Biomedical subjects
Publications and source records attributed to U Costabel.
Pneumotoxicity of cyclophosphamide is a rare complication of chemotherapy with this drug. 28 cases have so far been reported in world literature. We add one case in whom lung changes had appeared subacutely, after a single dose of cyclophosphamide, and were reversed by corticoids.
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This study investigated the usefulness of macrophage size determinations in lymphocyte-rich pleural effusions to improve the cytologic diagnosis of tuberculous pleurisy. The size of pleural macrophages was analyzed by quantitative morphometric planimetry in 18 effusions due to tuberculosis, 21 effusions following radiotherapy for malignant disease and 10 effusions due to congestive heart failure. Macrophages were identified and clearly separated from mesothelial cells by latex phagocytosis and immunostaining with the monoclonal antibody My4 (CD14). The mean macrophage area (+/- standard deviation) in tuberculous effusions (92 +/- 14 sq micron) was significantly smaller than in postradiation (141 +/- 28 sq micron) and heart-failure effusions (154 +/- 22 sq micron) (P less than .0001). There was also a smaller ratio of mesothelial cells in tuberculous effusions (0.5 +/- 0.9%) in comparison with effusions following radiotherapy (4 +/- 5%) or congestive heart failure (10 +/- 12%). In summary, this study demonstrated some cytomorphologic parameters that may be helpful in the differential diagnosis of tuberculous effusions.
In the pathogenesis of hypersensitivity pneumonitis (HP) several immune mechanisms are involved. The initial phase, 4-48 h after antigen inhalation, appears to be immune complex mediated and is characterized by an early increase in bronchoalveolar lavage (BAL) neutrophils and the histopathologic features of oedema, neutrophil infiltration of the alveolar wall, and vasculitis. After 12 h to several days, the immune response possibly shifts to a cell-mediated reaction, and the alveolitis consists of cytotoxic effector cells as well as suppressor cells which may be required to modulate the B cell response of antibody production by plasma cells. In this phase, lymphocytes of the OKT8 positive phenotype, natural killer cells, and occasionally a few plasma cells are increased in BAL fluid. The characteristic histopathologic finding is a mononuclear infiltrate consisting of lymphocytes, plasma cells, and foamy histiocytes. After weeks to months, a delayed type hypersensitivity reaction may lead to a slight predominance of OKT4 positive cells in BAL fluid and to granuloma formation. Finally, after months to years, repeated immune-mediated injury to the alveolar wall with release of proteolytic enzymes and fibroblast growth factors may result in pulmonary fibrosis and end stage lung with concomitant increase in BAL neutrophils as in other fibrotic diseases.
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The new Vacu-Cut biopsy needle differs from previous types by its simpler manipulation and the production of a stronger vacuum to extract the tissue core. This vacuum is caused by withdrawal of a stylet through an air-tight sealing membrane. The instrument is a hollow needle with an inner cutting-edge and a diameter of 0.95 mm. 49 patients with suspected lesions of the pulmonary parenchyma were biopsied transcutaneously under x-ray monitoring. The biopsy material allowed a clearcut diagnosis in 44 patients, including 2 repeat biopsies; the success rate was thus 86% of all biopsies performed. 7 attempts (14%) did not yield useful material as the lesions were too small (diameter below 2.5 cm) or were not penetrated. In 35% of all biopsies small pneumothoraces were observed after a few hours. In two cases transitory hemoptysis occurred.
The serum of 2 patients suffering from idiopathic pulmonary fibrosis (IPF) repeatedly demonstrated a positive antibody reaction against rat alveolar type II cells isolated by the use of a combination of elastase and trypsin for disaggregation and a Percoll density gradient for purification. Neither of the other 8 IPF patients examined nor any of the controls showed a positive reaction. Because the 2 patients with serum antibodies against alveolar type II cells did not show any antinuclear antibodies, it is concluded that the antibodies against the surface of rat alveolar type II cells found in the serum of IPF patients may be autoantibodies involved in the pathogenesis of IPF.
To study the local distribution of lymphocyte subsets in inorganic dust diseases, bronchoalveolar lavage (BAL) was performed in seven patients with asbestosis, and in 13 patients with mixed dust pneumoconiosis (anthracosidero-silicosis). Lymphocyte subsets in BAL and blood were determined by the monoclonal antibodies OKT3 (pan T), OKT4 (helper/inducer), OKT8 (suppressor/cytotoxic), B1 (B-cells), OKIa (HLA-DR antigens), and Leu-7 (natural killer). The BAL lymphocytes were moderately elevated to 15 +/- 8 percent (mean +/- SD) in mixed dust pneumoconiosis, and even more markedly increased to 28 +/- 21 percent in asbestosis. The OKT4/OKT8 ratio in BAL was significantly increased to 4.5 +/- 2.1 in asbestosis, and significantly reduced to 0.9 +/- 0.8 in mixed dust pneumoconiosis. In blood, the ratio of T-cell subsets remained unchanged, though total lymphocytes were decreased in asbestosis. These results suggest altered cellular immune processes in the lungs of patients with pneumoconiosis and may indicate different immunoregulatory changes depending on the nature of the inhaled dust.
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The methodology and techniques of bronchoalveolar lavage in obtaining and processing cells and fluids in interstitial lung diseases are reviewed. The effects of the following variables on the results of lavage processing are critically discussed: lavage location, lavage volume, mode of aspiration, filtration through cotton gauze, washing procedures, quantification of differential cell count by cytocentrifuge or millipore filters, and internal or external markers for dilution of non-cellular components.
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To study the value of knowing the proportions of bronchoalveolar T cell subsets when predicting the course of pulmonary sarcoidosis, we subjected 31 patients to clinical, physiologic, and radiographic evaluations, with controls, for at least 12 months. Initially, when all patients were untreated, BAL's were performed, and BAL lymphocyte subsets were marked by the following monoclonal antibodies: OKT3 (expressed by all T cells), OKT4 (to mark helper-inducer T cells), OKT8 (to mark suppressor-cytotoxic T cells), and OKIa (to mark Ia antigen-positive, activated T cells). A normal T4/T8 ratio was highly predictive of a favorable course: the conditions of 13 out of 15 patients with normal ratios remained stable or improved, and only 2 of these 15 patients had to be treated because of persistent symptoms. On the other hand, the conditions of 10 out of 16 patients with elevated T4/T8 ratios deteriorated during the follow-up period. The specificity of T cell subsets for predicting deterioration was improved by considering both the T4/T8 ratio and the number of Ia antigen-positive, activated T cells present. Deterioration occurred in 9 out of 11 patients with elevated T4/T8 ratios and elevated levels of activated T cells. These results suggest that the subtyping of BAL lymphocytes may be useful in determining prognosis in pulmonary sarcoidosis.