STUDIES IN CONTACT DERMATITIS. XV. DENTAL MATERIALS.
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BACKGROUND: The panel of patch test allergens used for the evaluation of patients with suspected photoallergy typically does not include plant and pesticide allergens. The prevalence of allergic contact dermatitis and photoallergic contact dermatitis to plant and pesticide allergens was determined for this subgroup of patients. OBSERVATION: Positive reactions were detected in 12 of 26 patients who were tested with our photoallergen series: 5 with allergic contact dermatitis, 5 with photoallergic contact dermatitis, and 2 with both. Four of the 12 patients had positive patch and photo-patch test reactions to plant allergens, pesticide allergens, or both. The positive patch test reactions were to the plants Taraxacum officinale (dandelion) and Tanacetum vulgare (tansy) and to the pesticides folpet and captafol. Positive photo-patch test reactions were to the pesticides folpet and captan. The histories of the patients suggested that 2 or 3 of the 4 patients had clinically relevant reactions. In the other 8 patients, positive reactions to the patch and photo-patch tests included fragrances, sunscreens, and antibacterial agents. CONCLUSION: Plant and pesticide allergens should be included in the patch and photo-patch test series used for the evaluation of patients with suspected photoallergy.
Immune responses to enviornmental agents affecting the skin may take various clinical forms, among which contact dermatitis is the most prominent representative of delayed-type hypersensitivity. Whereas in industrialized countries a relatively restricted amount of chemical agents is responsible for the majority of contact dermatitis cases, other factors from the environment such as natural flora, seasonal or nutritional factors may also play a role. Like other immune responses, contact dermatitis is strongly influenced by genetic factors and the existence of immune response genes, in part linked to the major histocompatibility complex, has been established in experimental animals. Whereas the formation of conjugates between skin-specific proteins and contactant allergens is held by some to represent an important feature in contact dermatitis, recent experiments suggest that the direct binding of contactants to monocyte and lymphocyte membranes represents the most efficient way in inducing sensitization of the T lymphocytes primarily responsible for contact hypersensitivity. At the effector level, complete inhibition of contact dermatitis and other delayed type hypersensitivity reactions by an antiserum prepared against guinea pig lymphokines (especially migration inhibition factor) offers strong evidence that lymphokines, as products of activated lymphocytes, also play a decisive role in vivo. The properties of antibodies raised against purified lymphokine fractions are reviewed. Localized contact dermatitis reactions, as well as accompanying phenomenons such as flar-up reactions and generalized maculopapular rashes, may, however, still involve other elements than T lymphocytes and lymphokines. The participation of other secondary cell types and of local antibody formation is briefly discussed.
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Occupational contact dermatitis in hair dressers and beauticians has increased in importance in the past years. Type IV-allergies against glyceryl monothioglycate components of permanent waves are most common. Other occupational allergens include bleach components such as ammonium persulfate and hair dye ingredients such as p-phenylenediamine (PPD) and p-toluylene-diamine (PTD) base. Allergies to hair dyes in customers of hair dressers have rarely been observed. Two female patients developed allergic contact dermatitis of the scalp and face after repeated use of Polycolor intensivtönung schwarz and of Movida color. We also review the current literature on type IV-allergies to components of hair dressing products components.
Lymphomatoid contact dermatitis refers to the relatively little known phenomenon of allergic contact dermatitis producing histological features suggestive of cutaneous T-cell lymphoma. We report the first case of lymphomatoid contact dermatitis in response to para-tertyl-butyl phenol resin.
Recent data suggest a key rôle for IL-1 beta in the induction phase of allergic contact dermatitis. In the present study, the protein levels of IL-1 beta were measured in skin lymph derived from normal untreated skin as well as from irritant and allergic (induction and elicitation phase) contact dermatitis. IL-1 beta increased in the course of both types of contact dermatitis, displaying the highest levels in irritant CD. Using a reverse transcriptase-polymerase chain reaction, low signal strength of IL-1 beta mRNA was demonstrated in lymph cells derived from normal skin and allergic CD. In lymph cells collected 2 x daily during the induction phase of allergic contact dermatitis, no upregulation of the IL-1 beta mRNA signal was found. Isolated CD1a+ lymph cells derived from normal skin as well as from the induction and elicitation phase of allergic contact dermatitis did not express IL-1 beta mRNA. Our results demonstrate that in human skin lymph, the IL-1 beta profiles do not discriminate between irritant and allergic contact dermatitis and that besides resident epidermal and dermal cells, circulating lymph cells may also contribute to IL-1 beta protein production.
Medical practitioners have a role in the recognition of occupational contact dermatitis. The longer the duration of symptoms before diagnosis, the poorer the outcome. Our objective was to understand practice patterns, barriers and needs for early diagnosis of occupational contact dermatitis. A survey to obtain information on practice patterns was developed based on the literature and interviews with dermatologists and family practitioners. The survey was sent to all dermatologists and a random sample of 600 family practitioners in Ontario. Fifty-seven per cent of dermatologists and 9% of family practitioners report seeing more than 20 patients per year with occupational contact dermatitis. The majority of practitioners report taking a workplace exposure history. Barriers to taking a workplace exposure history include time constraints and lack of knowledge. Reasons for referral to specialists include a lack of expertise, testing facilities and knowledge about workers' compensation, time constraints and inadequate reimbursement, whereas lack of access to specialists is a barrier for referral. Although most practitioners identify a need for further education, a low volume of patients and time constraints are key barriers to continuing education. Opportunities are identified to improve educational initiatives and health services delivery for occupational contact dermatitis, tailored to each practitioner group.
Allergic contact dermatitis is a delayed-type hypersensitivity reaction, secondary to hapten-specific T lymphocyte activation in sensitized individuals. The present study reports on the establishment of T cell lines from peripheral blood mononuclear cells (PBMC) of nickel-allergic patients, initially cultured with nickel, IL-2, or PHA and IL-2. It was possible to derive hapten-specific T cell lines from the three protocols, and the best proliferative responses to nickel were observed when PBMC were cultured in the presence of nickel in vitro. T cell lines initially cultured with IL-2 always gave better specific proliferative responses to nickel than those derived with PHA and IL-2. Phenotypical analysis of the nickel-specific T cell lines showed that they were mainly composed of activated CD8+ TcR alpha beta + T lymphocytes. These results emphasize the importance of initial culture conditions for the generation of hapten-specific T cell lines and suggest that CD8+ lymphocytes could play an important role in the pathogenesis of allergic contact dermatitis.
The clinical efficiency of mitigating contact dermatitis with a Ginkgo biloba extract and carboxymethyl-beta-1,3-glucan formulation was investigated in a double-blind versus placebo study using 22 subjects (Caucasian women aged 22-55 years) with allergic contact dermatitis from various substances in the European standard series. The formulation was applied to intact skin 2X a day for 2 weeks ("in use" application) prior to a single application of a selected contact allergen under a Finn Chamber for 24 h. Readings were carried out in a blind study by a dermatologist 2 and 3 days after patch removal. Representative photographs were taken of treated, placebo and untreated test areas. 68.2% of the panelists showed significantly reduced skin reactivity (p = 0.037*) on the treated site 2 days after patch removal, versus untreated and/or placebo sites. This finding indicates that the Ginkgo biloba/carboxymethyl-beta-1,3-glucan formulation can mitigate against allergic contact dermatitis.
Induction in mice of marked photoallergic contact dermatitis (PCD) to 3,3',4',5-tetrachlorosalicylanilide (TCSA) with UVA (320 to 400 nm) radiation requires pretreatment with cyclophosphamide (CY). Attempts to induce photoallergic contact dermatitis without CY result in only a small degree of sensitivity, accompanied by significant net splenic suppressor cell activity. These suppressor cells are antigen specific, inhibit the induction but not the elicitation of photoallergic contact dermatitis to TCSA, and are T lymphocytes. Exposure of mice to UVB (280 to 320 nm) radiation at a site distant from that of sensitization, before CY administration and sensitization, inhibits the development of photoallergic contact dermatitis. This is analogous to the suppression of allergic contact dermatitis (ACD) observed in mice after exposure to UVB radiation; such suppression is accompanied by the formation of antigen-specific splenic suppressor cells. However, in contrast to the findings with allergic contact dermatitis, splenic suppressor cells are not detected in mice that are treated with UVB radiation before CY administration and sensitization to TCSA. This is presumably because CY prevents their formation. This provides evidence that UVB-irradiated mice have a second form of anergy that is not mediated by suppressor cells.
9 of 10 patients who developed dermatitis following contact with Holigarna ferruginea and 5 of 35 asymptomatic volunteers showed a positive patch test reaction to 2% W/V acetone extract of the plant's resinous exudate. 6 albino rats were sensitized following 3 weekly applications of the same extract. Laccol (3-heptadecadienyl catechol) was identified as the active principle in the exudate.
LEARNING OBJECTIVES: Reading this article will reinforce the reader's knowledge of the definition, pathophysiology, differential diagnosis, evaluation, and management of the most common of all the "eczemas," contact dermatitis, which can have an allergic and/or an irritant pathogenesis. DATA SOURCES: Relevant articles and current texts on contact dermatitis were referenced and reviewed. The personal experiences of the authors in an Environmental Medicine Clinic, their private practices, and their teaching of residents and other physicians were evaluated. A MEDLINE database using subject keywords was searched from 1986 to date. STUDY SELECTION: Book chapters, pertinent articles, data source abstracts, guidelines for the management of contact dermatitis set by the American Academy of Dermatology, and the American Contact Dermatitis Society were critiqued. RESULTS: The recent elucidation of the pathoimmunology of contact dermatitis is concisely reviewed, highlighting its clinical implications. The protean clinical presentations of contact dermatitis, both "allergic" and "irritant" type are cited. The signs and symptoms warranting the search for a contactant are outlined. The most likely regional contactants are listed, but the need to reference a more complete textbook is often required. That patch testing is the gold standard to identify an allergenic agent causing allergic contact dermatitis is stressed. While the "who" and "when" to patch test is amply described, a cookbook "how" to patch test has been omitted in order to emphasize the importance of "hands on" experience for such testing. The advantages and limitations of the commercially available standard patch tests (Hermal, and T.R.U.E.) are described, plus the sources for "nonstandard" patch tests is made available. Therapeutic modalities, topical and systemic, for management of the uncomfortable patient are outlined. CONCLUSION: The physician who manages a patient with an "eczematous" rash must be aware of the complete differential diagnosis of that clinical presentation. Suspicion that a "contactant" is the cause must have high priority, especially when the rash is persistent, and fails to respond to "appropriate" therapy. The value of a skin biopsy is limited to confirming its eczematous (spongiotic) nature and ruling out other diseases. Appreciating the paradox of patch testing, namely the deceptive simplicity of application versus the required expertise for interpretation and recognition of clinical significance, is the key to the proper management of the patient with contact dermatitis.
Allergic contact dermatitis (ACD) is a T-cell-mediated disease in which expression of a distinct repertoire of chemokines results in the recruitment of effector T cells into the skin. While it is becoming clear which chemokines and receptors determine the development of ACD, the mechanisms involved in the retention of T cells in the skin after resolution of inflammation are still unknown. Unravelling these mechanisms will help us to understand local skin memory as observed in retest reactivity and flare-up reactions. This study was designed to evaluate the role of chemokine-chemokine receptor interactions in local T-cell retention. The results show that expression of the CCR10 targeting ligand CCL27 is not only increased during inflammation, but also remains increased several weeks after clinical responsiveness to patch testing. In parallel with increased CCL27 expression, an increased number of infiltrating cells could still be detected in skin that, clinically, had returned to normal 21 days after patch testing. These persisting cells were characterized as CD4+ cells expressing CCR10, while no CD8+ CCR10+ cells could be detected. The presence of these cells is most likely an allergen-mediated effect, as increased levels of CCL27 and CCR10 could not be detected 21 days after initiating an irritant contact dermatitis reaction. In contrast to CCL27, increased expression of CXCL9, CXCL10, and CXCL11 could only be observed during the clinically inflammatory phase of ACD. In conclusion, local CCL27-mediated retention of CCR10+ CD4+ T cells in sites previously challenged by ACD could be responsible for phenomena such as local skin memory observed in retest reactions and flare-up reactions in which the presence of persisting T cells results in an accelerated inflammatory response upon renewed allergen challenge.