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1/51. Hypersensitivity pneumonitis among workers cultivating tricholoma conglobatum (shimeji).

    We report five cases of hypersensitivity pneumonitis among workers cultivating tricholoma conglobatum (shimeji). After having worked for 5 to 20 years, they began to notice symptoms of cough, sputum, and dyspnea. They were diagnosed as having a hypersensitivity pneumonitis based on clinical features, bronchoalveolar lavage and transbronchial lung biopsy. By the double immunodiffusion test, precipitating lines between shimeji spore antigen and sera were observed in all of the patients. By enzyme-linked immunosorbent assay, the antibody activities against shimeji and three species of fungi (cladosporium sphaerospermum, penicillium frequentans, and scopulariopsis species) were significantly higher in the sera of the patients than in those of normal subjects who were cultivating shimeji. Although it is not clear what causes this disease, these findings may be helpful in determining the specific antigen.
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2/51. anaphylaxis to deer dander in a child: a case report.

    BACKGROUND: Hypersensitivity to deer dander is rarely reported, with only 26 cases in the literature. Ours is the youngest reported case and the first reported case of anaphylaxis on exposure to a live deer. OBJECTIVE: Evaluation of a case of anaphylaxis in a young boy upon exposure to a deer. methods AND RESULTS: A 4-year-old boy experienced hives, swelling, and shortness of breath requiring epinephrine following a deer exposure. He had one mild reaction 5 days prior to his anaphylaxis with an indirect exposure. A deer dander extract was made from fur supplied by the patient's mother. IgE-mediated reactivity was positive for deer and cattle by both selective skin prick method and RAST results. CONCLUSION: Hypersensitivity to wild animals can lead to life threatening anaphylaxis, even in children. Passive transfer of antigen may occur, but needs further investigation.
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3/51. A case report of olanzapine-induced hypersensitivity syndrome.

    Hypersensitivity syndrome is defined as a drug-induced complex of symptoms consisting of fever, rash, and internal organ involvement. The hypersensitivity syndrome is well recognized as being caused by anticonvulsants. Olanzapine is an atypical antipsychotic agent whose side effects include sedation, weight gain, and increased creatinine kinase and transaminase levels. To date, there have been no reports of hypersensitivity syndrome related to this drug. A 34-year-old man developed a severe generalized pruritic skin eruption, fever, eosinophilia, and toxic hepatitis 60 days after ingestion of olanzapine. After termination of olanzapine treatment, the fever resolved, the skin rash was reduced, eosinophil count was reduced to normal, and the transaminase levels were markedly reduced. Clinical features and the results of skin and liver biopsies indicated that the patient developed hypersensitivity syndrome caused by olanzapine.
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4/51. Pulmonary hypersensitivity associated with pancreatin powder exposure.

    A 25-year-old woman with obstructive, reversible pulmonary and nasal hypersensitivity apparently induced by casual, repeated inhalation of pancreatin powder (desiccated pork pancreas) is described. The powder was being employed as a dietary supplement for the patient's son, diagnosed as having cystic fibrosis. Two challenges of the diagnosed as having cystic fibrosis. Two challenges of the patient by reproducing home use of the powder resulted in repetition of a hypersensitivity symptom complex on both occasions. Vitalometry demonstrated an immediate and late response. Avoidance of pancreatin powder exposure resulted in subsidence of symptoms. Immunologic mechanisms are suggested but not proven.
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5/51. A baker's occupational allergy to flour moth (Ephestia kuehniella).

    BACKGROUND: Allergy to insects is common. However, few reports cover occupational sensitization to flour moth (Ephestia [syn. Anagasta] kuehniella). We describe a baker who suffered from IgE-mediated occupational respiratory allergy to flour moth. methods: The skin prick test (SPT) and serum IgE tests were used to evaluate the patient's sensitivity to flour moth. Allergen cross-reactivity with mites was evaluated in IgE-inhibition studies. Clinical sensitivity was evaluated by nasal challenge test. Pulmonary function tests were repeatedly monitored. RESULTS: SPT with flour moth gave a 6-mm wheal, and an elevated level of flour moth-specific IgE was measured in the patient's serum (1.9 PRU/ml, RAST class 2). immunoblotting with the patient's serum revealed at least seven heavy IgE-binding bands with molecular masses of 22, 35, 43, 53, 65, 77, and >86 kDa in the extract of flour moth. Allergen cross-reactivity with mites was demonstrated in inhibition studies. Immediate-type allergy to flour moth was confirmed by nasal challenge. Increased daily variability of PEF values was observed during workplace exposure. CONCLUSION: A baker's occupational respiratory allergy to flour moth was confirmed.
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6/51. Acute pulmonary hypersensitivity to carbamazepine.

    Acute pulmonary hypersensitivity to carbamazepine (Tegretol) is reported, manifested by diffuse pulmonary infiltrates, skin rash, and eosinophilia. The reaction cleared on cessation of the drug. A lymphocyte transformation test was reactive to carbamazepine.
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7/51. Occupational respiratory hypersensitivity in dental personnel.

    OBJECTIVE: The aim was to study the causes of respiratory hypersensitivity in dental personnel based on the statistics of the Finnish Register of Occupational Diseases (FROD; 1975-1998) and the patient material of the Finnish Institute of occupational health (FIOH; 1990-1998). methods: Details about the cases of respiratory hypersensitivity were compiled from the FROD. The occupational rhinitis diagnoses studied at the FIOH were based on work-related symptoms and a change in the status of the nasal mucosa during challenge testing; and the diagnosis of occupational asthma based on reactions in challenge testing, or on IgE positivity and peak flow monitoring at work and during days off. RESULTS: A total of 64 cases of occupational respiratory diseases (ORDs) was diagnosed in dental personnel during 1975 to 1998 according to the FROD; two cases in 1975 to 1989, and 62 in 1990 to 1998. Twenty-eight cases were of occupational asthma (18 caused by methacrylates), 28 occupational rhinitis (six caused by methacrylates), seven allergic alveolitis and one organic dust toxic syndrome (ODTS). The non-acrylate-material diagnosed in 1990-1998 at the FIOH comprised three cases of asthma and one of rhinitis caused by chloramine-T (sodium- N-chlorine- p-toluene sulphonamide); as well as one case of asthma, seven cases of rhinitis, and two cases of combined rhinitis and conjunctivitis caused by natural rubber latex (NRL). Furthermore, one case of occupational rhinitis caused by Nobetec containing colophony was diagnosed. The incidence rate (IR) of ORD increased from 0 in 1988 to a peak of 105.1 new cases per 100,000 working years in 1995. During the last observation year, i.e. 1998, the IR was 55 new cases per 100,000 workers. The IR in dental personnel was lower than in the whole working population in finland up until 1992, but since then has been greater than in the whole population, peaking in 1995 when the IR of dental personnel was 2.55 times greater than in the whole population. CONCLUSION: The present study shows the increasing frequency of respiratory hypersensitivity among dental personnel. Besides methacrylates, important causes of respiratory hypersensitivity are NRL and chloramine-T.
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8/51. Sinobronchial allergic mycosis: the SAM syndrome.

    We contend that the presence of concomitant allergic fungal sinusitis (AFS) and allergic bronchopulmonary mycosis in the same patient represents an expression of the same process of fungal hypersensitivity in the upper and lower airways. We have termed this process the SAM syndrome, an acronym for sinobronchial allergic mycosis. Diagnostic criteria have been established for the SAM syndrome, and the clinical characteristics of one previously unreported and four previously reported patients have been tabulated. patients with the SAM syndrome have chronic sinusitis involving multiple sinuses, asthma, immediate cutaneous reactivity to fungal allergens, peripheral eosinophilia, and radiographic evidence of bronchiectasis. Total serum IgE levels are usually elevated as well. A variety of chest radiographic abnormalities may occur, ranging from mass lesions to diffuse pulmonary infiltrates and even normal findings on chest radiographs. patients present for an evaluation of either sinus or lung disease and, at that time, demonstrate no clinical features that distinguish them from patients with isolated sinus or lung disease. All patients reported to date have had clinical responses to therapy with corticosteroids. We postulate that SAM is underdiagnosed in patients with AFS, a disease recently reported from medical centers in the southeastern and western united states. Moreover, since our patient had a mutation in the cystic fibrosis transmembrane conductor regulator (CFTR) gene, we further hypothesize that CFTR gene mutations may play an important role in the pathogenesis of the SAM syndrome.
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9/51. Fatal pulmonary hypersensitivity reaction to HL-A incompatible blood transfusion:report of a case and review of the literature.

    A girl with thalassemia major reacted to a transfusion of packed red blood cells with increasing respiratory distress until death 12 1/2 hours later. chills and fever were followed by dry cough, dyspnea, and pulmonary edema. The recipient had lymphocytotoxic antibodies specific for donor leukocyte antigens HL-A11 and possibly W14. At autopsy, the lungs showed pulmonary edema with extensive nonspecific acute alveolar injury. Similar cases in the literature are reviewed.
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10/51. Interstital lung disease due to contamination of forced air systems.

    Eight patients had hypersensitivity pneumonitis due to contaminated home or office forced-air heating or air-conditioning systems. We studied their clinical and laboratory features, and the results indicated that this disease may occur as an acute or insidious form differing in type and intensity of respiratory and systemic symptoms. Thermophilic actinomycetes contaminatinf the forced air systems were identified as the sensitizing agents in most cases. Precipitating antibodies to the organisms could be shown in the serums of the patients and the antigen identified by immunofluorescent studies in the three lung biopsies examined by this method.inhalation challenge studies with the cultured organism or other materials obtained from the forced air systems reproduced the clinical syndrome in the four patients tested. Avoidance of the contaminated system, and the use of corticosteroids in more severe cases,seems to be appropriate therapy for patients with this disease.
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