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)

Six South African White miners were studied with the 2-g L-tryptophan load test and tracer doses of L-tryptophan-7a-14C, L-kynurenine-keto-14C and hydroxy-L-kynurenine-keto-14C. The breath 14CO2 and 14 urinary metabolities were measured. When they were compared with a previous study of American women with scleroderma, similar 14CO2 and tryptophan metabolite excretion patterns were observed in the data from the miners. The labelled quinolinic acid excretion was more significantly elevated in the South African miners' urine than in the urine of the American women. The data from both studies suggest that some patients with scleroderma have an altered step in the tryptophan metabolic pathway after hydroxy-anthranilic acid. What relationship exists between the induction of pulmonary silicosis and the subsequent development of scleroderma, requires additional human studies.
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PMID:Metabolism of 14C-labelled L-tryptophan, L-kynurenine and hydroxy-L-kynurenine in miners with scleroderma. 84 60

Classically more common in women, scleroderma nevertheless affects with predilection men exposed to the inhalation of silica particles. The association scleroderma-silicosis is essentially a statistical finding. It has no particular clinical, radiological nor histological distinguishing characteristics, other than the syndromic juxtaposition of the stigmata of each of the two disorders. This serious pathological combination is not due merely to chance. It is the result of depressed cellular immunity, related to the cytotoxicity of silica and responsible for auto-immune reactions and the formation of circulating immune-complexes. In the presence of an underlying predisposition, the polyvisceral diffusion of inhaled toxic mineral particles could also facilitate the sclerodermic process by stimulating fibroblastic proliferation.
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PMID:The association: scleroderma-silicosis or Erasmus' syndrome (author's transl). 91 5

Such an association would not appear to be fortuitous since scleroderma is commoner in male miners than in women in general, whilst the predominance of the disease in the latter group is well known. The picture is that of generalised scleroderma without any special characteristics. Silicosis usually precedes the scleroderma. In general, the onset of scleroderma alters the chest X-ray appearance with the development of diffuse, non-cavitated macro-nodular opacities localised in the lower two-thirds of the lungs and in particular at the bases, without absolute symmetry. Several hypotheses may be advanced to explain this association. Irritation by dust in the presence of a particular underlying terrain may cause silicosis and the same terrain may be associated with the development of scleroderma. A second possibility is that of immune phenomena secondary to the pneumoconiosis which favourise the development of scleroderma.
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PMID:[Silicosis associated with scleroderma]. 117 57

Several environmental factors and chemicals have been described as being able to induce systemic scleroderma and scleroderma-like diseases. The present work reports 2 male patients with progressive systemic sclerosis and pulmonary silicosis. Both patients had occupational histories of exposure to silica and one of them of handling trichloroethylene as a degreasing agent. The clinical and analytical findings could not be distinguished from those present in idiopathic systemic scleroderma with the exception of interstitial images with calcified hilar lymph nodes in the chest X-ray suggestive of pulmonary silicosis.
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PMID:Silica and trichloroethylene-induced progressive systemic sclerosis. 845 56

In recent years, with the aging of patients with pneumoconiosis, autoimmune diseases as a complication have been observed. One of the reasons for this may be that autoimmune diseases are prone to develop among the elderly. On the other hand, it has been reported that dust itself, such as silica for example, has adjuvant effect. A review of the recent literature published in Japan and abroad was made to clarify the relationship between pneumoconiosis and autoimmune diseases and the following results were obtained. 1) Disorders which accompany pneumoconiosis: Scleroderma, rheumatoid arthritis, systemic lupus erythematosus (SLE), and disorders of the kidney and liver have been reported. In Japan, about 30 cases of pneumoconiosis accompanied with autoimmune diseases have been reported. In many of the reports, patients with pneumoconiosis and scleroderma have a past history of exposure to silica. In both case studies and case control studies, patients with rheumatoid arthritis and history of silica exposure are prone to develop pneumoconiosis. 2) Immunological studies of patients with pneumoconiosis: As for humoral immunity, elevation of polyclonal gamma-globulin, especially IgG, has been often reported together with high positive rate of autoantibodies such as antinuclear antibodies. In cellular immunity, decreased delayed type skin reaction and decreased CD4/8 ratio have been reported. In human leukocyte antigen (HLA) typing the elevated frequency of DR4 has been reported. In the study of BAL increased production of superoxide anion O2- by alveolar macrophages has been observed. 3) EXPERIMENTAL STUDIES: Silica is well known for its toxicity to cells and also for its adjuvant effect. In the German Democratic Republic, patients with scleroderma and history of long term silica exposure are recognized as patients with occupational disease even though pneumoconiosis is not clearly demonstrated on X-ray film. It is difficult from this review to nrake a definite conclusion regarding the relation between silicosis and autoimmune diseases. There is a need to repeat this review of the literature on autoimmune diseases and pneumoconiosis in the near future.
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PMID:[Relationship between autoimmune diseases and pneumoconiosis]. 140 2

Scleroderma-like diseases can be induced by a number of chemical compounds, such as plastics, solvents and drugs. Contaminated rapeseed oil was the cause of the toxic oil syndrome and L-tryptophan induces the so-called eosinophilia-myalgia-syndrome. On the other hand, paraffin and silicon can trigger so-called adjuvant disease, while long-term exposure to silica can lead to idiopathic scleroderma (associated with silicosis in some cases). In addition to the clinical features, some pathogenetic data in the literature, such as genetic factors (HLA, chromosomal anomalies, enzyme deficiencies) and the metabolism of chlorinated ethylenes via reactive epoxide intermediate products, and our own findings are reported. Silica-induced scleroderma cannot be distinguished from the idiopathic form by epidemiological, clinical or immunological studies or by parameters referring to the blood vessels or collagen metabolism. In cell culture studies it has been shown that macrophages/monocytes release IL1, IL6 and TNF after ingestion of silica, which affects fibroblasts, T-helper cells and endothelial cells. Comparative results from the silicosis literature are reported. Finally, the possibly stimulating role of ionizing irradiation (uranium mining) in favouring the development of scleroderma is discussed.
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PMID:[Chemically-induced scleroderma]. 150 11

A group of 191 patients with systemic scleroderma and 12 patients with silicosis-associated scleroderma were investigated for connective tissue turnover. The serum levels of type III collagen aminopropeptide (P-III-P), the laminin PI (Lam PI) fragment and the acid lysosomal beta-galactosidase (beta-Gal) were determined by specific radioimmunoassays and spectrofluorometry, respectively. Increased levels of type III collagen aminopropeptide strongly correlated with enhanced activity of beta-galactosidase. Both parameters correlated with the clinical course in idiopathic systemic scleroderma and in silicosis-associated scleroderma. Serum levels of Lam PI were also found to be elevated in both groups, although there was no correlation with the severity of the disease. Autoantibodies directed against the DNA topoisomerase Scl-70 and against centromeric proteins were found in a similar range in patients with idiopathic systemic and silicosis-associated scleroderma. These results suggest that P-III-P, Lam PI and beta-Gal are useful serological markers of fibrotic activity and demonstrate similarities between idiopathic systemic scleroderma and scleroderma associated with silica-dust exposure.
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PMID:Type III collagen aminopropeptide and laminin P1 levels in serum of patients with silicosis-associated and idiopathic systemic scleroderma. 211 68

In a survey done in East Germany between 1981 and 1988, we found that 93 of 120 male scleroderma patients had long-term exposure to silica dust. We describe our findings in 12 patients with scleroderma and silicosis. The exposure time to silica dust was between 3 and 34 years; the interval between the beginning of exposure and the onset of scleroderma averaged 27.3 years (range 9 to 40 years). Antinuclear antibodies in titers between 80 and 10,240 with nucleolar and/or speckled patterns were found in 10 patients, antibodies against double-stranded DNA in three, Scl-70 (topoisomerase I) in three, and anticentromere antibodies in five. The following markers of collagen metabolism were increased in serum: beta-galactosidase in 12 patients, laminin peptide-P1 in 10 patients, N-terminal procollagen type III peptide in 10, and urinary sialic acid excretion in 7. We propose that crystalline particles of silica less than 5 microns may be phagocytosed by macrophages and release lymphokines and monokines, which activate fibroblasts and enhance their collagen and glycosaminoglycan synthesis. In addition, silica may act as an adjuvant to increase immune reactivity.
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PMID:Silica-induced scleroderma. 215 53

For the stimulation of research on scleroderma and the prophylaxis of occupational scleroderma-like diseases and the prevention of iatrogenic injuries, respect., it is important to know the inducing environmental substances. Plastics (vinyl chloride, epoxy resins), solvents (chlorinated, aromatic and aliphatic hydrocarbons), drugs (bleomycin, pentazocine), cocaine (abuse) and contaminated rapeseed oil are more or less able to induce scleroderma-like diseases. Vinyl chloride disease is the best known among these. The toxic oil syndrome represents the most inglorious example of the recent time. Paraffin and silicon can act as adjuvants and induce a progressive systemic sclerosis. In our studies it could be shown, that silica is able to induce not only a silicosis, but also a true progressive systemic sclerosis after long term exposure. Acknowledgment of such cases as an occupational disease is justified and regulated by law in the German Democratic Republic.
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PMID:[Scleroderma and scleroderma-like diseases caused by environmental pollutants]. 242 99

Silicosis, a disease of historical importance, continues to occur cryptically today. Its pathogenesis is under ongoing study as new concepts of pathobiology evolve. In this article, the gross and microscopic features of the disease in the lungs and the lesions in lymph nodes and other viscera are described. These tissue changes are then discussed in the context of clinical disease and other possible or established complications of silica exposure (ie, scleroderma and rheumatoid arthritis, glomerulonephritis, and bronchogenic carcinoma). Silicates are members of a large family of common minerals, some of which have commercial importance. Silicates are less fibrogenic than silica when inhaled into the lungs, but cause characteristic lesions after heavy prolonged exposure. The features of these disease conditions are described herein. Various aspects of the mineralogy and tissue diagnosis of silicosis and lung disease due to silicates are reviewed. An overview of contemporary regulatory considerations is provided.
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PMID:Diseases associated with exposure to silica and nonfibrous silicate minerals. Silicosis and Silicate Disease Committee. 283 5


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