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Results for “Dermatitis, Allergic Contact”

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At least 19 recordsLinked to original sources
PubMed2001

Evaluation of efficacy of a skin lipid mixture in patients with irritant contact dermatitis, allergic contact dermatitis or atopic dermatitis: a multicenter study.

Disturbances of skin barrier function occur in several skin diseases, e.g., atopic dermatitis (AD), irritant/allergic contact dermatitis (ICD, ACD). Skin barrier damage triggers the production of cytokines that stimulate lipogenesis which may also cause inflammatory processes. The aim of this study was to evaluate the efficacy of a topical skin lipid mixture in the treatment of ICD, ACD and AD. 580 consecutive patients suffering from ICD, ACD or AD were treated with a skin lipid mixture containing ceramide-3 and patented nanoparticles. Patients received the lipid mixture alone or in combination with topical corticosteroids until clearance or for 8 weeks. Both treatment groups statistically improved all parameters considered at week 4 and 8 as compared to baseline. Between the 2 treatment groups, there was a statistically significant difference in favour of combined therapy for (ICD, ACD, AD, respectively): erythema, pruritus and overall disease severity; erythema and pruritus; erythema, pruritus, fissuring and overall disease severity. No statistically significant difference was found for (ICD, ACD, AD, respectively): dryness, scaling and fissuring; scaling, fissuring and overall disease severity; dryness and scaling. Between the 2 ACD treatment groups, there was a statistically significant difference in favour of the skin lipid mixture for dryness. In conclusion, the study shows that balanced lipid mixtures are effective in improving barrier properties and the clinical condition of the skin in contact dermatitis.

Administration, Topical↗
PubMed1996

Dissection of antigenic and irritative effects of epicutaneously applied haptens in mice. Evidence that not the antigenic component but nonspecific proinflammatory effects of haptens determine the concentration-dependent elicitation of allergic contact dermatitis.

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.

Administration, Cutaneous↗
PubMed2004

Allergic contact dermatitis.

Allergic contact dermatitis is a common skin condition that can be difficult to diagnose without the aid of a specific diagnostic tool called patch testing. The pathophysiology, clinical features, diagnosis, and treatment of allergic contact dermatitis are summarized in this review. The process of patch testing, the gold standard for diagnosing allergic contact dermatitis, is discussed in detail.

Administration, Oral↗
PubMed1991

Recent developments in the pathogenesis of allergic contact dermatitis.

Allergic contact dermatitis is both an important clinical problem and a model system for lymphocyte-mediated pathologic changes. Elicitation of allergic contact dermatitis requires interaction of antigen with epidermal Langerhans cells, followed by migration of the Langerhans cells to the lymph nodes to present antigen to T lymphocytes. These activated T lymphocytes must then home to the antigen-exposed skin. Adhesion molecules such as LFA-1 and ICAM-1 have a role in this homing. Only a small proportion of the T lymphocytes in the skin lesion are specific for the inducing antigen. Studies of poison ivy (urushiol dermatitis) have determined this fraction to be less than one per 100 infiltrating lymphocytes. By a variety of amplification mechanisms, it is possible for this small number of antigen-specific T lymphocytes to induce the pathologic changes of allergic contact dermatitis. Improved understanding of this condition should result in increased knowledge of the pathogenesis of a variety of T lymphocyte-mediated skin conditions.

Dermatitis, Contact↗
PubMed1999

Mechanisms of drug-induced allergic contact dermatitis.

Allergic contact dermatitis is induced by a wide variety of drugs that trigger specific immune responses following topical exposure. Identified chemical structures involved in such reactions include the mercuric and thiosalicylic acid groups of thimerosal, the diphenylketone group of the anti-inflammatory drug ketoprofen, the amide or ester structure of local anesthetics, and the side-chain and thiazolidine ring of beta-lactams. The T cell responses to such compounds involve CD4+ and CD8+ alphabeta+ T lymphocytes and also CD4 /CD8 gammadelta+ T cells. Although "T helper 2" cytokine production by drug-specific human T cells from patients with allergic contact dermatitis has been described, T helper 1-like and T cytotoxic 1-like responses clearly play key roles in this cutaneous reaction.

Allergens↗
PubMed2004

Immunoregulation of allergic contact dermatitis.

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.

CD4-Positive T-Lymphocytes↗
PubMed2001

Effector and regulatory T cells in allergic contact dermatitis.

Allergic contact dermatitis is a prototypic T-cell-mediated disease that has a socio-economic impact in industrialized countries. Here, Andrea Cavani and colleagues highlight recent developments in the T-cell-based effector and regulatory mechanisms of this common skin disorder.

Dermatitis, Allergic Contact↗
PubMed2003

[Pathomechanisms of the elicitation phase of allergic contact dermatitis].

Allergic contact dermatitis (ACD) is a T-cell mediated, antigen-specific inflammatory response to repeated epicutaneous exposure to haptens. Two immunologically distinct sequential steps are required to produce the clinical picture of ACD. In the sensitization phase, naïve antigen-specific T cells are primed and differentiate into memory or effector T cells. In the elicitation phase, reapplication of the same hapten leads to local recruitment of hapten-specific T cells which are cytotoxic, release cytokines and recruit other inflammatory cells. These events lead to clinically visible tissue inflammation characterized by edema, erythema, scaling, and blistering. For the clinician, the effector phase is especially important, because sensitization is generally asymptomatic, whereas elicitation produces the clinical picture of ACD. Detailed knowledge about the mechanisms of the elicitation phase of ACD is needed in order to develop novel therapeutic approaches.

Cytokines↗
PubMed2002

Allergic contact dermatitis.

Allergic contact dermatitis (ACD) is a common occupational and environmental health issue. In common with other forms of allergy the disease progresses in two stages; an initial phase during which sensitization is acquired, followed later (after subsequent exposure to the same chemical allergen) by elicitation of a cutaneous inflammatory reaction. The development of skin sensitization is associated with, and requires, the activation and clonal expansion of allergen responsive T lymphocytes and it is these cells that orchestrate the cutaneous allergic reaction. In recent years, much has been learned of the characteristics of immune responses to skin sensitizing chemicals and of the roles played by dendritic cells, cytokines and chemokines. Some of the more interesting cellular and molecular mechanisms are reviewed briefly in this article. A more detailed appreciation of responses induced by chemical allergens has in turn facilitated the design of novel approaches to the toxicological evaluation of skin sensitization. Real progress has been made, not only in the development of improved methods for hazard identification and characterization, but also in the application of new paradigms for risk assessment. The newer methods now available and the opportunities that exist for further advances are considered. Finally, progress has been made in the characterization of skin sensitization in humans and in the clinical management of ACD. This article seeks to consider skin sensitization and ACD in holistic fashion, bridging experimental observations with clinical disease and basic mechanisms with practical toxicology.

Allergens↗
PubMedDate not supplied

The role of CD4+ and CD8+ T cells in contact hypersensitivity and allergic contact dermatitis.

Allergic contact dermatitis (ACD) and contact hypersensitivity (CHS) are delayed-type hypersensitivity reactions which are mediated by hapten specific T cells. During the sensitisation phases, both CD4+ and CD8+ T cell precursors are activated in the draining lymph nodes by presentation of haptenated peptides by skin dendritic cells. Subsequent hapten skin painting induces the recruitment of T cells at the site of challenge which induces inflammatory signals and apoptosis of epidermal cells, leading to the development of a skin inflammatory infiltrate and of clinical symptoms. There have been major controversies on the respective roles of CD4+ and CD8+ T cells in the development of the CHS inflammatory reaction. Experimental studies from the last 10 years have demonstrated that, in normal CHS responses to strong haptens, CD8+ type 1 T cells are effector cells of CHS while CD4+ T cells are endowed with down-regulatory functions. The latter may correspond to the recently described CD4+ CD25+ regulatory T cell population. However, in some instances, especially those where there is a deficient CD8 T cell pool, CD4+ T cells can be effector cells of CHS. Ongoing studies will have to confirm that the pathophysiology of human ACD is similar to the mouse CHS and that the CHS response to weak haptens, the most frequently involved in human ACD, is similar to that reported for strong haptens.

CD4-Positive T-Lymphocytes↗
PubMed1990

Mechanisms involved in allergic contact dermatitis.

Allergic contact dermatitis is a common inflammatory skin disease caused by agents such as plants, chemical compounds, and topical medications. Histologic features typically include edema within the epidermis and dermis and a lymphohistiocytic infiltrate with an admixture of basophils. Langerhans cells and keratinocytes play pivotal roles in allergic contact dermatitis reactions. Langerhans cells synthesize and express class II molecules that allow the presentation of exogenous antigens to T lymphocytes. Additionally, keratinocytes and Langerhans cells produce interleukin-1, which is thought to be a second signal that activates T cells. Mast cells and basophils also may play a proinflammatory role. Treatment primarily consists of removal of the offending agent. At times, systemic corticosteroids may be required, especially in the acute phase. In more chronic cases, topical corticosteroids may be beneficial. Antihistamines may be useful because of their soporific effects, but their usefulness is limited.

Dermatitis, Contact↗
PubMed2000

Allergic contact dermatitis.

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.

Child↗
PubMed1996

Mango dermatitis: allergic contact dermatitis to Mangifera indica.

Mango Dermatitis' is the common term given to allergic contact dermatitis to the sap or skin of the fruit of Mangifera indica. Four patients presented with urticaria and eczematous rash following exposure to mangoes or the trees. Patch testing with diluted sap, crushed leaf, crushed stem and fruit skin was strongly positive.

Adult↗
PubMed2002

Allergic contact dermatitis to topical minoxidil solution: etiology and treatment.

After more than a decade of use, topical minoxidil solution has proven to be a safe and effective treatment for androgenetic alopecia. However, some patients present with complaints of pruritus and scaling of the scalp. The most common causes of these symptoms include irritant contact dermatitis, allergic contact dermatitis, or an exacerbation of seborrheic dermatitis. Patients suffering from allergic contact dermatitis may benefit from patch testing to determine the causative allergen. Among the patients we patch tested, propylene glycol was found to be the contactant in a majority of cases, not the minoxidil itself. Many of these patients may be candidates for treatment with alternative formulations using other solvents, such as butylene glycol, polysorbate, or glycerol. Although predictive, patch testing results do not ensure that the compounded preparations will be tolerated. Unfortunately, patients found to be allergic to minoxidil are no longer candidates for topical treatment of their alopecia with any preparations of minoxidil.

Administration, Topical↗