Cases reported "Pulmonary Eosinophilia"

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1/11. Acute eosinophilic pneumonia in a new york city firefighter exposed to World Trade Center dust.

    We report a sentinel case of acute eosinophilic pneumonia in a firefighter exposed to high concentrations of World Trade Center dust during the rescue effort from September 11 to 24. The firefighter presented with a Pa(O2) of 53 mm Hg and responded to oxygen and corticosteroids. Computed tomography scan showed patchy ground glass density, thickened bronchial walls, and bilateral pleural effusions. Bronchoalveolar lavage recovered 70% eosinophils, with only 1% eosinophils in peripheral blood. eosinophils were not degranulated and increased levels of interleukin-5 were measured in bronchoalveolar lavage and serum. Mineralogic analysis counted 305 commercial asbestos fibers/10(6) macrophages including those with high aspect ratios, and significant quantities of fly ash and degraded fibrous glass. Acute eosinophilic pneumonia is a rare consequence of acute high dust exposure. World Trade Center dust consists of large particle-size silicates, but fly ash and asbestos fibers may be found in bronchoalveolar lavage cells.
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2/11. Cigarette smoke-induced acute eosinophilic pneumonia accompanied with neutrophilia in the blood.

    smoking causes various changes in the lung. This report describes a case of cigarette smoke-induced acute eosinophilic pneumonia (CS-AEP) with neutrophilia in the blood. However, the precise mechanism is unknown, so we examined the effect of exposure to cigarette smoke extracts on the production of interleukin (IL)-4, IL-5, IL-8, IL-18, granulocyte macrophage-colony stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF) by human bronchial epithelial cells (HBECs) obtained from the patient. We found that IL-8 released from HBECs was involved in neutrophilia in the blood, and is a new factor in the development of AEP, especially in the early phase.
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3/11. Chronic eosinophilic pneumonia. Ultrastructural evidence of marked immunoglobulin production plus macrophagic ingestion of eosinophils and eosinophilic lysosomes leading to intracytoplasmic Charcot-Leyden crystals.

    A 60-year-old man was diagnosed as having chronic eosinophilic pneumonia by clinical presentation and open lung biopsy. Electron microscopic study of the tissue from biopsy revealed evidence of marked production of immunoglobulin, which may be part of the chemotactic process which attracted large numbers of eosinophils into the area. Also, there were macrophages which were phagocytosing degenerating eosinophils and eosinophilic lysosomes. Charcot-Leyden crystals were noted in the cytoplasm of many macrophages. The relationship of the production of immunoglobulin to the eosinophilia and the mechanism of intramacrophagic formation of Charcot-Leyden crystals is discussed.
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4/11. Chronic eosinophilic pneumonia.

    We described three cases of eosinophilic pneumonia of unknown aetiology investigated clinically and by lung biopsy. The illnesses lasted between six and 20 weeks and consisted of cough, dyspnoea, malaise, and in two cases prolonged pyrexia. All had blood eosinophilia and chest radiographs showing widespread bilateral shadowing; in two cases this had a characteristic peripheral distribution. One patient recovered spontaneously and the other two responded to steroids, with disappearance of pyrexia within 12 hours and radiological clearing within 14 days. Lung function tests during the acute illness showed volume restriction or gas transfer defects or both in two cases. After remission all three showed abnormalities if small airways function. Lung biopsies performed during the acute illness were examined histologically and by transmission electron microscopy, and in two cases by immunofluorescence. There was both intra-alveolar and interstitial eosinophilic pneumonia with bronchiolitis obliterans, microgranulomata, and a vasculitis. Electron microscopy showed numerous eosinophils, many degranulated, and macrophages with phagocytosed eosinophilic granules and intracytoplasmic inclusions. In one case IgM, IgG, and IgA were demonstrated in the bronchial walls and interstitium. No IgE or complement was present. We believe that eosinophil granules are responsible for the tissue damage and fever and suggest mechanisms for this and for the response to steroid therapy.
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5/11. IgA2-alveolitis and eosinophilic pneumonia--a possibly virus-triggered allergy.

    A case of severe therapy-resistant asthma in a young girl with a duration of two years prior to death is reported. At autopsy antibodies of the IgA2-subtype were demonstrated in the lungs on the alveolar basement membranes. We were able to demonstrate intracellular virus-like structures by electron microscopy; this virus infection is taken to be the cause of antibody production. Following antigen-antibody reaction a non-complement-mediated eosinophilic pneumonia with numerous macrophages developed. This inflammatory reaction showed the injurious effect of eosinophilic granulocytes causing fibrinoid necrosis; this is confirmed by the pronounced depletion of the Charcot-Leyden-granules, equivalent to the release of the major basic protein and the Charcot-Leyden crystal protein. death was caused by IgA2 deposition in the myocardial vessels with consequent eosinophilic myocarditis.
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6/11. Analysis of bronchoalveolar lavage cells in chronic eosinophilic pneumonia before and during corticosteroid therapy.

    Bronchoalveolar lavage was performed in patients with chronic eosinophilic pneumonia of unknown origin diagnosed histopathologically, and the alveolar fluid cells were investigated before and during corticosteroid therapy. The counts of eosinophils in bronchoalveolar lavage fluid decreased markedly during steroid therapy compared with before therapy, and the ratios of interleukin 2 receptor-positive T cells and HLA DR-positive T cells to all T lymphocytes in the lavage fluid also decreased. Both before and during steroid therapy, many macrophages in bronchoalveolar lavage fluid phagocytosed EG2-positive granules and stained immunohistochemically as CD71-positive 'responsive macrophages'. The decrease of activated T lymphocytes and the active phagocytosis of eosinophil granules by macrophages might play an important role in the mechanism of healing in chronic eosinophilic pneumonia.
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7/11. Eosinophilic lung reaction to aluminium and hard metal.

    A nonsmoker drill polisher with interstitial lung disease is presented. The environmental exposure was mainly to aluminum oxide, aluminum silicate, and hard metals. Bronchoalveolar lavage revealed high eosinophilia, and transbronchial biopsy specimen disclosed interstitial pneumonia with giant cell infiltrates and peribronchiolar accumulation of macrophages laden with opaque dust. Mineralogic studies done from the tissue revealed a high concentration of exogenous particles that were identified as hard metals and aluminum silicate. These findings are compatible with hard metal pneumoconiosis.
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8/11. Pulmonary eosinophils express HLA-DR in chronic eosinophilic pneumonia.

    BACKGROUND: Chronic eosinophilic pneumonia is a rare idiopathic disorder. role the eosinophil plays in the pathogenesis of this disease is unknown. The recent finding that nature eosinophils can express the class II major histocompatibility complex molecule HLA-DR suggests an immunologic role, perhaps through antigen presentation. The purpose of this research was to determine whether lung-derived eosinophils exhibit in vivo expression of HLA-DR. methods: eosinophils were obtained simultaneously from bronchoalveolar lavage and peripheral blood from a 59-year-old woman with asthma and chronic eosinophilic pneumonia. Eosinophil-enriched aliquots of peripheral blood were cocultured with human lung fibroblasts (with or without additional granulocyte-macrophage colony-stimulating factor). The percentage of cells expressing HLA-DR was quantitated by flow cytometric analysis. RESULTS: eosinophils derived from bronchoalveolar lavage displayed in vivo expression of HLA-DR (86%) in contrast to those from peripheral blood (7%), suggesting compartmentalization of eosinophil activation within the lung. Peripheral blood eosinophils retained the capacity for HLA-DR expression when coincubated with lung fibroblasts (83%) with augmentation by granulocyte-macrophage colony-stimulating factor (93%). CONCLUSION: These data demonstrate that lung eosinophil HLA-DR expression occurs in vivo; it may contribute to the pathogenesis of inflammatory lung injury.
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9/11. Cytokine production at the site of disease in chronic eosinophilic pneumonitis.

    Chronic eosinophilic pneumonitis (CEP) is characterized by longstanding respiratory symptoms accompanied by a massive pulmonary eosinophil infiltration. We hypothesized that cytokine(s) produced in the disease sites are implicated in the pathophysiology of CEP. We studied peripheral blood and bronchoalveolar lavage fluids (BALF) obtained from two lung segments of a patient with CEP. Seventy times more eosinophils were found in the BALF from an involved lung segment (showing patchy opacification on a chest roentgenogram) than from an uninvolved segment. The eosinophil-active cytokines interleukin-5 (IL-5), IL-6, and IL-10 were strikingly elevated in the BALF from the involved lung segment, whereas no or minimal levels of these cytokines were detectable in the BALF from the uninvolved segment or serum, respectively. leukocytes in the involved lung segment, but not those in peripheral blood, expressed messenger ribonucleic acid (mRNA) for IL-5, IL-6, and IL-10. In contrast, IL-2, IL-3, IL-4, interferon-gamma (IFN-gamma), granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor-alpha (TNF-alpha) were not detected in any sample. These findings suggest that increased production of several cytokines, such as IL-5, IL-6, and IL-10, in the involved lung segment, but not in the uninvolved lung segment or peripheral blood, is a critical pathophysiologic feature of CEP.
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10/11. Electron microscopic study of chronic eosinophilic pneumonia.

    Two cases of chronic eosinophilic pneumonia were examined electron microscopically to study the role of eosinophil granulocytes. eosinophils, together with macrophages and lymphocytes, were observed to have infiltrated prominently in the lung tissues of the two cases. Degeneration and necrosis of pneumocytes were observed, and denuded basement membranes and destroyed alveolar structures were occasionally found. In the alveolar septa, swelling of the endothelial cells of the blood capillaries, edema of the stroma and fibrin deposition were observed. eosinophils, released eosinophil granules and macrophages phagocytosing eosinophil granules were found frequently near the degenerated and necrotic alveolar tissues. These findings suggest that the tissue injuries were induced by the cytotoxic effects of the eosinophil granules.
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