Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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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PMID:Lung and blood lymphocyte subsets in asbestosis and in mixed dust pneumoconiosis. 379 62

The results of pulmonary function tests in patients with silicosis, pneumoconiosis in coal miners and arc welders, asbestosis, as well as in persons exposed to asbestos without abnormal x-ray findings of the chest, and in nonexposed healthy control persons and the development after 6 years are compared between each other and with the x-ray findings. There are significant differences between the several groups. There is no correlation (parallelism) between increase of lung function impairment and progression of x-ray findings.
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PMID:Lung function in different types of pneumoconiosis. 392 50

Diagnosis of pneumoconiosis was made in 2 dental technicians presenting with interstitial lung disease. The occupational origin of inhaled dust was confirmed by mineralogic analyses, which disclosed mainly large amounts of chromium-cobalt-molybdenum particles originating from Vitallium prostheses, but also showed abrasives (silica and silicon carbide) and asbestos in 1 patient. The presence of Vitallium and its chemical stability in bronchoalveolar lavage and lung several years after cessation of exposure confirm the resistance of this alloy to corrosion by body fluids. This contrasts with the high solubility of cobalt described in cobalt or hard metal disease. We suggest that dental technician's pneumoconiosis is a complex pneumoconiosis distinct from silicosis, asbestosis, or hard metal disease and that Cr-Co-Mo alloys play a role in its pathogenesis.
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PMID:Dental technician's pneumoconiosis. A report of two cases. 394 27

We applied energy-dispersive x-ray fluorescence to the determination of abnormally present elements or abnormal concentrations of elements in human broncho-alveolar lavage fluids. The low detection limits and the ability to perform multi-elemental analysis permit one to establish or confirm occupational exposure of workers. We also describe different methods used to check our method and our results. We report examples of abnormal compositions of broncho-alveolar lavages containing W, Ce, La, Nd, I, Fe, or Ni. We discuss the limits of the method for characterizing silicosis or asbestosis.
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PMID:Simultaneous determination of trace elements in lavage fluids from human bronchial alveoli by energy-dispersive x-ray fluorescence. 2: Determination of abnormal lavage contents and verification of the results. 395 15

Serum angiotensin conversion enzyme (serum ACE) is a dipeptidylcarboxypeptidase which activates angiotensin I to angiotensin II and inactivates bradykinine. It is a glycoprotein with an MW of 126,000 to 480,000. It is produced by all endothelial cells, and is located on the cell membrane. It is inhibited by EDTA (chelator of Zn-- cofactor), teprotide (snake venom nonapeptide) and captopril. Estimation of ACE has greatly benefitted from the use of synthetic tripeptides. An example is the method of Cushman and Cheung using hippuryl histidyl leucine. A raised serum ACE level in sarcoidosis has been demonstrated by Liebermann in 1975. The diagnostic value is limited by the existence of high levels in other pulmonary diseases (asbestosis, silicosis). Serum ACE levels in sarcoidosis are all higher when the disease is diffuse from a pulmonary and extrapulmonary standpoint. They decrease when the disease regresses spontaneously and rise if it worsens. Radiological improvement in pulmonary sarcoid lesions under the influence of corticosteroid therapy is accompanied by a fall in serum ACE levels. Persistence of this normalization as the dose is decreased is a favourable sign, whilst the reappearance of a high serum level may either reflect simple and isolated biological "rebound" or may accompany a recurrence of signs of the disease. Serum ACE measurement is thus an important factor in the surveillance of cases of treated sarcoidosis when the dose of corticosteroids is to be reduced.
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PMID:[Characteristics, assay and semeiologic value of angiotensin converting enzyme (ACE)]. 618 19

Serum angiotensin converting enzyme (SACE) assays, chest roentgenograms and gallium scans were obtained in 28 patients with active sarcoidosis, two patients with resolved sarcoidosis and 43 nonsarcoid patients. In patients with active sarcoidosis, 23 had elevated SACE activity and 26 had diffuse uptake of gallium in the lung parenchyma. Normal SACE and gallium scans were found in patients with resolved sarcoidosis. None of the nonsarcoid patients had a combination of elevated SACE activity and diffuse pulmonary parenchymal uptake of gallium, although some had elevated SACE activity and abnormal gallium scans. These results suggest that combination of elevated SACE activity and diffuse accumulation of gallium in the lung parenchyma are suggestive of sarcoidosis. However, in view of the reports of abnormal gallium accumulation, and occasional elevation of SACE activity in silicosis, asbestosis and miliary tuberculosis, it is still necessary to require histological evidence of noncaseating granuloma to confirm the diagnosis of sarcoidosis.
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PMID:Significance of serum angiotensin converting enzyme and gallium scan in noninvasive diagnosis of sarcoidosis. 627 2

Silicosis and asbestosis are two forms of fibrotic lung disease resulting from the inhalation of inert materials indigestible by pulmonary alveolar macrophages. Results of studies of the host response to these particulates have not always been consistent. It is clear, however, that after phagocytosis, both cause alveolar macrophage damage, with resultant release of macrophage products, including fibrogenic factors and chemotactic factors for neutrophils. The latter cells also release lysosomal enzymes and free radicals when exposed to silica and asbestos. The net effect of these observations suggests that the combination of tissue damage and fibroblast stimulation results in the pulmonary fibrosis characterizing these diseases. Patients with silicosis and asbestosis have normal or decreased cell-mediated and increased humoral immunity with a high incidence of circulating immune complexes and autoantibodies. Whether these abnormalities are related to the pathogenesis of pulmonary fibrosis or are epiphenomena remains to be determined.
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PMID:Current concepts about the pathogenesis of silicosis and asbestosis. 628 50

Biological data acquired in recent years has thrown new light on the pathogenesis of pulmonary fibrosis. The key element in the genesis of fibrosis may be the alveolar macrophage which, under the influence of different stimuli, secretes numerous factors, attracting polymorphonuclear leukocytes and eosinophils, stimulating fibroblasts and activating lymphocytes. Pulmonary fibrosis induced by inhalation of inorganic particles seems to proceed by identical mechanisms, with certain differences relating to the nature of each mineral. The morphological, cytological and immunological characteristics which defend the lung from silicosis and asbestosis are particularly discussed. The in vitro reactivity of several cell types (alveolar macrophages, mesothelial cells in culture, fibroblasts) equally has revealed differences between quartz and chrysotile. Nevertheless this in vitro response is difficult to interpret compared to an in vivo response: they vary according to the cellular system used and the physico-chemical state of the particular mineral (chrysotile and leached chrysotile by oxalic acid for example). The fibrosing action of other particles (talc, metals) is also reviewed. As opposed to an inflammatory granuloma secondary to the stimulation of alveolar macrophages which represents the usual response to mineral particles, there is also an immunological granuloma of the sarcoid type which may lead to secondary fibrosis: beryllium and talc in certain circumstances may act by this mechanism.
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PMID:[Pulmonary fibrosis and inorganic particles]. 630 30

Cohort studies in three American asbestos factories were undertaken to investigate the effect of fibre type and manufacturing process on lung cancer, mesothelioma, and asbestosis. Reports have been published on a chrysotile textile plant in South Carolina and a mainly textile plant in Pennsylvania, which also used amphiboles. In the third plant in Connecticut friction products and packings were made from chrysotile only. In a cohort of 3641 men employed for one month or more, 1938-58, 3513 (96.5%) were traced, 1267 (36%) had died, and death certificates were obtained for 1228 (96.9%). Individual exposures were estimated (in mcpf . years) from impinger measurements. Life table analyses using Connecticut mortality rates gave an SMR for all causes of 108.5 (USA 107.9). The SMR (all causes) for men who had worked for less than a year was 129.9 and for those who had worked for a year or more, 101.2. The equivalent SMRs for respiratory cancer were 167.4 and 136.7 respectively. Excluding men who had worked for less than a year, there was possible evidence of some increase in risk of lung cancer with increasing exposure, supported also by a "log-rank" (case-control) analysis, of the same order as that observed in chrysotile mining and milling. These findings may be compared with chrysotile textile manufacture where the risk of lung cancer was some 50-fold greater. It is suggested that the differences in risk are perhaps related to the higher proportion of submicroscopic fibres in textile manufacture that may result from the traumatic carding , spinning, and weaving processes. No case of mesothelioma was found, consistent with a much lower risk of this tumour with chrysotile than with amphiboles. Twelve deaths (nine in men with very short and low asbestos exposure) were given ICD code 523 (pneumoconiosis); all but two were ascribed to anthracosilicosis or silicosis and none to asbestosis.
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PMID:Dust exposure and mortality in an American chrysotile asbestos friction products plant. 632 94

The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of conducting airways (asthma) and some of these cause permanent distortion or obliteration of airways as well. Terminal bronchioles appear to be particularly susceptible to particles which cause goblet cell metaplasia, mucous plugging and ultimately peribronchiolar fibrosis. Cancer is the last outcome at the bronchial level and appears to depend upon continuous exposure to or retention of an agent in the airway and failure of the affected cells to be exfoliated which may be due to squamous metaplasia. Alveoli are populated by endothelial cells, Type I or pavement epithelial cells and metabolically active cuboidal Type II cells that produce the lungs specific surfactant, dipalmytol lecithin. Disturbances of surfactant lead to edema in distal lung while laryngeal edema due to anaphylaxis or fumes may produce asphyxia. Physical retention of indigestible particles or retention by immune memory responses may provoke hyaline membranes, stimulate alveolar lipoproteinosis and finally fibrosis. This later exuberant deposition of connective tissue has been best studied in the occupational pneumoconioses especially silicosis and asbestosis. In contrast emphysema a catabolic response, appears frequently to result from leakage or release of lysosomal proteases into the lung during processing of cigarette smoke particles. The insidious and probably most important human lung disease due to particles is bronchiolar obstruction and obliteration, producing progressive impairment of air flow. The responsible particle is the complex combination of poorly digestive lipids and complex carbohydrates with active chemicals which we call cigarette smoke. More research is needed to perfect, correct and quantify our preliminary picture of the pathogenesis of lung disease by particles, but a useful start has been made.
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PMID:Particles causing lung disease. 637 14


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