Cases reported "Dermatitis, Contact"

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1/10. 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.
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2/10. Contact urticaria to giraffe hair.

    BACKGROUND: Immediate-type hypersensitivity to animal proteins is a common problem in people occupationally exposed to animals. methods: A 19-year-old female working as a voluntary zookeeper in her off-time suffered from hives on her forearms following contact to the fur of a giraffe. For diagnostic evaluation, skin prick tests, assessment of specific serum IgE antibodies, and basophil activation tests were performed. RESULTS: skin prick tests with a standard series of common aeroallergens were positive for various pollens. Prick testing with native materials was positive for extracts of hair from two different giraffe subspecies in the patient, but not in control subjects. By CAP-FEIA, no specific serum IgE antibodies to dander of a large variety of animals were found in the patient. In the basophil activation test, expression of the activation marker CD63 was induced by extract of giraffe hair on the cells from the patient, but not on those from unaffected controls. CONCLUSIONS: This patient suffers from an 'exotic' immediate-type contact allergy to giraffe hair.
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3/10. Delayed skin reaction caused by a coelenterate.

    We report a delayed skin reaction, histologically characterized by liquefaction degeneration of the basal layer, which was observed in a 30-year-old man returning from guadeloupe. It was most likely due to contact with a marine animal.
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4/10. Contact allergy to furazolidone.

    A case of occupational contact allergy to furazolidone, used as an animal feed additive and as an antimicrobial drug in veterinary medicine, is described. The patient did not react to furazolidone 2% pet. Using PEG-400 and alcohol as patch test vehicles resulted in positive patch test reactions. No cross-reactions were observed to other nitrofuran derivatives (nitrofurazone, nitrofurantoin) or to furfural. The literature on contact allergy to nitrofurans is reviewed.
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5/10. IgA nephropathy associated with dental nickel alloy sensitization.

    We report a patient with documented IgA nephropathy in whom microscopic hematuria, proteinuria, and hypertension first occurred after placement of nickel alloy base dental crowns. Progressive proteinuria culminating in nephrotic-range proteinuria occurred parallel to increased nickel placement and dramatically resolved following nickel alloy removal. That immunologic alterations occur as a result of nickel exposure has already been suggested by the common occurrence of nickel contact dermatitis, often exacerbated by intraoral nickel placement, increased carcinogenesis in nickel refinery workers, and animal models of nickel-associated carcinogenesis. Our patient may represent an example of nickel-induced sensitization and associated IgA glomerulopathy. Further study of patients with immune-mediated glomerulopathy with attention to dental nickel exposure appears indicated.
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6/10. Contact sensitivity to quinidine sulfate from occupational exposure.

    Three workers exposed to quinidine sulfate became sensitized after short exposure times (2-3 months). They were patch test positive to quinidine in different vehicles, but negative to the diastereoisomer quinine. Guinea pig maximization tests demonstrated quinidine and quinine to be grade V allergens according to the classification of Magnusson & Kligman. When challenged for cross reactivity, the animals sensitive to quinine did not react to quinidine. Among the quinidine-sensitive guinea pigs, three of 20 (P greater than 0.05) reacted when challenged with quinine.
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7/10. Orchid allergy.

    A female office worker acquired contact allergy by handling Cymbidium cultivars for several years. The sensitizing properties of this ornamental orchid were demonstrated by experimental sensitization of guinea pigs. Chemical analysis of the ether extracts disclosed the presence of two quinones. The structure of the main quinone was elucidated as 2,6-dimethoxy-1,4-benzoquinone by x-ray crystallographic analysis. In the patient and in the sensitized animals, only this quinone elicited strong reactions, while tests with the second constituent were negative or gave only weak responses. Although 2,6-dimethoxy-1,4-benzoquinone is only a moderately strong sensitizer, its role as a contact allergen is emphasized, as it has been found in more than 50 different plant and wood species.
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8/10. The sensitizing capacity of alstroemeria cultivars in man and guinea pig. Remarks on the occurrence, quantity and irritant and sensitizing potency of their constituents tuliposide A and tulipalin A (alpha-methylene-gamma-butyrolactone).

    dermatitis in 8 female nursery workers handling alstroemeria ligtu cultivars has been proven/proved in 6 cases to be of allergic origin. Epicutaneous tests with cut flower extracts as well as with the isolated and purified sensitizer were positive. Successful animal experiments corroborated the sensitising capacity of alstroemeria cultivars. The responsible but unstable contact allergen, alpha-methylene-gamma-butyrolactone (tulipalin A), was found in short ether extracts of flower petals in concentrations up to 18%. Due to its instability, subsequent extractions were performed with methanol, yielding the sensitising constituent after purification in the glucosidic form (tuliposide A). This could be stored at room temperature for longer periods without loss of activity. Tuliposide A was determined in specimens of alstroemeria ligtu cultivars of 14 different origins of various colours; its content varied between 1 and 2%. Direct testing of the plant material in human patients carries the risk of false positive reactions and active sensitisation, as the threshold for both forms of the allergen is very high. Only a concentration of 0.01% can be considered safe.
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9/10. seizures and dermatitis after exposure to caprolactam.

    A 22-year-old man was initially seen with dermatitis, fever, and seizures after three days of occupational exposure to caprolactam, a nylon fiber precursor. A comprehensive neurological investigation showed no organic CNS abnormalities. Although caprolactam has been shown to induce convulsive disorders in experimental animals, to our knowledge, there are no reports of caprolactam-induced seizures in man. The coincidence of typical skin lesions with otherwise unexplained grand mal seizures in this strongly suggests that caprolactam was the cause.
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10/10. Contact leukoderma associated with the use of hair colors.

    Four cases of contact leukoderma associated with the application of hair rinses and permanent and semipermanent hair colors are described. To our knowledge, this association has not been previously reported. Although none had evidence of pigment loss in other sites, Koebner-induced vitiligo cannot be excluded. In our cases hair color ingredients seem to have had a selective toxic effect on melanocytes. Further study of pigment loss from hair colors is warranted, especially in animal and in vitro assays. Patch testing with putative depigmenting agents in patients should be done with caution, so as to minimize potential for depigmentation in cosmetically important anatomic sites.
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