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)

Four men developed silicosis after sandblasting tombstones for an average of 35 months; 3 of them died an average of 59 months after their first exposure to sandblasting. Lung tissue demonstrated noncaseating granulomas and silicotic nodules involving small arteries and veins in 3 patients and alveolar proteinosis in 2. X-ray energy spectrometry showed primarily elemental silicon in the lung parenchyma. One patient developed lupus erythematosus and another focal glomerulonephritis. Two developed pneumothorax. None had cultural or morphologic evidence of tuberculosis. Pulmonary function studies in all 4 patients revealed a restrictive pattern. Industrial investigations revealed that the patients wore inadequate personal protection equipment and were exposed to 5 times the threshold limit value for respirable silica.
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PMID:Acute silicosis in tombstone sandblasters. 84 57

In a 59-year old sand-blaster, histologically proven silicosis was complicated by systemic lupus erythematosus (SLE) and focal glomerulonephritis with IgG, IgA and ClQ deposits. Nothing likely to facilitate SLE was detected by investigating the familial background, the HLA phenotype and the complement system. This type of SLE differs from drug-induced lupus-like syndromes by a high level of anti-double helix DNA antibodies and by the renal lesions observed. The connection between silicosis and SLE lies in changes in humoral immunity, i.e. polyclonal activation and production of antinuclear antibodies. A decrease in the number of suppressor T-cells may also be held responsible.
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PMID:[Pulmonary silicosis and disseminated lupus erythematosus]. 663 73

A case associating asbestosis and clinical lupus erythematosus (SLE), both diagnosed according to standard criteria, is described. It is suggested that such an association may bear some analogy to the well-known 'Caplan-Collinet' syndrome, associating silicosis and rheumatoid arthritis.
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PMID:Asbestosis and systemic lupus erythematosus. 696 85

We have updated a study of 3,328 gold miners who worked underground for at least 1 year between 1940-1965 in South Dakota, extending the follow-up from 1977 to 1990. The exposures of concern were silica and nonasbestiform amphibole minerals. The lung cancer standardized mortality ratio (SMR) was 1.13 (95% confidence interval [CI] 0.94-1.36, 115 observed) when the U.S. population was used as the referent group, increasing to 1.25 (95% CI 1.03-1.51) when the county was used as the referent, and to 1.27 (1.02-1.55) for person-time with more than 30 years potential latency. However, lung cancer mortality did not show a positive exposure-response trend with estimated cumulative dust exposure. Data on smoking habits suggested that the miners smoked slightly more than the U.S. population in a 1960 cross-sectional survey. In contrast to lung cancer, other diseases known to be associated with silica exposure (tuberculosis and silicosis) were significantly increased (SMR = 3.44 and 2.61) and exhibited clear exposure-response trends. Nonmalignant renal disease, also associated with silica exposure, was elevated for those hired in early years and showed a significant positive exposure-response trend. Multiple-cause analysis revealed significant excesses of arthritis, musculoskeletal diseases (including systemic lupus and sclerosis), and skin conditions (including scleroderma and lupus), diseases of autoimmune origin which have been associated with silica exposure in other studies. Multiple cause analysis also showed a significant excess of diseases of the blood and blood-forming organs.
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PMID:Mortality study of gold miners exposed to silica and nonasbestiform amphibole minerals: an update with 14 more years of follow-up. 775 12

A 60-year-old stonemason, suffering for many years from joint pains and exertional dyspnoea, developed a high fever with weight loss. Physical examination revealed reddening of light-exposed skin areas, fine rales and overly warm and reddened hand and knee joints. Abnormal laboratory findings were increased erythrocyte sedimentation rate of 66 mm/h, C-reactive protein concentration of 1 mg/dl, haemoglobin of 9.4 g/dl and white cell count of 3300/microliters. Urine contained albumin (100 mg/dl) and cylinders. Titres of both antinuclear and anti-ds-DNA antibodies were elevated (1:2560 and > 97 U/ml, respectively). The chest radiography showed enlarged hili, as well as reticular and nodular shadows which histologically showed silicosis. Systemic lupus erythematodes was diagnosed and the patient was treated with prednisone (2 mg/kg daily), the dosage being reduced to 12 mg daily within 3 months. When the joint pains recurred, azathioprine (50 mg daily) was added for 24 months. At present he is receiving prednisone (12 mg daily) and there has been no recurrence for 4 years.
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PMID:[Systemic lupus erythematosus and silicosis]. 785 45

Exposure to silica minerals is associated with silicosis and autoimmune disorders, especially systemic scleroderma. Evidence of this association has been increasingly reported in the last decade. The aim of this paper is to discuss, on the basis of a literature review, the case of a 28-year-old female dental technician who suffered from episodes of weakness, arthralgia, pain, swelling and stiffness of the fingers, dyspnoea with cough, a positive Waaler-Rose reaction, increased rheumatoid factor and normal ESR. She was a non-smoker. A rheumatoid syndrome with lung interstitial disorder, associated with silica exposure from dental ceramic products, was diagnosed. The patient had the HLA-A2-A31, HLA-B51-B18 and HLA-DR3-DR11 haplotypes, some of which are associated with autoimmune disease susceptibility. A 6-month follow-up, with adequate protection and without treatment, showed disappearance of the symptomatology and negative tests for Waaler-Rose reaction and rheumatoid factor. Exposure to silica should, therefore, be sought in the history of any patient with autoimmune or lupus-like syndrome and pulmonary changes. Symptoms associated with silica dust exposure from dental ceramic products should be recognised as being due potentially to an occupational disease, and dental technicians should be protected as workers at risk.
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PMID:Rheumatoid syndrome associated with lung interstitial disorder in a dental technician exposed to ceramic silica dust. A case report and critical literature review. 1195 93

This article collects the evidence that shows that the biological reactions to Silica are due to the stimulation of the Immune System. Both Innate and Adaptive Immunity are involved. The following sets of events take place sequentially: (1) Silica is recognized as a PAMP (pathogen-associated molecular pattern) by the Receptors of Innate Immunity; (2) This causes the stimulation first and then the death of the key cells of Innate Immunity (the macrophages); (3) While stimulated, macrophages produce cytokines (IL-1 and TNF) that stimulate fibroblasts; (4) The same and possibly other cytokines produced by silica- activated macrophages induce the maturation of dendritic cells, which are the connecting elements between the Innate and the Adaptive (lymphoid) Immune Systems; (5) It follows a polyclonal activation of the Adaptive Immunity; (6) The end result is the formation of fibro-hyaline tissue. In view of the double involvement of the Innate and the Adaptive Immune Systems and their cooperation in the stimulation of fibrosis, Silicosis can be considered as a "Collagen" Disease, related to other diseases of that group like Rheumatoid Arthritis, Lupus erythematosus and Scleroderma. Not surprisingly the incidence of these Diseases has been shown to be significantly increased in human exposed to Silica.
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PMID:Silica and the immune system. 1635 May 48

Silicosis patients (SILs) and patients who have been exposed to asbestos develop not only respiratory diseases but also certain immunological disorders. In particular, SIL sometimes complicates autoimmune diseases such as systemic scleroderma, rheumatoid arthritis (known as Caplan syndrome), and systemic lupus erythematoses. In addition, malignant complications such as lung cancer and malignant mesothelioma often occur in patients exposed to asbestos, and may be involved in the reduction of tumor immunity. Although silica-induced disorders of autoimmunity have been explained as adjuvant-type effects of silica, more precise analyses are needed and should reflect the recent progress in immunomolecular findings. A brief summary of our investigations related to the immunological effects of silica/asbestos is presented. Recent advances in immunomolecular studies led to detailed analyses of the immunological effects of asbestos and silica. Both affect immuno-competent cells and these effects may be associated with the pathophysiological development of complications in silicosis and asbestos-exposed patients such as the occurrence of autoimmune disorders and malignant tumors, respectively. In addition, immunological analyses may lead to the development of new clinical tools for the modification of the pathophysiological aspects of diseases such as the regulation of autoimmunity or tumor immunity using cell-mediated therapies, various cytokines, and molecule-targeting therapies. In particular, as the incidence of asbestos-related malignancies is increasing and such malignancies have been a medical and social problem since the summer of 2005 in Japan, efforts should be focused on developing a cure for these diseases to eliminate nationwide anxiety.
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PMID:Immunological effects of silica and asbestos. 1776 16

Causal links have been documented between silica and rheumatoid arthritis, lupus erythematosus, systemic sclerosis and glomerulonephritis. Two different effects of silica have been suggested, an enhanced inflammatory response in the pulmonary region (e.g. activation of alveolar macrophages) and dysregulation of autoimmunity. Based on our previous reports showing in vitro activation of peripheral T cells by silica and reduced regulatory function of the peripheral CD4(+)CD25(+) fraction in which FoxP(3)+ regulatory T cells (Treg) are located, reconstitution of the CD4(+)CD25(+) fraction in silicosis patients (SILs) was investigated. Since T cells in peripheral CD4(+)CD25(+) and CD4(+)CD25(-) (effector T cells; Teff) fractions from SILs showed higher expression of pd-1 (a marker gene for T cell activation) in comparison to that of healthy donors (HDs), chronic T cell activation was considered to have occurred in SILs. In this study, a higher expression of the CD95/Fas molecule in Treg was recorded from silicosis patients (SILs) compared to healthy donors (HDs), and excess loss of FoxP3(+) Treg in freshly isolated peripheral blood mononuclear cells (PBMCs) from SILs relative to HDs was demonstrated when these cells were cultured with silica ex vivo, whereas CD25(+) cells were not reduced due to contamination of activated Teff in the CD4(+)CD25(+) fraction. The activation of both Teff and Treg results in reconstitution of the peripheral CD4(+)CD25(+) fraction, loss of Treg and contamination of activated Teff, resulting in reduction of the number and function of Treg. These results contribute to our understanding of the development of autoimmune diseases found in SILs.
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PMID:Reductive alteration of the regulatory function of the CD4(+)CD25(+) T cell fraction in silicosis patients. 2124 59