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1/75. Aerobiological analysis in a salami factory: a possible case of extrinsic allergic alveolitis by penicillium camembertii.

    A 39-year-old man was hospitalized with a history of fatigue, dyspnoea and low grade fever which seemed to be related to his working environment. The patient was employed in a salami factory, working near the area where the salami are seasoned with fungal inocula. Chest X-ray showed diffuse initial changes of reticulonodular pattern that disappeared after a brief course of steroids therapy. Precipitating antibodies to penicillium notatum and aspergillus fumigatus were found both in plasma and bronchoalveolar lavage fluid. This, together with the finding of a lymphocytic alveolitis with CD4 depletion and CD8 increase, suggested the possibility of extrinsic allergic alveolitis of fungal aetiology. Qualitative and quantitative monitoring with an impinger of both the working and outside environment for aerial fungal concentration demonstrated a very high level of contamination (up to 1.14x10(9) fungal propagules m-3 of air) and an inside/outside ratio from 21 to about 2000. penicillium camembertii was the most common species found in all the indoor sites (60-100% of the fungal load). The patient's BALF and serum both displayed precipitating antibodies to P. camembertii from the powder used for the inoculum and the air samples. These results together with the patient's working history gave some evidence of relationship between the indoor P. camembertii concentration and the patient's symptoms.
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2/75. Hard metal alveolitis accompanied by rheumatoid arthritis.

    Hard metal lung diseases (HML) are rare, and complex to diagnose. We describe the case of a patient with allergic alveolitis accompanied by rheumatoid arthritis. A sharpener of hard metal by trade, our patient was a 45-year-old, nonsmoking Caucasian female who experienced symptoms of cough and phlegm, and dyspnea on exertion. Preliminary lung findings were inspiratory rales in both basal areas, decreased diffusion capacity and a radiological picture resembling sarcoidosis. A high-resolution computed tomography scan indicated patchy alveolitis as well. An open lung biopsy revealed non-necrotizing granulomas consisting of epitheloid cells and surrounded by lymphocytes, plasma cells and a few eosinophils. These cells also occupied the thickened alveolar interstitium. macrophages in the alveolar spaces, some of them multinuclear, contained dust particles. Hard metal alveolitis is clinically well known and, in this patient, has been described histologically. After the patient had quit working with hard metal and following corticosteroid therapy, pulmonary symptoms and signs were relieved. During this recovery period, however, she contracted rheumatoid arthritis.
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3/75. hydroxyurea-induced hypersensitivity pneumonitis: A case report and literature review.

    hydroxyurea is a cytotoxic agent indicated in the treatment of a variety of malignant and nonmalignant conditions. Apart from dose-related bone marrow suppression, this antineoplastic agent is generally well tolerated. This report describes a patient with chronic myeloid leukemia who developed severe pneumonitis within four weeks of beginning therapy with hydroxyurea. Pathological examination of a lung specimen obtained by video-assisted thoracoscopic lung biopsy revealed extensive active alveolar and interstitial inflammation, and poorly formed granulomas. After the cessation of hydroxyurea and treatment with systemic corticosteroids, both clinical and radiological resolution of pneumonitis occurred. physicians using hydroxyurea must be aware of its potentially life-threatening pulmonary toxicity.
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4/75. Extrinsic allergic alveolitis from a proteolytic enzyme.

    BACKGROUND: subtilisins are proteolytic enzymes of bacterial origin found in detergents. They are high-molecular-weight antigens and have been implicated in allergic rhinitis and asthma. OBJECTIVE: This report describes a case of extrinsic allergic alveolitis due to subtilisins in a liquid cleaner. methods: Clinical, radiologic, and serologic information were used to make the diagnosis. CASE REPORT: A 53-year-old woman developed respiratory symptoms while working with a cleaner containing subtilisins. Her symptoms intensified in the work environment and improved away from work. A computed tomography scan demonstrated alveolar and interstitial infiltrates with subsequent scarring. A pulmonary function study revealed a restrictive pattern with diminished diffusion capacity. Bronchoalveolar lavage showed lymphocytosis and all cultures were negative. Precipitating antibodies to the enzyme were found in the patient's serum. Her symptoms improved once she changed her occupation. CONCLUSIONS: The combination of the patient's clinical history, physical, laboratory, and radiologic findings support the diagnosis of extrinsic allergic alveolitis from the enzyme contained in the cleaner.
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5/75. Organic antigen-induced interstitial lung disease: diagnosis and management.

    BACKGROUND: Traditionally, chronic idiopathic interstitial pneumonia/fibrosis (IIP/F) had included usual interstitial pneumonia, desquamative interstitial pneumonia, and nonspecific interstitial pneumonia (NSIP). More recent classifications have included bronchiolitis obliterans-organizing pneumonia (BOOP), respiratory bronchiolitis-associated interstitial lung disease, and acute interstitial pneumonia. Some chronic eosinophilic pneumonias (CEP)/pulmonary infiltrate with eosinophilia (PIE) have obvious causes, but many lack an identifiable etiology. We felt that hypersensitivity pneumonitis (HP) was being underdiagnosed and was hidden within this large heterogeneous group of interstitial lung disorders of unrecognized cause. OBJECTIVE: We sought to prove that detailed environmental histories and investigations would reveal causative contaminations in the home or workplace of some patients with idiopathic interstitial lung disease and remediation of the contamination would stabilize the disorder. methods: Consecutive cases of IIP/F were investigated. patients were identified by compatible signs and symptoms, roentgenographic studies, pulmonary function tests, and lung biopsies. They were further evaluated with detailed environmental histories, serologic tests, and investigation into the suspected causative environment. Environmental and specific antigen challenges were done in some cases. Remediation of contaminations or moving into another environment were the methods used as therapy. RESULTS: Eighty-six consecutive patients with IIP/F were evaluated. Twelve patients were subsequently diagnosed with specific causes for interstitial lung disease. Fifty-seven of 74 patients were identified by clinical evaluation and lung biopsy with HP, CEP/PIE, NSIP, BOOP, UIP, and nonclassifiable morphologic patterns. Seventeen patients were not biopsied or had an inadequate transbronchial biopsy but had consistent findings radiographically and clinically of idiopathic interstitial lung disease. Contamination of the home was causative in 69 of 74 and the workplace in 3 of 74 cases. There were 9 positive and 33 negative environmental challenges with 4 positive and 1 negative specific challenges. Fifty of 74 (67%) patients are receiving no treatment and are free of active disease after remediation of the environmental contamination, with a mean survival of 8.2 years. CONCLUSIONS: Our data show that UIP, BOOP, NSIP, CEP/PIE, and nonclassifiable morphologic patterns represent a spectrum of interstitial lung disease that may be caused by inhalation of organic dusts in the home or workplace as described with HP. Remediation of, or moving from the contamination, can lead to arrest of the active inflammatory process and stability of the lung disorder.
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6/75. trichosporon asahii-induced asthma in a family with Japanese summer-type hypersensitivity pneumonitis.

    BACKGROUND: trichosporon species frequently induce summer-type hypersensitivity pneumonitis (SHP), which is the most prevalent type of hypersensitivity pneumonitis (HP) in japan, but have not been reported to induce asthma. OBJECTIVE: Evaluation of a case of asthma induced by trichosporon asahii. methods AND RESULTS: This report describes a 46-year-old Japanese man who developed asthma induced by T. asahii, following symptoms of HP attributable to the same pathogen, in a case of familial occurrence of SHP. This patient lacked typical findings of HP in his radiograph but had an elevated level of eosinophils in his bronchoalveolar lavage fluid. Open lung biopsy, however, revealed typical pathologic findings of HP when he was free of asthmatic symptoms. His serum was also positive for anti-T asahii antibody, as are the sera of SHP patients. Nevertheless, provocation tests, including returning home and inhalations of T. asahii antigen, reproduced asthmatic features such as airway hyperresponsiveness and reversible bronchoobstruction, but not the features of HP. A skin test with the same antigen also evoked an immediate allergic reaction. An IgE mechanism was suspected but could not be proven by radioallergosorbent test. The patient's son and daughter displayed typical features of SHP, associated with compatible results in their radiographs, bronchoalveolar lavage fluid analysis, serologic and pathologic examinations, and provocation and skin tests. CONCLUSIONS: To our knowledge, this is the first case of extrinsic asthma, and of coexistent asthma and HP, induced by T. asahii. The patient initially displayed symptoms typical of SHP, which were subsequently replaced by more typical asthmatic symptoms.
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7/75. fever and neutrophilic alveolitis caused by a vanadium based catalyst.

    AIMS: To investigate a worker who experienced systemic and respiratory symptoms when exposed to a vanadium containing powder used as a catalyst in the production of maleic anhydride. methods: The investigation included inhalation challenge with the suspected compound combined with monitoring of lung function tests and post-challenge bronchoalveolar lavage. RESULTS: Exposure to the vanadium containing catalyst for 120 minutes resulted in a sustained decline in forced vital capacity and forced expiratory volume in one second, while the transfer factor for carbon monoxide did not change significantly. The subject developed fever and peripheral blood neutrophilia. Bronchoalveolar lavage performed 48 hours after the end of challenge exposure showed a marked increase in neutrophils (60% of total cell count). CONCLUSIONS: Exposure to vanadium can cause a metal fume fever-like syndrome associated with neutrophilic alveolitis.
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8/75. Treatment of allergic alveolitis with methylprednisolone pulse therapy.

    We report on a 13-year-old-boy who had been admitted to our hospital for dyspnea, hypoxia, and pulmonary infiltrates. The diagnosis of allergic alveolitis was based on history (provocation by exposure), lung function tests, bronchoalveolar lavage, and transbronchial lung biopsy. No specific allergen could be identified. Five courses of methylprednisolone pulse therapy (15 mg/kg on three consecutive days) stabilized the patient with normalization of lung function and blood gas analysis. Between pulses the boy returned to his home on a farm without relapse. It is estimated that the effect of a single pulse lasted for at least 2-4 weeks. We conclude that pulse therapy can be used instead of continuous therapy in this rare disease in childhood.
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9/75. hypersensitivity pneumonitis induced by hexamethylene diisocyanate.

    A case of hypersensitivity pneumonitis (HP) induced by hexamethylene diisocyanate (HDI) is described. Serial determinations of the lymphocyte surface phenotypes by two-color assay revealed the following: 1) increased activated cytotoxic T lymphocytes in the bronchoalveolar lavage fluid (BALF), and 2) increased percentage and absolute number of non-major histocompatibility complex (MHC)-restricted natural killer (NK) cells in the peripheral blood (PB) during the recovery phase of the disease. These findings were considered to be related to the activity of the disease.
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10/75. hypersensitivity pneumonitis induced by Shiitake mushroom spores.

    hypersensitivity pneumonitis due to the inhalation of Shiitake mushroom spores was demonstrated in a 38-year-old woman. Symptoms of cough, nausea and malaise, and clinical findings of cyanosis, bibasilar crackles, reduced lung volumes, hypoxemia, leukocytosis, elevated ESR, positive c-reactive protein, and bilateral diffuse reticulonodular shadows on chest roentgenogram improved after the patient was removed from exposure. Alveolitis was demonstrated by transbronchial lung biopsy, as well as an increase in lymphocytes in bronchoalveolar lavage. serum precipitins and specific IgG antibodies to an extract of Shiitake mushroom spores, but not to other common molds or mushroom body, were detected in serum. Provocative inhalation test with the extract of mushroom spores caused the same clinical symptoms and signs as experienced in the workroom. This is the first report of typical hypersensitivity pneumonitis induced by Shiitake mushroom spores. Mushroom spores as well as thermophilic actinomycetes must be considered a causative agents for mushroom worker's lung.
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