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Biomedical subjects

U Costabel

Publications and source records attributed to U Costabel.

At least 217 records · Page 12Linked to original sources
PubMed1981

Different therapies and factors influencing response to therapy in idiopathic diffuse fibrosing alveolitis.

The success of 3 different treatment regimens was compared in 15 patients with diffuse fibrosing alveolitis. Improvement or deterioration of lung function (vital capacity (VC) and PaO2 changes during exercise) were used as a control of therapy. The combination of prednisolone and azathioprine proved to be most effective: in 4 of 6 patients both VC and PaO2 improved. Combinations with D-penicillamine resulted in a high number of unwanted side effects: in 5 of 13 treated patients it had to be withdrawn. 6 patients were treated with prednisolone alone; only 1 of them improved. Patients with a short duration of symptoms prior to therapy and initially mild impairment of lung function showed a higher degree of improvement during therapy. The consequence for the management of lung fibrosis is to establish diagnosis and treatment as early as possible.

Adult↗
PubMed1978

The pulmonary air-blood barrier of human shock lungs (a clinical, ultrastructural and morphometric study).

Interstitial edema in the alveolar septa is the first morphologically recognisable change to be observed in cases of shock. It is brought about by the altered function of the membranes of the damaged epithelium and endothelium in the alveolar wall. At the same time there is an impairment of gaseous exchange, which is rendered more difficult by the exudative process in the interstitium. Pari passu with these events there is injury to the cells of both the alveolar epithelium and the alveolar capillary endothelium. Both these processes are still reversible. The point of irreversibility appears to be reached--so far as time is concerned--at the end of the first week, after which the injurious effects on the cell are established, since the thin alveolar wall necessary for the exchange of gases becomes overgrown with bulky alveocytes (Tpye II), and the fibroblasts in thealveolar interstitium push the capillaries away from the surface of the alveolus. In most of the advanced cases of shock this process of thickening of the alveolar wall exceeds the critical value, and respiratory exchange is so impaired that satisfactory functioning of the lungs is no longer possible.

Adult↗
PubMed1975

Cell number in human heart in atrophy, hypertrophy, and under the influence of cytostatics.

The DNA content was determined in 30 human hearts from different age groups and of different weight classes. Among these cases were included 4 hearts of children and 5 hearts of adults who had been treated with cytostatics. The total DNA content was determined biochemically and the nuclear DNA content was measured by means of Feulgen cytophotometry. By combining both methods, the total number of heart muscle cells was determined. We obtained the following results: (1) The DNA concentration remained the same in all the hearts, while the total amount of DNA rose up to three-fold with increasing heart weights. (2) Cytophotometric DNA measurements revealed that, in hearts of infants up to the age of 7, a diploid DNA content is found in 80% of the muscle nuclei. In children of higher ages and in adults, 60% of the muscle nuclei are tetraploid. In hypertrophied hearts, there occurs an increased polyploidization of the muscle nuclei, with up to 8% of 32-ploid nuclei. Thus, polyploidisation is caused by chronic hyperfunction of the heart. In atrophic hearts, on the other hand, no regression of polyploidisation was observed. (3) The number of connective tissue cells in a given heart increases from 1 x 10(9) just after birth to 5 x 10(9) in adults, reaching its maximum of 10 x 10(9) in extremely hypertrophied hearts. The number of heart muscle cells is 2 x 10(9) in normal hearts of children and adults, and may rise to 4 x 10(9) in excessively hypertrophied hearts. (4) During treatment with cytostatics, the DNA content of the myocardium is reduced only in hearts of children; in adult hearts, no decrease of DNA is observed. Cytostatics prevent polyploidisation of the heart muscle nuclei and exhibit no other influence upon the DNA content of the heart muscle cell nuclei. (5) Cytostatics cause a decrease in the number of connective tissue and heart muscle cells of up to 57% of the original value in hearts of children. The cell number of adult hearts remains the same under cytostatic treatment.

Adult↗
PubMedDate not supplied

Phenotypic analysis of bronchoalveolar lavage lymphocytes from acquired immunodeficiency patients with and without Pneumocystis carinii pneumonia.

A study was performed to reveal possible differences in lymphocyte subpopulations from bronchoalveolar lavage (BAL) of acquired immunodeficiency patients with and without Pneumocystis carinii pneumonia. Forty-one consecutive human immunodeficiency virus-seropositive patients were studied. Pneumocystis carinii infection was detected in the BAL fluid from 18 patients. The BAL lymphocyte subpopulations were determined by surface marker analysis with the immunoperoxidase slide assay. No significant differences in the percentage of CD4+ and CD8+ lymphocytes were found between the two groups. The percentage of CD57+ natural killer (NK) cells was significantly higher in the Pneumocystis carinii-negative group than in the -positive group. Since NK cells protect from microbial infections, it is conceivable that the loss of CD57+ NK cells may be one of the phenomena leading to the immunodeficiency state that underlies the pulmonary complications characteristic of the acquired immunodeficiency syndrome.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Increased surfactant protein A content in human alveolar macrophages in hypersensitivity pneumonitis.

Surfactant protein A (SP-A) appears to have an important function in the assembly and maintenance of the alveolar surfactant monolayer. SP-A has also been implicated in modulating the activity of immunoactive cells, such as increasing the bactericidal capacity of alveolar macrophages. In this immunocytochemical study the SP-A content of alveolar macrophages from seven patients with hypersensitivity pneumonitis was compared with the results obtained from six healthy controls. A polyclonal rabbit antibody against human SP-A was used for detection of SP-A in the cytoplasm of alveolar macrophages, applying the immunoperoxidase adhesive slide assay. In hypersensitivity pneumonitis a significant increase in the percentage of SP-A+ alveolar macrophages was observed as compared with the percentage in healthy controls. The intensity of the staining reaction was also increased in the alveolar macrophages of hypersensitivity pneumonitis. We conclude that the observed abnormalities in SP-A content in alveolar macrophages may play a role in the pathogenesis of hypersensitivity pneumonitis.

Adult↗
PubMedDate not supplied

Immunocytochemical analysis of ascitic fluid due to cirrhosis. A contribution to understanding the origin of markedly atypical cells.

In some cases of ascitic fluid due to cirrhosis, benign mesothelial clusters may be observed, accompanied by markedly atypical cells that have been proposed to be abnormal macrophages, mesothelial cells or necrotic cells of hepatic origin. The aim of this study was to determine the origin of these cells with the use of a panel of monoclonal antibodies (MAbs) against cell surface antigens. Furthermore, the lymphocyte subpopulations were analyzed for a possible correlation with the presence of abnormal cells. Markedly atypical cells were found in 4 of 12 cases. They showed no phagocytosis of latex particles and were negative for MAbs My4 (CD14), HLE-1 (CD45), Leu M1 (CD15), CEA 3-13 and HEA-125. They reacted positively with BMA-120 and HLA-1. This staining pattern demonstrated the mesothelial origin of the markedly atypical cells. The profile of the lymphocyte subpopulations in the cases with markedly atypical cells was not different from the other cases. We propose that these cells are abortive cluster formations of mesothelial cells.

Adult↗
PubMedDate not supplied

[Drug-induced lung changes in rheumatology].

In rheumatologic disorders cytostatics and immunosuppressive agents are frequently applied and may lead to damage of the lung parenchyma. In the pathogenesis, toxic and immunologic mechanisms are discussed. In the differential diagnosis, pulmonary manifestations of the underlying disorder and infections are important. The diagnosis is confirmed by historical, clinical, histological, and cytologic findings (bronchoalveolar lavage). This review focuses on aspirin, gold, D-penicillamine, methotrexate, cyclophosphamide, and azathioprine treatments. Pulmonary side effects are rare, but early diagnosis is important, because withdrawal of the drug may lead to full recovery of the patient. The prognosis is poor in D-penicillamine or cyclophosphamide induced pneumonitis with a lethal course in 40-50%. The interval between start of treatment and manifestation of lung damage can range from a few weeks to several years. Beside pulmonary symptoms such as cough and dyspnea, fever may occur. Pulmonary function tests show restriction and impairment of diffusion. Gold and methotrexate can induce blood eosinophilia. In bronchoalveolar lavage, the most frequent finding is an increase in lymphocytes with a decrease of the CD4/CD8 ratio. Some drugs, however, can also lead to an increase of the neutrophils and/or the eosinophils in the lavage fluid. Bronchoalveolar lavage can contribute to the exclusion of infections or pulmonary manifestations of the underlying disorder.

Anti-Inflammatory Agents↗
PubMedDate not supplied

Malignant pleural effusions due to small cell carcinoma of the lung. An immunocytochemical cell-surface analysis of lymphocytes and tumor cells.

Thirteen malignant pleural effusions due to small cell carcinoma (SCC) of the lung were immunocytochemically studied using the peroxidase-antiperoxidase adhesive slide assay for the determination of cell surface antigens. A panel of monoclonal antibodies (MAbs) was used to determine the lymphocyte subpopulations and the reactivity of the tumor cells. Of the lymphocytes, 87 +/- 1% were CD3+ T cells, with 72 +/- 10% CD4+ helper/inducer T cells and 20 +/- 5% CD8+ suppressor/cytotoxic T cells. Only a minority of T lymphocytes were activated in terms of expressing the surface markers CD38 and HLA-DR. The distribution of the lymphocyte subpopulations was not significantly different from the distribution in other malignant and nonmalignant pleural diseases previously studied, indicating that the reaction pattern of the lymphocytes in the pleural cavity is similar in different diseases. The tumor cells from all cases were positive for LeuM1, CD16 and HLA-DR; 10 of 11 cases were positive for HEA-125, Sam 2 and Sam 10. Positivity for epithelial membrane antigen was observed in 11 cases, for OKT9 in 8 cases and for carcinoembryonic antigen in 6 cases. A total or partial loss of the reactivity with HLA-1 was found in nine cases. The reactivity pattern of the tumor cells with the MAbs used in this study is not specific for SCC of the lung because other carcinoma cells also reacted with these markers. Additional morphologic criteria, such as cell size and cell configuration, are needed to recognize the immunocytochemically positive-reacting cells as tumor cells from SCC of the lung. However, the immunostaining allows a better identification of the tumor cells, especially in cases with a small quantity of tumor cells.

Antibodies, Monoclonal↗