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At least 1,225 records · Page 68Linked to original sources
PubMed1986

Contact dermatitis from Grevillea 'Robyn Gordon'.

Grevillea 'Robyn Gordon' is an Australian hybrid plant which may cause allergic contact dermatitis. Over the past 8 years, it has been planted extensively in Australia and is now being exported to the United States and other Western countries. Recently, an explosion in incidence of contact dermatitis due to this plant has been seen. 24 patients who were suspected of being sensitive to it were patch tested to fresh plant and extracts with confirmation of sensitivity. A cross sensitivity to Toxicodendron was demonstrated clinically and on patch testing. The allergen in Toxicodendron, 3 pentadecylcatechol, is closely linked in chemical structure to 5-pentadecylresorcinol, present in Grevillea banksii and tridecylresorcinol in Grevillea robusta. Patch testing in patients sensitive to Grevillea 'Robyn Gordon' with tridecylresorcinol produced positive reactions, thus implicating the sensitizing rôle of long chain alkyl resorcinols in Grevillea 'Robyn Gordon' allergy. There is a likelihood that this sensitizing potential extends to other plants of the Grevillea genus, e.g., Grevillea robusta. With the spread of Grevillea 'Robyn Gordon' to other markets, this problem will become increasingly common.

Adult↗
PubMed1985

Contact dermatitis to anaerobic sealants.

High-performance polymerizable anaerobic sealants originated in 1953 and are used to lock metal parts together chemically. A case of hand contact dermatitis from Loctite RC/601, 242, and 504 is reported in a 60-year-old machine assembler. This diagnosis was documented by positive patch tests of the product and of three of the components: polyethylene glycol dimethacrylate, hydroxypropyl, and hydroxyethyl methacrylate. This is the third report of contact dermatitis caused by these sealants in the United States, is the second in the world on hydroxypropyl methacrylate, and is another example of the wide environmental use of potentially sensitizing acrylic resins.

Acrylates↗
PubMed1976

Biosynthesis of prostaglandins in human allergic contact dermatitis.

The biosynthesis of prostaglandins by human inflamed skin was studied in 5 patients with allergic contact dermatitis induced by patch tests. Inflamed skin from these patients evidenced an increased ability to synthesize prostaglandins. In the presence of exogenous arachidonic acid in the incubation medium, the activity formed was about 60% greater in inflamed skin than in noninflamed control skin. In prostaglandin E1-equivalents the concentration amounted to 9.19 +/- 2.02 ng/mg protein nitrogen and 5.74 +/- 1.97 ng/mg protein nitrogen, respectively (mean values +/- S.E.). When inflamed skin was incubated without excess of exogenous precursor acids in the incubation medium the activity formed was about 130 times lower and the values were similar to those of non-inflamed skin. Thus, the present results support the view that the prostaglandin system is activated in allergic contact dermatitis, thereby providing a basis for future therapeutic attempts to control this disorder.

Dermatitis, Atopic↗
PubMed1989

[Contact dermatitis caused by isophorone diamine].

Two patients with allergic contact dermatitis to IPD (Isophoronediamine), a hardener present in plastics industries are presented. Its high capacity of sensitization perhaps is not well known because it is not enough tested in our contact clinics.

Adult↗
PubMed1981

The cellular infiltrate in experimental allergic and toxic contact dermatitis. Effect of systemically administered corticosteroids.

The effect of systemically administered corticosteroids on allergic and toxic contact dermatitis in the guinea pig was studied. Dermatitis was provoked with dinitrochlorobenzene (DNCB). The influence of corticosteroids on the sensitization phase was also investigated. The epicutaneous test reactions were assessed with the naked eye, low-power microscopy, and a method based on the counting of infiltrating cells in the upper corium. Prednisolone injected in a dose of 5 mg/kg body weight daily for 4 days starting on the 1st day of sensitization or the 1st day of testing tended to shorten the duration of the contract allergic skin reaction as seen with the naked eye. Microscopically, a decrease in the number of infiltrating basophil granulocytes was found. Prednisolone had no convincing influence on the toxic contract eczematous reaction macroscopically or microscopically. Responses to weakly toxic doses of DNCB tended to fade earlier and to show small displacements of granulocytes in the differential count of infiltrating cells compared to controls. The results suggest that prednisolone given systemically influences only slightly the inflammatory cell infiltration in contact dermatitis in the guinea pig.

Acanthosis Nigricans↗
PubMed1991

Allergic contact dermatitis from non-diglycidyl-ether-of-bisphenol-A epoxy resins.

In addition to previously presented patients with allergic contact dermatitis from cycloaliphatic epoxy resins (ERs), during 1974-1990, we have seen 4 patients with allergic contact dermatitis (ACD) caused by products containing uncured non-diglycidyl-ether-of-bisphenol-A ER. The patients were negative on patch testing with the standard ER based on diglycidyl ether of bisphenol A (DGEBA-ER). The following non-DGEBA-ERs were included in the causative agents: heterocyclic dimethylhydantoin ER, phenol novolak ER, and brominated ER. We were unable to specify the type of ER in an epoxy primer used by the 4th patient. Apart from the ACD caused by the brominated ER, 1 of the patients also had IgE-mediated occupational rhinitis caused by methyl hexahydrophthalic anhydride (MHHPA), an epoxy hardener. The diagnosis was verified by positive prick tests and specific IgE determinations with MHHPA. Intense rhinitis evoked by a bronchial challenge with MHHPA confirmed the diagnosis. We stress the importance of performing patch testing with the relevant epoxy resins to which the patient has been exposed, in addition to patch testing with the standard ER.

Adult↗
PubMed1979

Contact dermatitis due to nitroglycerin ointment.

Topical nitroglycerin ointment is among the most effective long-acting vasodilators currently available. We report two cases of contact dermatitis in which patch testing showed allergy to nitroglycerin-containing compounds. The severity of this dermatitis necessitated the discontinuation of topical nitroglycerin therapy in both patients. A potent corticosteroid cream applied once to previous nitroglycerin application sites prevented or minimized this dermatitis and enabled continuation of topical nitroglycerin therapy. Contact dermatitis due to topical nitroglycerin preparations may be more common than is presently realized.

Aged↗
PubMed1998

Patients with allergic contact dermatitis to nickel and nonallergic individuals display different nickel-specific T cell responses. Evidence for the presence of effector CD8+ and regulatory CD4+ T cells.

To investigate the mechanisms underlying the expression of allergic contact dermatitis, we compared the characteristics of nickel (Ni)-specific T cell responses in 10 patients with allergic contact dermatitis to Ni and in 10 healthy, nonallergic individuals. CD4+ T cells purified from peripheral blood of both allergic and nonallergic subjects proliferated similarly to NiSO4 in vitro, with the responses mostly restricted to CD4+ CD45RO+ memory T cells. In contrast, Ni-specific CD8+ T cell responses were detected only in allergic patients. Limiting dilution assay confirmed a high frequency of Ni-specific CD4+ T cells in both individual categories, and of Ni-specific CD8+ T cells in allergic patients, but not in nonallergic persons. Ni-specific CD4+ T cell clones prepared from nonallergic subjects displayed lower interferon-gamma and higher interleukin-10 production compared with T cell clones from allergic patients. The T cell skin-homing receptor, cutaneous lymphocyte-associated antigen, was expressed on the large majority of specific CD4+ clones from both the groups. Finally, Ni-specific CD8+ clones prepared from patients also expressed the cutaneous lymphocyte-associated antigen receptor, and released high interferon-gamma and no interleukin-4. In aggregate, the results suggest that the presence of specific CD8+ T cells and a distinct pattern of cytokine release (e.g., an augmented production of interleukin-10) by CD4+ T cells can be important elements in determining whether a hapten induces allergy or a silent immune response.

Adult↗
PubMed1978

The sensitizing capacity of Compositae plants. I. Occupational contact dermatitis from Arnica longifolia Eaton.

Three patients with occupational contact dermatitis due to Arnica longifolia Eaton and Arnica montana L. are reported. During cultivation, harvesting of the flower heads, chemical investigation of the sesquiterpene lactone constituents and preparation of therapeutic tinctures, they had frequent contact with the plant materials. Patch tests with the two sesquiterpene lactones carabron and helenalin, isolated during investigation from A. longifolia Eaton, were positive in all three patients, though the second patient had never shown visible allergic reactions of the skin. Sensitization experiments with carabron in five guinea pigs were successful. The investigation results revealed that carabron, helenalin and the acetyl derivative of helenalin must be considered as the sensitizers of A. longifolia, and helenalin acetate and properly arnifolin as sensitizers of A. montana. Studies on cross reactivity in the sensitized animals with six related sesquiterpene lactones showed that only those compounds gave a positive test response which contain an alpha-methylene gamma-lactone group. Cross reactions were obtained with a crude extract of Chrysanthemum indicum L. The case reports supported by the patch test and investigation results demonstrate that persons handling a new drug from the Compositae family run a risk of developing an allergy after intensive contact with the plant and its constituents.

Adult↗
PubMed2005

Allergic contact dermatitis from natural rubber latex in atopic dermatitis and the risk of later Type I allergy.

The aims of the study were to assess whether contact dermatitis in children could be due to a delayed hypersensitivity reaction to natural rubber latex (NRL) and to define risk factors for later occurrence of Type I hypersensitivity to this allergen. Among 1800 children investigated for contact dermatitis, 55 were referred on suspicion of rubber allergy and had patch tests to NRL, as well as prick tests and blood tests for specific immunoglobulin E (IgE). A 2-year follow-up was then carried out. Delayed hypersensitivity to NRL was confirmed in 32 children. Patch testing with NRL proved to be positive, and clinical improvement confirmed the diagnosis and relevance of patch tests. 30 of these 32 patients had associated atopic dermatitis (AD). Prick tests and blood tests for specific IgE to latex were negative at the time of diagnosis. A 2-year follow-up showed that 10 of 27 patients presenting initially with a positive patch test without associated Type I sensitization later developed immediate hypersensitivity. Children with AD are at high risk for allergy to NRL protein. Exclusion of this allergen should be strongly advised in atopics because of the dual risk of dermatitis and later evolution into severe Type I hypersensitivity.

Allergens↗
PubMed1996

Hyporesponsiveness in contact hypersensitivity and irritant contact dermatitis in CD4 gene targeted mouse.

To determine the role of CD4 molecules in the generation and regulation of contact hypersensitivity (CHS), we treated mice lacking the CD4 gene as a result of targeted disruption with dinitrofluorobenzene to induce CHS. The mutant mice lacking CD4 (CD4(-) mice) showed marked hyporesponsiveness in CHS compared with normal syngeneic C57BL/6 mice (38.3 +/-9.0% of normal at 24 h after the challenge assessed by net ear swelling; p < 0.025). CD4(-) mice had a larger CD4-8- double negative T-cell receptor alpha beta+ cell population in the lymph nodes than did normal mice, and the increase of this cell population was observed in CD4(-) mice after sensitization. Draining lymph node cells from sensitized normal mice restored the responsiveness in CD4(-) mice, but those from sensitized CD4(-) mice were less effective in restoring the CHS response in normal mice. Langerhans cell numbers were normal, and function, as assessed by the ability to present soluble hapten, was not impaired in CD4(-) mice. Skin cytokine profiles demonstrated an increase in interferon-gamma, interleukin-2, and interleukin-4 mRNA levels after challenge in normal mice, whereas this response was blunted in CD4(-) mice. CD4(-) mice also showed hyporesponsiveness in inflammatory reaction to irritant chemicals. These results suggest that the CD4 molecule is required for optimal induction of CHS as well as irritant contact dermatitis and may influence the development of CHS by modulating the cytokine profiles in the skin.

Animals↗
PubMed1980

Allergic contact dermatitis to dimethoxane in a spin finish.

A textile worker exposed to dimethoxane in an aqueous system developed allergic contact dermatitis. Patch testing to this compound and its possible products in an aqueous system demonstrated sensitization to acetaldehyde and crotonaldehyde.

Antifungal Agents↗
PubMed2000

The diagnostic evaluation, treatment, and prevention of allergic contact dermatitis in the new millennium.

Identifying the etiology of allergic contact dermatitis is a rewarding yet challenging endeavor. Not all allergic contact reactions are eczematous in appearance. The most reliable clinical clue to the allergic nature of the dermatitis is its geographic distribution. Once a list of culprit allergens has been identified by patch testing, the practitioner must identify the relevant allergen(s) and counsel the patient in avoidance. For most individuals, allergen avoidance results in resolution of the dermatitis; however, some patients will require continuing symptomatic therapy despite avoidance. For those patients unable to avoid known allergens, immunosuppressant therapies (including phototherapy) or barriers can be beneficial. Currently, hyposensitization is not a viable alternative for the treatment of allergic contact dermatitis.

Dermatitis, Allergic Contact↗
PubMed2003

Clinical and immunologic features of systemic contact dermatitis from ingestion of Rhus (Toxicodendron).

Oral or parenteral exposure to certain contact allergens may elicit an eczematous skin reaction in sensitized individuals. This phenomenon has been called systemic contact dermatitis (SCD) and is relatively rare when compared with classical contact dermatitis. We reviewed and analysed the clinical and immunologic features of 42 patients with SCD caused by ingestion of Rhus (Toxicodendron), 24 males and 18 females, average age 44 years (range 24-72). Several of such patients (33%) had a known history of allergy to lacquer. The patients developed skin lesions such as generalized maculopapular eruptions (50%), erythroderma (29%), vesiculobullous lesions (14%) and erythema multiform (EM)-like lesions (7%). Many patients (57%) developed leucocytosis with neutrophilia (74%). In some patients (5%), abnormalities of liver function developed. We also analysed lymphocyte subsets in the peripheral blood of 12 patients. The lymphocyte subsets studied were T cells (CD3), B cells (CD19), natural killer (NK) cells (CD3-CD16+/CD56+), helper/inducer cells (CD4), cytotoxic/suppressor cells (CD8) and helper/suppressor ratio (CD4/CD8). The lymphocyte subsets of all 12 patients studied were within the normal range. Moreover, there were no differences between patients with a history of allergy to lacquer and those without a history of allergy to lacquer. Therefore, rather than an immunologic response, the skin eruption seems to be caused by a toxic reaction because of Rhus.

Administration, Oral↗