Cases reported "Asthma"

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1/21. Facial dermatitis, contact urticaria, rhinoconjunctivitis, and asthma induced by potato.

    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.
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2/21. Sensitization to triglycidylisocyanurate (TGIC) with cutaneous and respiratory manifestations.

    The case is presented of a man with allergic contact dermatitis and occupational asthma due to triglycidylisocyanurate (TGIC), which is used as a hardener in thermosetting powder paint. The contact dermatitis was confirmed by patch testing (TGIC 0.5% and 5% in petrolatum), and the occupational asthma was confirmed by bronchial provocation testing: two challenges to an aerosol of lactose containing TGIC (0.05% and 0.1%, w/w, each for 0.5 1 2 4 min) led to a maximal decrease in FEV1 of 22% and 31% after 6 and 4 h, respectively. Skin prick tests with unconjugated TGIC were possibly positive. This case confirms that exposure to TGIC in powder paints may cause not only contact dermatitis, but also occupational asthma.
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keywords = patch test, patch
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3/21. Analgesic-induced asthma caused by 2.0% ketoprofen adhesive agents, but not by 0.3% agents.

    A 74-year-old woman was admitted with an asthma attack. She had a 40-year history of sinusitis, nasal polyp and analgesic-induced asthma; however, asthma had never occurred when she used a 0.3% ketoprofen adhesive patch (Mohrus) for stiff shoulder or lumbago. In the hospital, a life-threatening asthma attack suddenly occurred two and a half hours after application of a 2.0% ketoprofen adhesive tape (Mohrus tape) to her shoulder. She was treated with bronchodilator and glucocorticoid and extubated after 20 hours. A drug lymphocyte stimulating test (DLST) was strongly positive for ketoprofen. We suspected that drug-induced hypersensitivity coexisted in the present case, but it was not clear whether or not the hypersensitivity was related to the pathogenesis of analgesic-induced asthma.
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keywords = patch
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4/21. asthma from diisocyanates is not mediated through a Type IV, patch-test-positive mechanism.

    The mechanism of occupational asthma from diisocyanates (DI)(1-10)(Fig. 1) is not fully known; only about 10%-30% of such patients have specific IgE antibodies to DI (3, 11, 12). A T-cell mediated response has been considered to be involved in DI asthma (13) and we therefore wondered whether patch testing might be of any help in its diagnosis.
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keywords = patch test, patch
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5/21. Occupational contact urticaria caused by airborne methylhexahydrophthalic anhydride.

    Acid anhydrides are low-molecular weight chemicals known to cause respiratory irritancy and allergy. Skin allergy has on rare occasions been reported. A total of 3 subjects with occupational exposure to methylhexahydrophthalic anhydride (MHHPA) and hexahydrophthalic anhydride (HHPA) from an epoxy resin system were studied to evaluate the nature of their reported skin and nose complaints (work-related anamnesis, specific IgE, contact urticaria examinations, and ambient monitoring). Using a Pharmacia CAP system with a HHPA human serum albumin conjugate, specific IgE antibody was detected in serum from 1 (33.3%) out of the 3 workers. One unsensitized worker displayed nasal pain and rhinorrhea only when loading liquid epoxy resins into the pouring-machine (2.2 mg MHHPA/m3 and 1.2 mg HHPA/m3), probably being an irritant reaction. Two workers had work-related symptoms at relatively low levels of exposure (geometric mean 32-103 microg MHHPA/m3 and 18-59 microg HHPA/m3); one complained of only rhinitis, and the other was sensitized against HHPA and displayed both rhinitis and contact urticaria (the face and neck). The worker's skin symptoms were evidently due to airborne contact, since she had not had any skin contact with liquid epoxy resin or mixtures of MHHPA and HHPA. These urticaria symptoms were confirmed by a 20-min closed patch test for MHHPA, but not by that for HHPA. The causative agent was considered to be MHHPA, although the specific IgE determination to MHHPA was not performed.
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keywords = patch test, patch
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6/21. Dentist's occupational asthma, rhinoconjunctivitis, and allergic contact dermatitis from methacrylates.

    BACKGROUND: Allergic contact dermatitis (ACD) caused by (meth)acrylates (MA) is common in dental personnel. MAs have also caused asthma and rhinoconjunctivitis, but asthma, rhinoconjunctivitis and ACD caused by MAs in the same patient appears to be very rare. methods: Occupational asthma and rhinoconjunctivitis were diagnosed in a dentist according to patient history, PEF monitoring, and a work-simulated bronchial provocation test. ACD was diagnosed by skin-patch testing with MAs with the occlusive Finn Chamber-technique. RESULTS: The patient's skin-prick test reactions to common environmental allergens and MAs were negative. The total IgE was not elevated. Occupational asthma was diagnosed by a specific inhalation challenge test in which the patient handled liquid dental MAs for 30 min causing a delayed 23% reduction in FEV1. The provocation test also resulted in rhinoconjunctivitis. On patch testing, positive reactions were provoked by several MAs including 2-hydroxyethyl methacrylate (2-HEMA) to which the patient was occupationally exposed. The patient has not been able to continue her work with dental MAs. CONCLUSIONS: A case of occupational asthma, rhinoconjunctivitis and ACD caused by dental acrylate compounds is presented. patients with respiratory hypersensitivity from MAs have to stop working with MAs, whereas patients with ACD from MAs need to avoid direct contact with MAs, but can often continue in their present job if they use no-touch techniques.
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keywords = patch test, patch
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7/21. Histopathology of severe childhood asthma: a case series.

    BACKGROUND: To date, little has been published describing the pathology of severe childhood asthma. The currently accepted model of asthma holds that persistent airway inflammation leads to various symptoms of asthma, airway hyperresponsiveness, and airway remodeling that ultimately results in permanent loss of lung function. methods: Evaluation of six children referred to the National Jewish Medical and research Center with difficult-to-control asthma, despite aggressive anti-inflammatory therapy, who underwent bronchoscopy with endobronchial biopsy to better characterize their disease. RESULTS: In every case, endobronchial biopsies revealed changes consistent with airway remodeling characterized by thickening of the basement membrane, smooth-muscle hypertrophy, with varying degrees of goblet-cell and submucous gland hyperplasia. The degree of subbasement membrane thickening did not appear to correlate with baseline FEV(1), ultimate FEV(1) following aggressive therapy, or lability in lung function. In five of six cases, there was minimal to no histologic evidence for airway inflammation with mild and patchy submucosal lymphocytic infiltration noted; eosinophils and neutrophils were not present. Further, the majority of the patients achieved normal FEV(1) values despite significant subbasement membrane thickening, counter to the current beliefs regarding airway remodeling and irreversible loss of lung function. CONCLUSIONS: This case report highlights some of the shortcomings of the current inflammatory paradigm for severe asthma. Despite little evidence of ongoing airway inflammation, many of the subjects displayed significant lung function lability. The lack of inflammation argues against steroid resistance at a cellular level, although it could be argued that inflammation may have been distal to the site sampled. Additionally, normal to nearly normal lung function was achieved despite the presence of significant remodeling. These findings suggest the need to look beyond inflammation to fully treat severe asthma and ultimately alter its progression.
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keywords = patch
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8/21. Occupational asthma in a hairdresser caused by persulphate salts.

    Persulphate salts, which are common constituents of hair bleaches, have occasionally been reported to cause occupational asthma in hairdressers. We describe the clinical and immunological studies carried out in a hairdresser who developed cutaneous and respiratory symptoms, about 1 year after being employed in a hairdressing salon. Skin prick tests with 1:5 w/v potassium and sodium persulphate extracts were positive in our patient at 15 min and negative in control subjects. The European standard contactans (ECDRG) and a battery of hairdressing agents were patch tested with positive result to KATHON CG (isothiazolinone). The methacholine-inhalation test showed airway hyperresponsiveness. Bronchial provocation test with a 1:50 w/v potassium persulphate extract elicited a nonimmediate asthmatic reaction, followed by recurrent nocturnal fall in FEV1 lasting up to 3 days after the test. plethysmography results revealed air trapping caused by a marked increase of airway resistance 3 h after the specific bronchial challenge. histamine release test was not conclusive, and the determinations of specific IgA, IgM, IgG and IgG subclasses by EIA and IgE by RAST against persulphate salts were negative.
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keywords = patch test, patch
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9/21. Occupational asthma induced by the fungicide tetrachloroisophthalonitrile.

    A 48 year old male farmer had recurrent episodes of dyspnoea, shortness of breath, and wheezing after being in his plastic greenhouse when the fungicide tetrachloroisophthalonitrile had been sprayed. A bronchial provocation test with a control challenge and a patch skin test confirmed that his asthma was induced by tetrachloroisophthalonitrile.
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keywords = patch
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10/21. Fixed drug eruption due to loratadine.

    We present the clinical case of a 8-years-old boy suffering a fixed drug reaction attributed to the oral intake of loratadine. He is an atopic child with perennial rhinitis and asthma and marked hypersensitivity to the house-dust mite dermatophagoides pteronyssinus who is receiving inhaled corticosteroids and b2-agonists ad libitum plus specific immunotherapy with the mite. When the boy received loratadine to alleviate his nasal symptoms he suffered a well-defined erythematous and oedematous plaque in his right elbow that disappeared without treatment in one week. Several methods such as the patch-tests, the UBCT or ultra-brief-challenge test (our version of the peroral provocation one) and the skin biopsy were applied. The UBCT and the skin histopathology were the most important techniques to assure the suspected diagnosis. Other antihistamines such as ebastine and cetirizine as well as some excipients used as controls were all negative. Conventional prick or intradermal skin tests with the drug were not performed because we considered that they were useless in this case.
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keywords = patch
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