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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We cared 2 patients with diffuse pulmonary lymphangiomyomatosis (LAM) through the perioperative period. LAM is a disease of uncertain origin and poor prognosis because of respiratory failure. Therefore, it is important to provide not only a good anesthetic care but also a good preoperative respiratory care. In the first case (a 35-yr-old woman), an open lung biopsy was performed after dyspnea and sputum had disappeared with preoperative medications of a bronchodilator and some antibiotics. In the second case (a 35-yr-old woman), oophorectomy was performed after FEV1.0% had remarkably increased with preoperative medication of a bronchodilator. Both patients did well through the perioperative period without any trouble or complications, such as pneumonia or severe hypoxemia, presumably owing to our perioperative management system.
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PMID:[Two cases of diffuse pulmonary lymphangiomyomatosis]. 143 86

The histopathologic and ultrastructural features of intraluminal organizing and fibrotic changes were studied in open lung biopsies and autopsy specimens from 373 patients with interstitial lung disorders, including hypersensitivity pneumonitis (n = 44), idiopathic pulmonary fibrosis (n = 92), collagen-vascular diseases (n = 20), chronic eosinophilic pneumonia (n = 10), pulmonary histiocytosis X (n-90), pulmonary sarcoidosis (n = 62), pneumoconioses (n = 25), Legionnaire's disease (n = 5), drug- and toxin-induced pneumonitis (n = 4), radiation-induced pneumonitis (n = 2), lymphangioleiomyomatosis (n = 11), and chronic organizing pneumonia of unknown cause (n = 8). Three patterns of intraluminal organization and fibrosis were recognized: 1) intraluminal buds, which partially filled the alveoli, alveolar ducts and/or distal bronchioles; 2) obliterative changes, in which loose connective tissue masses obliterated the lumens of alveoli, alveolar ducts or distal bronchioles, and 3) mural incorporation of previously intraluminal connective tissue masses, which fused with alveolar, alveolar ductal, or bronchiolar structures and frequently became reepithelialized. All three patterns had common morphologic features, suggesting that, regardless of their severity, they resulted from a common pathogenetic mechanism, ie, the migration of activated connective tissue cells, through defects in the epithelial lining and its basement membrane, from the interstitial into the intraluminal compartment. Intraluminal buds were observed most frequently in hypersensitivity pneumonitis, chronic eosinophilic pneumonia, and organizing pneumonia of unknown cause. Mural incorporation and, to a lesser extent, obliterative changes were observed in most interstitial disorders and were very prominent in idiopathic pulmonary fibrosis. Mural incorporation and obliterative changes play an important role in pulmonary remodeling, especially when several adjacent alveoli and/or other air spaces are involved. Under these circumstances, intraluminal organization can mediate the fusion of adjacent alveolar structures by intraluminal connective tissue.
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PMID:Intraluminal fibrosis in interstitial lung disorders. 395 68

Langerhans' cells were found in lung biopsies in one of nine control patients and in 20 of 160 patients with fibrotic lung disorders, including 13 of 56 patients with idiopathic pulmonary fibrosis, two of nine patients with collagen vascular diseases, two of seven patients with hypersensitivity pneumonitis, and each of three patients with end stage fibrosis of uncertain cause. Langerhans' cells were not found in any of the 41 patients with sarcoidosis, the 35 patients with interstitial lung diseases associated with inhalation of inorganic dusts, the seven patients with pulmonary lymphangioleiomyomatosis, or the two patients with chronic eosinophilic pneumonia. In the control patient, Langerhans' cells were found between epithelial cells in bronchioles. In patients with fibrotic lung disorders, Langerhans' cells were found in the epithelial layer of bronchioles and alveoli containing proliferating epithelial cells, i.e., either cuboidal epithelial cells of bronchiolar origin or type II alveolar epithelial cells. Severe fibrosis or squamous metaplasia were not prerequisites for the presence of Langerhans' cells. The motility of Langerhans' cells apparently was restricted, as they were not found in the air spaces in any of the biopsies, and they were not recovered from bronchoalveolar lavage fluid of any of the 97 patients studied, even though some of these patients had relatively numerous Langerhans' cells in lung biopsies. These observations are in sharp contrast to those in pulmonary histiocytosis X, in which histiocytosis X cells (HX cells) occur in granulomas, in alveolar interstitium, and between epithelial cells of the lower respiratory system. HX cells also migrate into air spaces, as shown by their occurrence in bronchoalveolar lavage fluid. The HX bodies in HX cells are morphologically similar to Langerhans' cell granules, but are more numerous and pleomorphic. HX cells are considered to be reactive or activated Langerhans' cells.
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PMID:Pulmonary Langerhans' cells in patients with fibrotic lung disorders. 697 Mar

Ultrastructural studies were made of the types of alveolar epithelial cells in fibrotic lungs from 34 patients, including 20 with idiopathic pulmonary fibrosis, five with collagen-vascular diseases, six with sarcoidosis, one with lymphangioleiomyomatosis, one with histiocytosis X, and one with chronic eosinophilic pneumonia. In 28 patients, proliferation of type II alveolar epithelial cells was recognized on the basis of lamellar bodies in the cytoplasm, microvilli in the luminal surface, focal microfoldings of the basal plasma membrane, close interaction with underlying mesenchymal cells, and unilayered arrangement. Two types of cuboidal epithelial cells were recognized and were considered to be derived from bronchiolar basal cells (type A cuboidal cells) and from cuboidal cells in respiratory bronchioles (type B cuboidal cells). Type A cuboidal cells frequently contained large numbers of cytoskeletal filaments, and their basal plasma membranes possessed hemidesmosomes in close association with anchoring fibrils. Type B cells lacked hemidesmosomes and anchoring fibrils, Proliferation of either or both types of cuboidal cells was found in 30 patients. In 10 patients (average degree of fibrosis = 3.5 on a scale of 0 to +4), the proliferation involved type A cells; in 10 other patients (average degree of fibrosis = 2.5), type B cells in nine patients (average degree of fibrosis = 3.4), both type A and type B cells; in one patient cuboidal cells were identified only by light microscopy. In 17 patients, proliferating cuboidal cells formed foci of epithelial pseudostratification. Type II alveolar epithelial cells did not participate in the process of multilayering. Thus, type II alveolar epithelial cells and two types of cuboidal epithelial cells are sources of epithelial renewal in damaged alveoli in fibrotic lungs. Type II cells proliferate mainly in areas of less severe degrees of fibrosis; cuboidal cells become the main source of epithelial renewal in areas of very severe lung damage.
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PMID:Structure of alveolar epithelial cells in patients with fibrotic lung disorders. 705 89

A study was undertaken to evaluate the safety and efficacy of thoracoscopic lung biopsy for interstitial lung disease. The relation between operative findings, pathologic findings, and preoperative computed tomographic scan findings was examined. Twenty-six patients, 10 male and 16 female, underwent thoracoscopic lung resection to diagnose interstitial lung disease. Sixteen patients were outpatients for an elective procedure; 10 were inpatients including 2 who were ventilator dependent. The mean length of operation was 54 minutes and the mean length of chest tube duration, 1.3 days. There were no deaths. Staphylococcal pneumonia developed in 1 patient postoperatively. One patient with systemic pulmonary hypertension was ventilator dependent for 48 hours. A double-lumen endotracheal tube was used in all but 2 patients. Twelve-millimeter trocar ports were used to allow easy interchange of staplers and endoscopic instruments. Biopsy of at least two lobes was performed in each patient with resection of a piece of grossly abnormal lung. A single chest tube was left routinely. The pathologic diagnosis was usual interstitial pneumonitis in 7 patients. Four patients had interstitial fibrosis and 4, granulomas. Three patients had diffuse alveolar damage and 3, Wegener's granulomatosis. Two patients had bronchiolitis obliterans with organizing pneumonia. One patient each had lymphangioleiomyomatosis, eosinophilic granuloma, and cytomegalovirus. Sixteen patients underwent preoperative computed tomographic scanning. The scans were assessed by 2 radiologists who were blinded to the surgical results. Computed tomography accurately predicted the site of disease in most instances. Four patients had at least one lobe with no evidence of disease on computed tomography but with interstitial lung disease found thoracoscopy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of thoracoscopy in the diagnosis of interstitial lung disease. 784 48

To study the role of transforming growth factor-beta 1 (TGF-beta 1) in the pathogenesis of pulmonary fibrosis we have examined lung biopsies from nine patients with systemic sclerosis and interstitial lung disease, eight with 'lone' cryptogenic fibrosing alveolitis, two with cystic fibrosis, two with extrinsic allergic alveolitis, two with Langerhans' cell histiocytosis, one with lymphangioleiomyomatosis, one with giant cell interstitial pneumonia, and one adenocarcinoma of the lung. In cryptogenic fibrosing alveolitis, both 'lone' and associated with systemic sclerosis alveolar macrophages, bronchial epithelium and hyperplastic type II pneumonocytes expressed intracellular TGF-beta 1. Extracellular TGF-beta 1 was found in the fibrous tissue immediately beneath the bronchial and hyperplastic alveolar epithelium. In normal lung, however, the alveolar epithelium and alveolar interstitium were negative for both forms of TGF-beta 1. There was strong expression of TGF-beta 1 in hyperplastic mesothelium and its underlying connective tissue and in Langerhans' cells in the two cases of histiocytosis. In the organizing pneumonia in cystic fibrosis, the intraalveolar buds of granulation tissue reacted strongly for the extracellular form of TGF-beta 1 and the overlying hyperplastic epithelium expressed the intracellular form. In lymphangioleiomyomatosis, the aberrant smooth muscle cells strongly expressed intracellular TGF-beta 1 and the extracellular form was expressed in the adjacent connective tissue. In giant cell interstitial pneumonia, the numerous alveolar macrophage including the multinucleate forms, expressed intracellular TGF-beta 1, as did the hyperplastic alveolar epithelium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunohistochemical localization of transforming growth factor-beta 1 in the lungs of patients with systemic sclerosis, cryptogenic fibrosing alveolitis and other lung disorders. 818 7

The purpose of this study was to evaluate the role of high-resolution computed tomography (HRCT) in the clinical diagnosis of diffuse infiltrative lung disease (DILD). Diagnostic accuracy was compared using both chest radiography and HRCT. One hundred thirty-four cases of DILD, representing 21 different diseases, were selected for study, and the disease state was confirmed either histologically or microbiologically. The HRCT images and chest radiographs, available in all cases, were reviewed separately and in random order by 20 physicians who were provided only with information on each patient's age and sex. Overall, a correct first-choice diagnosis was made in 38 percent using radiographs and in 46 percent using HRCT images (p < 0.01). The correct diagnosis was among the top three choices in 49 percent when chest radiographs were used, and in 59 percent when HRCT images were viewed (p < 0.01). The correct first-choice diagnosis increased remarkably when the HRCT was used in usual interstitial pneumonia, sarcoidosis, alveolar proteinosis, bronchiolitis obliterans organizing pneumonia, hypersensitivity pneumonitis, and pulmonary lymphangiomyomatosis. High-resolution computed tomography was confirmed to be superior to conventional radiography in the accurate diagnosis of DILD in clinical practice.
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PMID:The diagnostic accuracy of high-resolution computed tomography in diffuse infiltrative lung diseases. 840 83

Worldwide almost no epidemiologic data are available on the prevalence or incidence of interstitial lung diseases (ILD) in the general population. Therefore, a registration programme of ILD-prevalence was organised by the VRGT (Vereniging voor Respiratoire Gezondheidszorg en Tuberculosebestrijding), among about 100 Flemish pneumologists since 1990. Most categories of the classification by Crystal et al. (1) were included and the diagnostic criteria (histology, laboratory tests, clinic, radiology) were registered. The present paper presents the results of 1992-1994: twenty pneumologists had forwarded the summary files of 237 patients to the central office in 1992 (n = 68), 1993 (n = 90) and 1994 (n = 79). The diagnoses that were most frequently made were: sarcoidosis in 27%, idiopathic pulmonary fibrosis in 20%, hypersensitivity pneumonitis in 14% (of which 68% by birds) and collagen-vascular disease in 10% (of which 54% in rheumatoid arthritis). Less frequent causes were eosinophilic pneumonia (4%), inhalation of inorganic material (4%, anthracosilicosis being excluded), histiocytosis X (3%), drugs (3%), angiitis and granulomatosis (2%), pulmonary hemosiderosis (1%), lymphocytic infiltrative lung disease (1%) and lymphangioleiomyomatosis (1%). The order of relative frequencies of the different categories of diseases was the same in the 3 registration years. In 9% of the patients the diagnosis was confined to "undefined fibrosis". The diagnosis was confirmed by histology in 63% of the cases. The overall male-female ratio was nearly one, with, however, a male preponderance in hypersensitivity pneumonitis (22/12), UIP(8/3) and "undefined fibrosis" (14/7).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of interstitial lung disease (ILD) in flanders: registration by pneumologists in 1992-1994. Working group on ILD, VRGT. Vereniging voor Respiratoire Gezondheidszorg en Tuberculosebestrijding. 853 25

A 49-year-old woman was admitted to our hospital because of coughing and dyspnea. A chest roentogenogram showed emphysematous changes and a diffuse reticular shadow. A high-resolution CT scan of the chest showed many small cysts throughout the lungs. Lymphangiomyomatosis was diagnosed after examination of a specimen obtained by transbronchial biopsy. Abdominal distention due to chylous ascites developed during the hospital stay despite anti-estrogen therapy. Because the ascites was resistant to conservative therapy, we decided to begin peritoneo-venous shunting with a Denver Shunt system. After the operation, the abdominal distention was controlled for 1 year and 11 months, at which time the patient died of respiratory and heart failure with pneumonia. At autopsy, the shunt was patent and functional although about 900 ml of serous ascites fluid was present. An adenocarcinoma was found in the upper lobe of the right lung, but it may not have been related to the lymphangiomyomatosis. Peritoneovenous shunting with a Denver Shunt can be used to treat chylous ascites due to lymphangiomyomatosis when conservative therapy is insufficient.
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PMID:[Lymphangiomyomatosis with chylous ascites treatment successfully by peritoneo-venous shunting]. 875 14

Because the list of interstitial lung diseases is so extensive, encompassing more than 180 chronic lung diseases in which the interstitium is altered by inflammation and/or fibrosis, this chapter focuses on several inflammatory lung diseases of unknown etiology: usual interstitial pneumonitis, respiratory bronchiolitis, idiopathic bronchiolitis obliterans with organizing pneumonia, pulmonary Langerhans' cell granulomatosis, hypersensitivity pneumonitis, and lymphangioleiomyomatosis.
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PMID:Interstitial lung disease. 895 12


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