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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43-year-old stone cutter with 13 years of exposure to silica developed a pulmonary silicosis and a glomerulonephritis with moderate renal failure. Renal biopsy demonstrated in light microscopy a segmental and focal mesangial proliferation and in electron microscopy distinct alterations of the proximal tubular cells. Renal histology suggest silica may play a part in the pathogenesis of renal damage. Clinicians should therefore include silica exposure in the differential diagnosis of unexplained glomerulonephritis.
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PMID:[Pulmonary silicosis and glomerular nephropathy. Apropos of 1 case]. 185 70

A 55-year-old white male, with silicosis diagnosed 10 years earlier, presented massive proteinuria with microscopic hematuria, moderate renal failure and distal polyneuropathy. Bilateral renal angiography showed multiple intraparenchymal saccular aneurysms. Renal biopsy disclosed a focal segmental necrotizing glomerulonephritis and arteriolitis. After combined corticosteroid and immunosuppressive treatment, renal function improved and remained stable 6 months later.
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PMID:Polyarteritis nodosa and necrotizing glomerulonephritis associated with long-standing silicosis. 256 70

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

A 54-year-old foundry worker with extensive silica exposure, but no pulmonary disease, developed the nephrotic syndrome and renal failure over a 3-month period. Renal biopsy demonstrated a proliferative glomerulonephritis; energy dispersive x-ray analysis detected silicon within the renal tubules. Measurements of respirable silica at the foundry revealed levels up to 2.5 times the current occupational standard. Similar glomerular disease has been reported in silica-exposed animals and workers with silicosis. This case suggests that clinicians should include silica exposure in the differential diagnosis of unexplained diffuse proliferative glomerulonephritis, renal disease may occur without clinically evident pulmonary disease in silica exposure, and silica-induced glomerulonephritis warrants further clinical and epidemiologic research.
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PMID:Silica and glomerulonephritis: case report and review of the literature. 303 97

We present case histories of 5 patients with silicosis who developed systemic lupus erythematosus and microscopic polyarteritis in two cases each, and rapidly progressive glomerulonephritis (limited Wegener's granulomatosis) in one case. An association between silica exposure and autoimmune disease is emphasized.
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PMID:[Silicosis and systemic diseases]. 834 94

A combination of risk factors are involved in susceptibility to a primary or secondary form of vasculitis. Most forms of vasculitis are probably genetically based but environmentally triggered. This review discusses currently available evidence for a pathophysiologic role of one possible environmental trigger, silica. Since 1960, several patients with pulmonary silicosis have been described that developed pauci-immune necrotizing crescentic glomerulonephritis, i.e., with either completely negative immunofluorescence findings or nonspecific granular IgM or C3 deposits along the capillary wall. Recently it was reported that these patients have antineutrophil cytoplasmic antibodies (ANCAs) that are in most cases directed to myeloperoxidase. Further, patients with pulmonary silicosis may develop microscopic polyangiitis, the syndrome of lung hemorrhage and nephritis, or Wegener's granulomatosis. To further substantiate the relation between silicon exposure and renal failure or vasculitis, several case-control studies have been reported. Exposure to silicon-containing compounds was found to be related to chronic renal failure (odds ratio, 1.7:2.5) or vasculitis (odds ratio, 6.5:14.0). The mechanisms by which silica may induce ANCA-associated glomerulonephritis or vasculitis are not well known. Silicon-containing compounds have a pronounced adjuvant effect on immune responses, and silica particles are potent stimulators of lymphocytes and monocytes or macrophages. Further, silica may induce apoptosis of monocytes or macrophages and possibly neutrophils. In conclusion, at present there is ample evidence that occupational exposure to silicon-containing compounds is related to the development of ANCA-associated glomerulonephritis and vasculitis, and silica is one of the first well-documented environmental triggers in these diseases.
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PMID:Silicon exposure and vasculitis. 944 85

A 63-year-old man was referred to our hospital for rapid deterioration of his renal function. He had worked as a metal founder for more than 40 years, and had been diagnosed as having silicosis. Laboratory data on admission showed severe anemia, thrombocytopenia, and end-stage renal failure (BUN 88.8 mg/dl, serum creatinine 9.0 mg/dl). Myeloperoxidase anti-neutrophil cytoplasmic antibody(MPO-ANCA) was also detected in his sera. On the next day after admission, he complained of sudden dyspnea and hemoptysis. Mechanical ventilation with pure oxygen was insufficient to improve hypoxia without concomitant use of percutaneous cardio-pulmonary support(PCPS) and continuous hemofiltration(CHF). We diagnosed his condition as MPO-ANCA-associated rapidly progressive glomerulonephritis with diffuse alveolar hemorrhage. Treatment with plasmapheresis, pulse methylprednisolone and pulse cyclophosphamide effectively improved his hemoptysis as well as chest X-ray findings and blood gas analysis. However on his later clinical course, he was complicated with superimposed complex infection and passed away. Autopsy findings showed crescentic glomerulonephritis in the kidneys and silica nodules in the lungs. Recently it has been postulated that some relationship exists between ANCA-associated(especially MPO-ANCA-associated) glomerulonephritis and silica exposure. The reported cases of glomerulonephritis in the patients with silica exposure showed a rapidly progressive clinical course and pauci-immune necrotizing crescentic glomerulonephritis in their histology. Gregorini et al. reported that 12 of 37 (32%) male patients with RPGN had either silicosis or significant silica exposure, and 7 of 8 patients examined were ANCA-positive(6 of 7 were MPO-ANCA-positive). Therefore silica seems to cause glomerulonephritis by disrupting the immune response. Including this case mentioned above, we have experienced 10 cases of MPO-ANCA-associated glomerulonephritis, at least 3 cases out of which had suffered from silicosis in the past(30%). These results indicate that silicosis should be considered a relevant pathogen of MPO-ANCA-associated glomerulonephritis beyond the race.
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PMID:[A case of silicosis with MPO-ANCA-associated glomerulonephritis and alveolar hemorrhage]. 1143 4

Silicosis and other occupational diseases are still important even in the most developed countries. In fact, at present, silica exposure may be a risk factor for human health not only for workers but also for consumers. Furthermore, this exposure is associated with many other different disorders besides pulmonary silicosis, such as progressive systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis, glomerulonephritis and vasculitis. The relationships between these silica-related diseases need to be clarified, but pathogenic responses to silica are likely to be mediated by interaction of silica particles with the immune system, mainly by activation of macrophages. As regards renal pathology, there is no single specific clinical or laboratory finding of silica-induced nephropathy: renal involvement may occur as a toxic effect or in a context of autoimmune disease, and silica damage may act as an additive factor on an existing, well-established renal disease. An occupational history must be obtained for all renal patients, checking particularly for exposure to silica, heavy metals, and solvents.
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PMID:Silica and renal diseases: no longer a problem in the 21st century? 1150 45

We encountered two patients with microscopic polyangiitis (MPA) associated with unusual pulmonary manifestations. The first patient was a 45-year-old man who had worked in amine for 3 years when he was young. On admission, chest X-rays showed long-standing silicosis and a new patchy infiltration. The second patient was a 52-year-old female. On admission, chest X-rays showed bilateral patchy infiltrations. Since then, variable patterns of patchy infiltration have waxed and waned repeatedly. The renal biopsy revealed that both patients had glomerulonephritis associated with small vessel vasculitis but with few or no immune deposits. There was neither granulomatous inflammation nor eosinophilic infiltration. Myeloperoxidase-antineutrophil cytoplasmic antibody (ANCA) was positive in both patients. After treatment with glucocorticoids and cyclophosphamide, radiological findings were minimal and stable. These two cases show that patients with MPA have a wide spectrum of radiological findings.
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PMID:Two patients with microscopic polyangiitis and unusual pulmonary manifestation. 1191 61

Work in Department of Energy (DOE) facilities has exposed workers to multiple toxic agents leading to acute and chronic diseases. Many exposures were common to numerous work sites. Exposure to crystalline silica was primarily restricted to a few facilities. I present the case of a 63-year-old male who worked in DOE facilities for 30 years as a weapons testing technician. In addition to silica, other workplace exposures included beryllium, various solvents and heavy metals, depleted uranium, and ionizing radiation. In 1989 a painful macular skin lesion was biopsied and diagnosed as leukocytoclastic vasculitis. By 1992 he developed gross hematuria and dyspnea. Blood laboratory results revealed a serum creatinine concentration of 2.1 mg/dL, ethrythrocyte sedimentation rate of 61 mm/hr, negative cANCA (antineutrophil cytoplasmic antibody cytoplasmic pattern), positive pANCA (ANCA perinuclear pattern), and antiglomerular basement membrane negative. Renal biopsy showed proliferative (crescentric) and necrotizing glomerulonephritis. The patient's diagnoses included microscopic polyangiitis, systemic necrotizing vasculitis, leukocytoclastic vasculitis, and glomerulonephritis. Environmental triggers are thought to play a role in the development of an idiopathic expression of systemic autoimmune disease. Crystalline silica exposure has been linked to rheumatoid arthritis, scleroderma, systemic lupus erythematosus, rapidly progressive glomerulonephritis and some of the small vessel vasculitides. DOE workers are currently able to apply for compensation under the federal Energy Employees Occupational Illness Compensation Program (EEOICP). However, the only diseases covered by EEOICP are cancers related to radiation exposure, chronic beryllium disease, and chronic silicosis.
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PMID:Silica exposure and systemic vasculitis. 1464 69


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