Papular and follicular contact dermatitis: irritation and/or allergy? Swiss Contact Dermatitis Research Group.
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Since oral cyclosporin A (CsA) has demonstrated its effectiveness in psoriasis and atopic dermatitis, efforts have been made to develop a topical CsA formulation, thus avoiding systemic adverse events. A limited number of publications are available on the use of topical CsA in allergic contact dermatitis and atopic dermatitis. Moreover the response rate of humans to topical CsA is about 50% or less. We now report our results with three new topical CsA formulations on allergic contact dermatitis and atopic dermatitis. No significant improvement was found in 16 atopic dermatitis patients and 7 allergic contact dermatitis (nickel sulphate) patients.
BACKGROUND: About 20% of patients using transdermal estradiol complain of adverse local side effects. CASE: A 47-year-old, postmenopausal woman developed eczematous lesions at the sites of application of a estradiol therapeutic transdermal system and successively at the sites of application of a gel containing estradiol. Due to the topical intolerance, the therapy was switched to oral estrogen, which caused a systemic pruritic rash. Positive patch tests with estradiol led to the diagnosis of type IV allergic dermatitis due to transdermal estradiol and to a gel containing estradiol. Systemic contact dermatitis due to oral estradiol was also diagnosed. CONCLUSION: Even though allergic contact dermatitis from estradiol is extremely rare, local side effects from estradiol systems must be kept in mind and correctly diagnosed. Patch tests allow identification of the causative agent. In the case of primary sensitization to topical estradiol, oral estrogens must be prescribed cautiously to avoid systemic reactions.
A case of allergic contact dermatitis to a keyboard wrist rest containing neoprene is reported. The patient, who had a history of sensitivity to rubber products, developed an acute vesicular reaction of the palmar aspects of her distal wrists, followed by eczematous patches of her extremities and face. Treatment with prednisone, a 3-week tapering dose (60, 40, 20 mg), cleared the dermatitis. The widespread uses of neoprene are discussed and suggest that neoprene will become a common source of contact dermatitis as the potential sources of exposure increase.
Allergic contact dermatitis and irritant contact dermatitis in the small animal may result in clinical lesions with similar anatomical locations. Allergic contact dermatitis is generally noted in ventral and lightly haired regions as a papular, erythematous, and sometimes vesicular dermatitis. It is intensely pruritic and is the result of many months (and usually years) of exposure to the contact allergen. Total avoidance of the allergenic substance is the only successful long-term management. Irritant contact dermatitis occurs when an irritating substance is applied to the skin. It is a sequela that would occur in the majority of a population having contact with the compound. It is generally more painful than pruritic. Removal of the irritant will permit resolution of the signs.
BACKGROUND: Contact dermatitis accounts for a considerable portion of outpatient clinic visits to dermatologists. The state of education in contact dermatitis at the level of dermatology residency training in the United States has not been examined. OBJECTIVE: To assess the state of education in contact dermatitis in dermatology residency programs in the United States. METHOD: Cross-sectional survey of directors and chief residents of 105 dermatology training programs accredited by the American College of Graduate Medical Education. RESULTS: Seventy-seven percent of directors and 74% of chief residents responded to the survey. In general, both sets of respondents gave concordant responses although responses from directors were more positive. With respect to didactic education, the vast majority of programs (> 73%) held lecture conferences on contact dermatitis. Less than one-third included contact dermatitis-focused journals in journal club conferences. A bare majority of programs (57% of directors, 53% of chief residents) identified a faculty expert in contact dermatitis, with almost all experts conducting patch-test clinics and providing lectures on contact dermatitis. Seventy-five percent of experts were members of the American Contact Dermatitis Society (ACDS). Although residents in most programs (> 78%) performed patch tests to diagnose contact dermatitis, there were 14 programs in which none of their graduates performed such tests. Moreover, only 27% of programs had rotations dedicated to contact dermatitis and/or patch testing. Finally, directors and chief residents predicted that most graduates will incorporate the TRUE Test and not the more extensive or customized patch tests in their practices. CONCLUSIONS: Several opportunities for improving contact dermatitis education in residency programs were identified, including recruitment or development of more faculty experts in contact dermatitis, creation of rotations dedicated to contact dermatitis, and greater inclusion of contact dermatitis-focused journals in journal club conferences. As the principal interest group for contact dermatitis in the United States, the ACDS is the logical organization to spearhead improvement of contact dermatitis education in residency programs.
The spontaneous 3H-thymidine (3HT) labelling of some lymphocyte subpopulations has been studied in the peripheral blood of five patients with atopic dermatitis and five with widespread allergic contact dermatitis and compared with that in 10 healthy subjects. One hour after addition of 3HT to heparinized blood, lymphocytes were separated and processed with two different rosetting techniques (E-rosette test and Active E-rosette test). The cell suspensions were cytocentrifugated and autoradiography undertaken. An increased number of 3HT labelled lymphocytes was observed in the peripheral blood of patients with dermatitis as compared to controls. These labelled lymphocytes were E-rosette-forming cells (T cells) and E-non-rosette-forming cells (non-rosette-forming T cells and non-T cells). The ratio between the labelling index (LI) of E-rosette- to the LI of non-E-rosette-forming cells was in favour of T cells in allergic contact dermatitis (ratio = 3.09) whereas in atopic dermatitis (ratio = 0.93) the DNA synthesis was relatively greater in the non-rosette-forming cells. It is suggested that this increased LI of peripheral blood lymphocytes could be related to the increased derman mononuclear cell 3HT-labelling that has been reported previously in these inflammatory skin diseases.
BACKGROUND: Idiopathic CD4+ lymphocyte deficiency is a newly described entity of apparently non-human immunodeficiency virus-associated helper T-cell depletion. The clinical spectrum continues to evolve, but, to date, it has included patients ranging from those with minimal symptoms to those who have died with acute opportunistic infections. Several individual cases have been previously reported, many with distinctive, primarily infectious, cutaneous manifestations. OBSERVATIONS: We describe a patient with idiopathic CD4+ lymphocyte deficiency distinguished by a unique clinical presentation of atopic dermatitis exacerbated by contact urticaria and allergic contact dermatitis. She has a persistent markedly diminished CD4+ lymphocyte count (absolute count less than 50), no serologic evidence of, or risk factors for, human immunodeficiency virus infection, and no history of opportunistic infections. CONCLUSIONS: We present a possible new cutaneous manifestation of idiopathic CD4+ lymphocyte disease and summarize the previously reported cases, with an emphasis on the cutaneous features.
BACKGROUND: Activation and skin-selective homing of T cells and effector functions in the skin represent sequential events in the pathogenesis of atopic dermatitis and allergic contact dermatitis. OBJECTIVE: T cell-mediated keratinocyte apoptosis plays a key pathogenetic role in the formation of eczematous dermatitis. IFN-gamma released from activated T cells upregulates Fas on ke-ratinocytes, which renders them susceptible to apoptosis. The lethal hit is given to keratinocytes by means of Fas ligand expressed on the T-cell surface or released to the inflammatory microenvironment. We sought to investigate whether drugs used for the treatment of eczematous disorders interfere with this pathogenic pathway. METHODS: T cell-mediated, Fas-induced keratinocyte apoptosis in a keratinocyte-T cell coculture system serves as an in vitro model of eczematous dermatitis. We tested, in this model, whether immunomodulatory agents (dexamethasone, cyclosporine A, rapamycine, tacrolimus/FK506, intravenous immunoglobulin [IVIG], and theophylline) are able to inhibit apoptosis of keratinocytes. Additionally, skin biopsy specimens from patients with untreated and successfully treated eczematous dermatitis were evaluated for keratinocyte apoptosis. RESULTS: Dexamethasone, cyclosporine A, FK506, rapamycine, and IVIG are inhibitors of keratinocyte apoptosis induced by activated T cells. This effect is mediated by 2 major mechanisms directed on T cells or keratinocytes. T-cell activation was mainly inhibited by dexamethasone, FK506, cyclosporine A, and rapamycine. Interestingly, high-dose dexamethasone and IVIG directly inhibited Fas-mediated keratinocyte apoptosis. In vivo keratinocyte apoptosis was significantly reduced after successful topical treatment of eczematous lesions. CONCLUSION: These results demonstrate mechanisms of action of current treatment approaches and provide a future for more focused therapeutic applications.
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Allergic contact dermatitis is a classical type IV delayed hypersensitivity immune response. This cell-mediated response is also known as hapten-type delayed hypersensitivity. Allergic contact dermatitis may be viewed as hyperreactivity of the skin immune system. In the present view of allergic contact dermatitis, individuals are born in a state of tolerance to environmental haptenic allergens. During life, sensitization to any hapten(s) may occur. Subsequent elicitation of a sensitized individual then leads to dermatitis, often accompanied by severe pruritus. Human epidermal Langerhans cells play a central role during the sensitization stage. These antigen presenting dendritic cells, loaded with environmental haptens, continuously leave the epidermis through the lymph vessels and, upon arrival in the paracortical T-cell areas of the skin draining lymph nodes, they differentiate into interdigitating cells. There is now in-vitro evidence for such a maturation of human Langerhans cells into interdigitating cells. Any given individual may be sensitized to any particular hapten by this route. Allergic contact dermatitis is probably a skin-specific disease because of the capacity of Langerhans/interdigitating cells to induce relatively naive T-cells to become memory T-cells. Factors determining the ultimate outcome in this continuous hapten presenting process, i.e. whether or not the original state of tolerance will persist, are still enigmatic. During elicitation, when the allergenic hapten is applied epicutaneously to a sensitized individual, a focal accumulation of immune response associated cells producing a wide variety of cytokines and inflammatory mediators ultimately results in the clinical condition of allergic contact dermatitis. Langerhans cells do not seem to play a major role during this stage.(ABSTRACT TRUNCATED AT 250 WORDS)
The relationship between atopic dermatitis (AD) and allergic contact dermatitis (ACD) has long been and continues to be an unsolved and frequently discussed issue. Whereas AD patients have traditionally been considered to have a decreased frequency of ACD, recent studies revealed that these individuals are more or equally likely to develop ACD. The aim of the present review was to determine whether the results of recent experimental studies and theoretical considerations might lead to a parallel shift in our concept on the causal relationship between AD and ACD. It has been shown that Th2 and Th1-type immune responses are not mutually exclusive, and that at least in AD a mixture of both Th2 and Th1 occurs and the interactions between them account for the clinical characteristics of the disease. This new concept on the immunopathomechanism of AD challenges our previous belief that the cytokine pattern of the affected skin is unsuitable for the development of delayed-type hypersensitivity. Since we do not know the exact quantitative balance between Th1 and Th2 reactions along a time axis, we cannot predict whether the cytokine pattern of AD patients favors or inhibits the development of ACD. What we do know with a greater degree of certainty, is that when the eczematous excoriated skin of AD patients, with its defective epidermal barrier (enhancing the penetration of many antigenic substances) is chronically exposed to skin care products and various sensitizing topical medications, it is more likely to develop a superimposed ACD.
Occupational contact dermatitis is often of multifactorial origin, and it is difficult to determine the relative significance of the various contributing factors. Contact allergies are relevant in 20-50% of recognised occupational contact dermatitis cases. The reported frequency in different studies varies, depending on differences in how occupational diseases are notified and recognised, in types of occupation in a geographical area, and the "quality" of the dermatological examination, including the accuracy of the diagnostic patch-test investigation. However, the clinical relevance of the reported contact allergies is often uncertain. Many occupational contact dermatitis patients with documented contact allergies develop chronic eczema, in spite of work changes and attempted allergen avoidance. Recognition/non-recognition of a notified case may be based on circumstantial evidence, because of difficulties in the establishing of a firm proof of work exposure and subsequent development of skin disease. Reliable quantitative exposure measuring techniques are needed. Methods are developed for the measurement of exposure to allergens such as nickel and acrylates, which makes it possible for exposure-effect relationships to be established with increased certainty. For prevention of allergic contact dermatitis it was a major step forward, with mandatory ingredient labelling of cosmetic products. However, improved labelling of the presence of contact allergens in household and industrial products is needed. For the identification of hazardous contact allergenic compounds, guinea pig or mice assays are still required. The local lymph node assay (LLNA), which is an objective and sensitive mouse assay has now been internationally validated and accepted.
Corticoid allergic contact dermatitis (ACD) may be topically or systemically elicited. Allergic contact dermatitis to topical corticosteroids is relatively common, whereas reports of orally elicited ACD to corticosteroids are rarer. Patients allergic to one corticosteroid often exhibit cross-reactivity to other corticoids. We have previously reported a 46-year-old woman with contact allergy documented by patch and provocative use testing to multiple topical corticosteroids. On further testing, she was thought to have multiple corticoid orally elicited ACD to triamcinolone, methyl prednisolone, dexamethasone, and prednisone. Oral provocation tests were performed in a single-blind fashion following the method of Alanko and Kauppinen [Diagnosis of drug eruptions: clinical evaluation and drug challenges. In, Skin Reactions to Drugs (Kauppinen K, Alanko K, Hannuksela M, Maibach HI, eds). Boca Raton, FL, CRC Press, 1998.]. The five oral corticosteroids tested were triamcinolone, methyl prednisolone, dexamethasone, prednisone, and hydrocortisone. Four of the five challenged corticosteroids (i.e., triamcinolone, methyl prednisolone, dexamethasone, and prednisone) produced a generalized maculopapular eruption in a delayed manner. The fifth challenged corticoid, hydrocortisone, had no adverse effect on this patient. This patient was unusual in that she exhibited polysensitivity to a spectrum of oral and topical corticosteroids. Hydrocortisone was identified as a corticosteroid for future clinical use. This is an important finding since corticosteroids are important emergency drugs.
BACKGROUND: Potato contains multiple heat-labile proteins which can induce immediate hypersensitivity reactions. Rhino-conjunctivitis, asthma, contact urticaria and protein contact dermatitis have been described in association with potato exposure. OBJECTIVE: A patient with possible airborne facial dermatitis to potato is described. RESULTS: A middle-aged atopic housewife with pre-existent atopic dermatitis suffered from rhino-conjunctivitis, asthma, and contact urticaria when pealing raw potatoes, but her main complaint was intense, treatment-resistant dermatitis of the face. The investigations showed a positive prick test, a positive patch test, and positive specific serum IgE to raw potato. Potato avoidance led not only to the resolution of the immediate symptoms, but also of the facial dermatitis, suggesting she had dermatitis due to this vegetable. CONCLUSIONS: Potato may induce contact dermatitis with positive immediate and delayed hypersensitivity tests.