Cases reported "Silicosis"

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1/7. Accelerated silicosis with mixed-dust pneumoconiosis in a hard-metal grinder.

    We describe a fatal case of accelerated silicosis with a component of mixed-dust pneumoconiosis in a young hard-metal grinder that we believe is the first case of its kind in israel and one of the rare cases reported worldwide. The patient's diagnosis was based on typical features: restrictive lung function, abnormal chest roentgenogram suggesting lung fibrosis, a history of exposure to silica and hard metals, bronchoalveolar lavage (BAL) fluid findings, and mineralogical studies. BAL cells showed an abundance of giant multinucleated macrophages. The CD4/CD8 ratio of T lymphocytes was 1.1, with a high percentage of CD8 and CD8/38 positive cells (37% suppressor/cytotoxic and 12% cytotoxic T lymphocytes, respectively). mRNA transcripts isolated from BAL cells were positive for interleukin-1 (IL-1) and transforming growth factor (TGF) Il-5, IL-2, and IL-10 but not for IL-6, IL-4, and interferon. Polarizing light microscopic studies of BAL and induced sputum cells showed polarizing particles, which are typical for silica. Mineralogical studies of electron microscopy performed on BAL fluid and on dust collected at the patient's workstation revealed silica particles as well as aluminum-titanium and other particles. The latter might have contributed to the patient's lung disease.
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2/7. silicosis in ceramic-industry workers with particular reference to the diagnostic value of bronchoalveolar lavage.

    We could identify, via bronchoalveolar lavage, crystals in the lavage fluid and in the alveolar macrophages. Thus, BAL could be another method for diagnosing silicosis patients.
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3/7. Acute silicoproteinosis.

    A case of alveolar lipoproteinosis associated with silicosis is reported. A 58-year-old man had been exposed to silica for seven years and died three years after the onset of symptoms. light microscopy of biopsy and necropsy material showed small silicotic nodules, silica particles, and alveolar lipoproteinosis, and ultrastructural studies were performed to define changes in alveolar epithelium and macrophages. The case provides a further example of alveolar lipoproteinosis developing as a response of the lung to injury by an external agent.
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4/7. The utility of bronchoalveolar lavage and transbronchial lung biopsy combined with energy-dispersive X-ray analysis in the diagnosis of silicosis.

    We used analytical electron microscopic techniques, including energy-dispersive X-ray analysis, to evaluate a patient with diffuse infiltrates and a history of silica exposure. We identified silica particles in digested bronchoalveolar lavage fluid, sectioned alveolar macrophages recovered by lavage, and parenchymal specimens obtained by transbronchial biopsy. This analysis confirmed our clinical suspicion (a sporadic case of accelerated silicosis) and eliminated the need for additional, more complicated, diagnostic procedures.
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5/7. Treatment of mixed-dust pneumoconiosis with whole lung lavage.

    A patient with silicosis and progressive dyspnea on exertion is described in whom open lung biopsy revealed active chronic inflammation with many macrophages filling alveolar spaces. Because of the extensive involvement by the disease of small air spaces, bilateral whole lung lavage was performed. The lung lavage effluent was striking in its blackish brown color. It was composed predominantly of macrophages containing silica, silicates, and graphite. Particles in the tissue and lavage were analyzed using scanning electron microscopy and energy dispersive X-ray analysis. The dry weight of the material removed was approximately 25 g, of which an estimated 135 mg was silica. The procedure resulted in immediate symptomatic improvement in the patient. Although his pulmonary function did not change significantly, it is hoped that removal of this material will improve his long-term prognosis.
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6/7. silicosis following employment in the manufacture of silica flour and industrial sand.

    We describe silicosis in a patient with chronic obstructive pulmonary disease who worked as a maintenance mechanic for less than 5 years in a plant in south carolina that manufactures silica flour and industrial sand. An open lung biopsy showed an early stage of silicosis manifested by perivascular and peribronchial collections of macrophages as well as early granuloma formation. An antinuclear antibody profile compatible with sjogren's syndrome or systemic lupus erythematosus occurred with no symptoms of either disease. Excessive occupational exposure levels of respirable free silica were documented.
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7/7. Silica-induced pleural disease: an unusual case mimicking malignant mesothelioma.

    A 57-year-old man with a history of exposure to silica for 32 years presented with pleural thickening of the lower lobe of the left lung and a chronic right-sided pleural effusion without any radiographic evidence of parenchymal nodules in either lung. light microscopic examination of a left visceral pleural biopsy specimen revealed markedly thickened pleura with fibrosis and macrophages containing birefringent silica and silicates. Occasional rounded intrapleural silicotic nodules were present. The underlying lung tissue did not show fibrosis or silicotic nodules. An energy-dispersive x-ray analysis confirmed the presence of silica. In the absence of lung involvement, this case represents a very unusual pathologic reaction caused by silica and silicates and adds to the clinical differential diagnosis of chronic pleuritis and malignant mesothelioma.
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