Cases reported "Pulmonary Eosinophilia"

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1/84. Acute eosinophilic pneumonia associated with shock.

    OBJECTIVE: To describe an unusual case of acute eosinophilic pneumonia (AEP) associated with hemodynamic instability. DESIGN: Case report, clinical. SETTINGS: Tertiary care intensive care unit (ICU). PATIENT: A single patient admitted to the ICU. INTERVENTIONS: Intravenous corticosteroids. MEASUREMENTS AND MAIN RESULTS: Resolution of distributive shock and respiratory failure. CONCLUSIONS: AEP with respiratory failure was first reported in 1989 as a distinct clinical entity. patients with this variant of eosinophilic lung disease develop acute hypoxemic respiratory failure with a rapid response to treatment with corticosteroids, The characteristic feature of this syndrome is a predominance of eosinophils found in bronchoalveolar lavage fluid and lung biopsy. Despite the increasing number of reported cases, to our knowledge, distributive shock has not been reported as a feature of AEP. We report a unique case of AEP associated with shock and review the pertinent literature.
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2/84. eosinophilia in Wegener's granulomatosis.

    Significant eosinophilia is a prominent feature in churg-strauss syndrome but has only rarely been described in Wegener's granulomatosis (WG). We describe two Wegener's granulomatosis patients with > 30% eosinophilia on their initial presentations. Other etiologies that could account for their eosinophilia were excluded. Both patients had pulmonary alveolar hemorrhage, sinusitis, arthritis, high-titer cytoplasmic antineutrophil cytoplasmic antibodies (cANCA), and proteinase-3 antibodies, but no evidence of renal disease. Herein we discuss eosinophilia, the differential diagnosis of pulmonary infiltrates and eosinophilia, the role of cANCA in vasculitis and autoimmune disease, compare Wegener's granulomatosis and churg-strauss syndrome, and review possible pathogenic mechanisms.
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3/84. Rapidly evolving adult respiratory distress syndrome with eosinophilia of unknown cause in previously healthy active duty soldiers at an Army training center: report of two cases.

    BACKGROUND: Two previously healthy soldiers presented with rapidly evolving adult respiratory distress syndrome (ARDS) within days of their return from the National Training Center at Fort Irwin, california. There have been six similar cases reported in the National Training Center area, five with fatal outcomes. methods: Both patients were treated in an intensive care unit setting. Extensive diagnostic testing was performed, and patients were treated empirically with doxycycline, ceftriaxone, and ribavirin. RESULTS: Both patients had complete recovery. intensive care unit course was notable for circulatory collapse, respiratory distress requiring ventilatory support, approximately 10% eosinophils on bronchoalveolar lavage, and dramatic peripheral eosinophilia. All cultures, including serology cultures for hantavirus, were negative. CONCLUSION: There have been no previously described syndromes comprising "viral" prodrome, rapid progression to ARDS, and eosinophilia. Based on the geographic, temporal, and clinical similarity of these two cases, we believe that they share a common, yet undetermined, cause. Both environmental exposures and any undescribed pathogens warrant further investigation.
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4/84. Nuclear hypersegmentation precedes the increase in blood eosinophils in acute eosinophilic pneumonia.

    In this case of acute eosinophilic pneumonia (AEP), eosinophils with hypersegmented nuclei emerged in the blood before the increase of eosinophil count. An 18-year-old woman complaining of fever, cough and dyspnea was admitted because of diffuse ground-glass opacities in her chest roentgenogram. On admission, her blood cell count revealed a marked increase of neutrophils. Although the number of eosinophils was normal, some of them contained three- or four-lobed nuclei. She was diagnosed to have AEP through bronchoalveolar lavage and transbronchial lung biopsy. The combination with acute clinical course, pulmonary infiltration and the presence of hypersegmented eosinophils in blood may imply the diagnosis of AEP.
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5/84. Acute eosinophilic pneumonia associated with smoke from fireworks.

    We report a case of acute eosinophilic pneumonia (AEP). Although the patient had been a habitual cigarette smoker for over 4 months, he had had not any respiratory distress. After he inhaled smoke from fireworks for 3 consecutive nights, the patient began to complain of cough, fever and dyspnea. He showed leukocytosis of 16,200/microl and hypoxemia of 58.1 torr. Chest radiograph showed bilateral infiltrates with Kerley A and B lines. The bronchoalveolar lavage fluid revealed 38.5% eosinophils. He was diagnosed as AEP. In this patient, inhaling of smoke from fireworks was clinically suspected to be associated with the induction of AEP.
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6/84. Activation of lymphocytes and increased interleukin-5 levels in bronchoalveolar lavage fluid in acute eosinophilic pneumonia.

    Acute eosinophilic pneumonia (AEP) is a recently described illness and the number of case reports has increased during the last few years. However, the role of interleukin (IL)-5 and activated lymphocytes in the pathogenesis or activity of AEP is still not clear. The clinical features, lymphocyte surface analysis and IL-5 concentrations in bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) of a young female patient with AEP are described before and at 2 weeks, 4 weeks and 6 months after a 3-day course of i.v. methylprednisolone. serum and BALF concentrations of IL-5 before treatment were 5,200 and 8,400 pg x mL(-1), respectively. Activated CD4 lymphocytes bearing CD25 and human leukocyte antigen (HLA)-DR in BALF were higher than in PB. Treatment caused a rapid fall in these cells and levels of IL-5 in BALF returned to normal levels in parallel with clinical improvement. There was no evidence of recurrence after cessation of steroid therapy. In contrast, eosinophilia in BALF persisted for 4 weeks after steroid therapy in spite of normalization of the chest radiograph and arterial blood gases. The number of CD8 CD11b- (suppressor/cytotoxic) T-cells subsequently increased while the number of CD8 CD11b cells decreased. These results suggest that activated CD4 cells and interleukin-5 elevation contribute to the development of acute eosinophilic pneumonia rather than persistent eosinophilia in the lung and that a short course of steroid therapy may effectively control acute eosinophilic pneumonia.
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7/84. Chronic eosinophilic pneumonia: a case report.

    Chronic eosinophilic pneumonia (CEP) is a disorder, characterized by a history of pneumonia (> 2 months) and eosinophilic pulmonary infiltration without any organic causes. We describe a 28-year-old woman who presented with cough, dyspnea and fever for 2 months. She was diagnosed with mild asthma and allergic rhinitis 2 years before being diagnosed with CEP. For a period of 9 months she took no medication. Her chest roentgenogram at this admission revealed patchy infiltration in both upper lung fields. Laboratory data revealed blood eosinophilia (4,284/mm3), and her serum IgE was mildly elevated (245.8 IU/ml). A computerized tomography of the chest did not show bronchiectasis. CEP was diagnosed from significant eosinophilia in bronchoalveolar larvage fluid and transbronchial biopsy revealed eosinophilic infiltration without any demonstrable infectious agent. The patient was treated with prednisolone 45 mg/day. Her symptoms disappeared and her chest roentgenogram showed nearly complete resolution in 2 and 4 days, consecutively.
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8/84. indomethacin induced bulky lymphadenopathy and eosinophilic pneumonia.

    indomethacin is one of the most popular non-steroidal anti-inflammatory drugs (NSAID). Although NSAID occasionally provoke bronchospasm and hypersensitivity pneumonia, they seldom cause lymphadenopathy. This is the first report in which NSAID induced both eosinophilic pneumonia and bulky intrathoracic lymphadenopathy simultaneously. A 76-year-old Japanese man experienced high fever and dyspnoea after using an indomethacin suppository. Computed tomography scan of his chest revealed massive mediastinal and hilar lymphadenopathy along with diffuse infiltration in both lungs. He was diagnosed to have eosinophilic pneumonia because of eosinophilia in his peripheral blood and bronchoalveolar lavage fluid (BALF). Without using glucocorticoids, the pulmonary infiltration and lymphadenopathy subsided spontaneously. As the blastoid transformation test using the lymphocytes in his BALF was positive to indomethacin, we judged that both his eosinophilic pneumonia and mediastinal lymphadenopathy were due to a hypersensitivity reaction to indomethacin. An allergic reaction to NSAID should be considered as a rare cause of mediastinal lymphadenopathy.
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9/84. Acute eosinophilic pneumonia associated with amitriptyline in a hemodialysis patient.

    Drugs are well known causes of eosinophilic lung disease. In many patients, drug-induced eosinophilic lung disease presents with transient eosinophilic infiltrates that disappear after discontinuation of the drug. Some patients, however, experience a fulminant, acute eosinophilia-like disease. Recently, we experienced a case of amitriptyline-associated acute eosinophilic pneumonia with respiratory failure in a diabetic hemodialysis patient. Eight days after treatment with amitriptyline, sudden fever, chill, dry cough and dyspnea developed. Subsequently, multiple patch consolidations appeared on the chest radiographs. Bronchoalveolar lavage (BAL), established a diagnosis of acute eosinophilic pneumonia. After immediate discontinuation of amitriptyline, a rapid clinical and radiological improvement was observed. The present case indicates that the possibility of acute eosinophilic pneumonia should be fully considered in dialysis patients developing unexplained respiratory symptoms while on amitriptyline therapy.
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10/84. Analysis of T cell receptor V(beta) gene expression and clonality in bronchoalveolar fluid lymphocytes from a patient with chronic eosinophilic pneumonitis.

    Chronic eosinophilic pneumonitis (CEP) is characterized by longstanding respiratory symptoms accompanied by a massive pulmonary eosinophil infiltration. T lymphocytes in bronchoalveolar lavage (BAL) from patients with chronic eosinophilic pneumonitis are considered to recognize unknown antigens. To analyze the pathogenesis of CEP, we examined the T cell receptor (TCR) repertoire and T cell clonotype of BAL lymphocytes and peripheral blood lymphocytes (PBLs) in a 66-year-old woman patient with CEP. The expression of TCR BV gene was analyzed by the family PCR method using specific primers for 20 TCR BV genes and BC gene. The clonotype of BAL and peripheral T cells was examined by the PCR-single-strand conformation polymorphism (SSCP) method. Functional sequences of some T cell clones were also carried out. A TCR repertoire of BAL T cells was heterogeneous as well as PBLs. However, SSCP analysis showed that distinct T cell clonotypes were detected in BAL T cells, TCR BV3, BV4, BV6, BV8, BV9, BV14, and BV18-positive T cell clones especially, expanded clonally in BAL from the patient. Sequencing analysis showed that GVD, LGG, RDXS, and SSG amino acid sequence motif were found in the CDR3 in lung-specific T cells. BAL-specific T cell clones accumulated in the patient with CEP. Thus, we can conclude that BAL T cells are induced by the antigen-driven stimulation and these cells might play a crucial role in the generation of CEP.
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