium-tanned leather. A 27-year-old woman golfer presented with recurrent, pruritic, erythematous plaques that had been occurring on both hands for several years. The lesions developed whenever she had worn golf gloves for an extended period of time, especially during tournament season. To identify the causative agent, patch tests were performed and the results demonstrated a strong positive reaction to potassium dichromate 0.5% and to her own glove. The amount of chromium in her golf glove was analyzed to be 308.91 ppm and based on this, a diagnosis of allergic contact dermatitis due to a chromium-tanned leather glove was made. She was treated with oral antihistamines combined with topical steroids and advised to wear chromium-free leather gloves. There has been no evidence of recurrence during a six month follow-up period.
Chromium; Contact dermatitis; Leather; Tanning
We report 2 cases of elicitation of allergic contact dermatitis to acrylates from disposable blue diathermy pads used on patients who underwent routine surgery. Their reactions were severe, and took approximately 5 weeks to resolve. Both patients gave a prior history of finger tip dermatitis following the use of artificial sculptured acrylic nails, which is a common, but poorly reported, cause of acrylate allergy. Patch testing subsequently confirmed allergies to multiple acrylates present in both the conducting gel of disposable blue diathermy pads, and artificial sculptured acrylic nails. We advocate careful history taking prior to surgery to avoid unnecessary exposure to acrylates in patients already sensitized.
Dinitrochlorobenzene-induced contact hypersensitivity is widely considered as a cell-mediated rather than antibody-mediated immune response. At present, very little is known about the role of antigen-specific antibodies and B cells in the development of dinitrochlorobenzene-induced hypersensitivity reactions, and this is the subject of the present investigation.
Data obtained from multiple lines of experiments unequivocally showed that the formation of dinitrochlorobenzene-specific Abs played an important role in the development of dinitrochlorobenzene-induced contact hypersensitivity. The appearance of dinitrochlorobenzene-induced skin dermatitis matched in timing the appearance of the circulating dinitrochlorobenzene-specific antibodies. Adoptive transfer of sera containing dinitrochlorobenzene-specific antibodies from dinitrochlorobenzene-treated mice elicited a much stronger hypersensitivity reaction than the adoptive transfer of lymphocytes from the same donors. Moreover, dinitrochlorobenzene-induced contact hypersensitivity was strongly suppressed in B cell-deficient mice with no DNCB-specific antibodies. It was also observed that treatment of animals with dinitrochlorobenzene polarized Th cells into Th2 differentiation by increasing the production of Th2 cytokines while decreasing the production of Th1 cytokines.
In striking contrast to the long-held belief that dinitrochlorobenzene-induced contact hypersensitivity is a cell-mediated immune response, the results of our present study demonstrated that the production of dinitrochlorobenzene-specific antibodies by activated B cells played an indispensible role in the pathogenesis of dinitrochlorobenzene-induced CHS. These findings may provide new possibilities in the treatment of human contact hypersensitivity conditions.
Offspring of asthmatic mothers have increased risk of developing asthma, based on human epidemiologic data and experimental animal models. The objective of this study was to determine whether maternal allergy at non-pulmonary sites can increase asthma risk in offspring.
BALB/c female mice received 2 topical applications of vehicle, dinitrochlorobenzene, or toluene diisocyanate before mating with untreated males. Dinitrochlorobenzene is a skin-sensitizer only and known to induce a Th1 response, while toluene diisocyanate is both a skin and respiratory sensitizer that causes a Th2 response. Both cause allergic contact dermatitis. Offspring underwent an intentionally suboptimal protocol of allergen sensitization and aerosol challenge, followed by evaluation of airway hyperresponsiveness, allergic airway inflammation, and cytokine production. Mothers were tested for allergic airway disease, evidence of dermatitis, cellularity of the draining lymph nodes, and systemic cytokine levels. The role of interleukin-4 was also explored using interleukin-4 deficient mice.
Offspring of toluene diisocyanate but not dinitrochlorobenzene-treated mothers developed an asthmatic phenotype following allergen sensitization and challenge, seen as increased Penh values, airway inflammation, bronchoalveolar lavage total cell counts and eosinophilia, and Th2 cytokine imbalance in the lung. Toluene diisocyanate treated interleukin-4 deficient mothers were able to transfer asthma risk to offspring. Mothers in both experimental groups developed allergic contact dermatitis, but not allergic airway disease.
Maternal non-respiratory allergy (Th2-skewed dermatitis caused by toluene diisocyanate) can result in the maternal transmission of asthma risk in mice.
Atopic dermatitis (AD) is a chronic inflammatory pruritic skin disease with extensive interindividual variation and multiple internal and external factors. In this study, we evaluated whether the atopic dermatitis severity (SCORAD index), gender, age, age onset or the presence of Allergic rhinitis (AR), Allergic conjunctivitis (AC) or Asthma has an influence on contact sensitization to common contactant allergens.
30 AD patients were evaluated in the Division of Allergy of Federal University of São Paulo. AD was diagnosed according to the Hanifin and Rajka's criteria and all patients were currently under regular treatment. Questionnaire (age, gender, age at onset, presence of AR, Asthma or AC), clinical examination and skin patch tests were carried out on all patients at the beginning of the study. Patients in regular use of oral CE; topical CE and/or calcineurin inihibitor use or having active AD lesions in the back were excluded from the study. Patch test was applied onto the upper back with 8 mm chambers attached with hypoallergenic tape and removed after 48 hours. The interpretation of the test reactions was performed at 48th and 96th hour.
Positive Patch-test reaction occurred in 14/30 (46.6%). Among those with positive patch-test, Nickel was responsible for 42.8% and Thimerosal for 28.5%. All patients finished the study and no adverse reactions occurred. Positive and negative Patch-test groups found no statistically significant difference (P > 0.05) when comparing: SCORAD index, sex, age, age of onset and presence of AC, AR or asthma.
According to our results, sensitization to common contact allergens in AD patients was more frequent than in normal subjects. Although we did not found an explanation to these findings, indiscriminate exposure to topic products should be avoided so that new sensitization or risk of deteriorating AD occurs. The benefits of avoidance to the contactants considered positive should be evaluated in the follow-up of these patients.
Allergic contact dermatitis to textile dyes is considered to be a rare phenomenon. A recent review reported a prevalence of contact allergy to disperse dyes between 0.4 and 6.7%. The relevance of positive patch testing was not reported in all studies. Textile dye allergy is easily overlooked and is furthermore challenging to investigate as textile dyes are not labelled on clothing. In this report, we present a case of allergic contact dermatitis to a textile necklace. The patch test showed strong reactions to the necklace and the azo dyes Disperse Orange 1 and Disperse Yellow 3. Despite the European legislation and the reduced use of disperse dyes in Third World countries, disperse azo dyes still induce new cases of allergic contact dermatitis.
Allergic contact dermatitis; Textile dermatitis; Disperse dyes; Disperse Yellow 3; Disperse Orange 1
Background—Over the last few years, changes in cutaneous homoeostasis resulting from sports activities have been reported. In particular, alterations in sweating mechanisms, the hydrolipid barrier, and surface bacterial flora, together with exposure to atmospheric conditions and the need to use medicaments, detergents, and other topical substances, predispose subjects to allergic contact dermatitis.
Objective—To evaluate the incidence of allergic contact dermatitis in a group of young people practising sports activities.
Methods—Patch tests were performed to confirm the diagnosis of irritant or allergic dermatitis; in addition, the radioallergoabsorbent test (RAST) to latex was evaluated in the group studied.
Results—Allergic contact dermatitis caused by thiourams (23.3%) and mercaptobenzothiazole (20.9%) was prevalent. Other haptens, such as benzocaine and nickel, which are contained in clothing, equipment, topical medicaments, and creams used for massage, were also allergenic. In two cases, RAST positivity to latex was registered.
Conclusions—The results suggest that close contact with sports equipment may increase the incidence of allergic contact dermatitis. Students practising certain sports may have "professional" allergic contact dermatitis to additives used in the production of rubber.
Key Words: skin; allergic contact dermatitis; latex; patch test; equipment; thiourams