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

Exposure to silica can induce fibrosis and/or emphysema. Various factors such as proteases, other hydrolases and oxidants may be involved in the destruction of lung parenchyma. On the other hand, antiproteases play an important role in the protection of lung parenchyma against the action of proteases. We have developed an animal model of silicosis in monkey Macacus cynomolgus and followed these factors by bronchoalveolar lavage (BAL). We have studied glycosidases activities, elastase-like activity, immunoreactive alpha 1-protease inhibitor (alpha 1PI), neutrophil elastase inhibitory capacity (NEIC) and myeloperoxidase. Bronchoalveolar cells in serial BAL were also studied. Six monkeys were exposed to quartz aerosols (100 mg.m-3) for 18 wks. They were followed until they developed X-ray changes, which occurred between 21-64 wks after the end of the dust exposure. Cellular "silicotic nodules" were observed in lung biopsies. A control animal underwent serial BAL. Changes were seen in the differential cell count. The release of superoxide anion by bronchoalveolar cells obtained during the experiment was increased. Separation on a gradient of Percoll showed the presence of young macrophages, which exhibited enhanced release of superoxide anion as compared to the totality of bronchoalveolar cells. The biochemical analysis of BAL fluids obtained during and after the period of dust exposure showed an increase in glycosidases, alpha 1PI and NEIC. Some free elastase-like activity was simultaneously detected in BAL fluids from exposed animals but not from the control. This elastase-like activity was very low compared to NEIC. The increase in enzymatic and antiprotease activities occurred at different points in time for each animal, suggesting large differences in individual responses to dust, but occurred before the chest X-ray abnormalities.
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PMID:An attempt to evaluate lung aggression in monkey silicosis: hydrolases, peroxidase and antiproteases activities in serial bronchoalveolar lavages. 164 17

1. Serial bronchoalveolar lavages were performed on a subhuman primate (Macacus cynomolgus) in order to give an experimental model for silicosis. 2. We have measured glycosidases, proteases, peroxidase and antiproteases of the BAL fluids from seven normal monkeys. 3. The results obtained were similar to those found in human control BAL fluids. 4. For monkeys, the repetition of the bronchoalveolar procedure does not seem to have an important influence on the values obtained. 5. The present results will now permit sequential follow up studies during the course of experimental silicosis.
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PMID:Comparison of hydrolases, peroxidase and protease inhibitors in bronchoalveolar fluid from Macacus cynomolgus and human controls. 332 59

The effect of infective, immunological, and irritative factors on the onset and development of silicosis after intratracheal inoculation with 50 mg of tridymite was investigated on 220 specific pathogen free (SPF) female Sprague-Dawley rats. Even after 12 months the rats, always kept in SPF conditions after intratracheal injection of the dust, showed mainly granulomas with little tendency to confluence or to fibrohyalinosis. Chronic infective stimulation was obtained by keeping groups of SPF animals injected with tridymite for three, six, or 12 months in a conventional animal house, where they were exposed to the endemic bacterial flora. In these animal silicosis developed much more rapidly and produced much more severe confluent lesions than in rats always kept in SPF conditions. Horseradish peroxidase and ferritin given by intratracheal injection and by inhalation were histochemically shown mainly in the dust granulomas but did not accelerate the development of silicosis. Exposure to ozone increased the prevalence of lung infections and thus enhanced the silicosis in conventionally kept animals, without modifying the evolution of silicosis in SPF animals. These experiments showed that the presence of bacterial flora, and particularly bronchopulmonary infections, accelerated the development of silicosis and led to the suggestion that individuals subject to frequent bronchopulmonary infections are unfit for occupations necessitating exposure to silica dust.
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PMID:Role of infective, immunological, and chronic irritative factors in the development of silicosis. 709 51

We studied the effects of a nutrient supplemented diet on the function of alveolar macrophages of silicosis rats and on the blastogenic response of lymphocytes, glutathione peroxidase (GSH-PX) activity, and lipid peroxidase (LPO) activity in the blood of silicosis patients. The results showed that a nutrient supplemented diet increased the phagocytosis rate (p < 0.01) and index (p < 0.05) of alveolar macrophages of silicosis rats. A nutrient supplemented diet also enhanced significantly the GSH-PX activity (p < 0.001) and the blastogenic response of lymphocytes (p < 0.01), and decreased substantially the LPO content (p < 0.05) in the blood of silicosis patients. We conclude that a nutrient supplemented diet may play an important role in antilipid peroxidation, decreased free radical reaction, stabilizing cell membrane, delaying lung fibrosis, and enhancing immune functions of the body.
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PMID:Effects of dietary supplementation on the function of alveolar macrophages of silicosis rats, on the blastogenic response of lymphocytes and on the peroxidase activity in blood of silicosis patients. 772 89

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

We reported two cases of silicosis exhibiting MPO-ANCA associated disorder. Case 1 was a 69 year-old man with silicosis and chronic interstitial pneumonia. He was admitted because of fever, dry cough, left chest pain, dyspnea and body weight loss. He was diagnosed as acute exacerbation of interstitial pneumonia, pericarditis and gastrointestinal bleeding. Case 2 was a 67 year-old man with silicosis. He repeated attack of fever, hoarseness, dysphagia and headache. The cell counts of cerebrospinal fluid increased and the thickness of cerebellar tent and left dura mater was observed in the brain MRI. Therefore, he was diagnosed as pachymeningitis and neuropathy of cranial nerves. Both cases were complicated by silicosis and the laboratory findings showed high serum levels of P-ANCA, ANA and rheumatoid factor and inflammatory responses, indicating they were suspected vasculitis. The two cases were treated by steroid and immunosuppressive therapy and had good clinical response. Silicosis may affect multiple organ involvement associated with P-ANCA.
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PMID:[Two cases of silicosis exhibiting MPO-ANCA associated disorder]. 1069 8

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

ANCA are associated with small sized vessel vasculitis; one subtype is an antibody against myeloperoxidase(MPO), which stains in a perinuclear pattern(P-ANCA) indirect immunofluorescence(IIF) using a neutrophil substrate, and the other subtype is an antibody against proteinase-3(PR-3), which stains in a diffuse granular cytoplasmic pattern ANCA by IIF. PR-3 ANCA is more specific in Wegener's granulomatosis(WG) than the other primary vasculitides. MPO-ANCA can be found in microscopic polyangiitis (MPA), Churg Strauss Syndromes(CSS), drug-induced vasculitis, and environmental factor-induced such as silicosis vasculitis more frequently than WG. The value of the IIF test for ANCA detection can be greatly increased by the addition of a standardized antigen-specific ELISA. The intra-assay and inter-assay CV of the MPO and PR-3 ELISA were 6.6 to 4.8%, respectively. Close ANCA titer correlation was shown between MPO-ANCA ELISA and the activity of ANCA associated vasculitis. Renal manifestations and pulmonary manifestations are observed in 70-90% of AAV as the initial manifestation. The changes in titers of ANCA seem to reflect disease activity in 60-70% of AAV patients. A combination of steroids and immunosuppressive drugs is effective in relieving the clinical symptoms of AAV.
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PMID:[Antineutrophil cytoplasmic antibody(ANCA)]. 1292 48

Two cases of hypertrophic pachymeningitis (HP) associated with pulmonary silicosis in tunnel workers are described. In both cases the myeloperoxidase antineutrophil cytoplasmic autoantibody (MPO-ANCA) was positive. Two patients with pulmonary silicosis developed headache and neurological disturbance, and a diagnosis of HP was made. In both cases the serum CRP level and the MPO-ANCA titer were elevated. Corticosteroid therapy produced a rapid improvement in all the clinical and laboratory parameters. Although an association has been noted between exposure to silica dust and ANCA-associated vasculitis, particularly glomerulonephritis, central nervous system involvement is rare. However, there have been some recent reports of HP cases that were positive for ANCA, and the association between HP and vasculitis has been discussed in the medical literature. HP may be one feature of multiorgan involvement in ANCA-associated disease, and the association between silica dust exposure and HP should be considered, as with other forms of ANCA-associated vasculitis.
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PMID:Two cases of hypertrophic pachymeningitis associated with myeloperoxidase antineutrophil cytoplasmic autoantibody (MPO-ANCA)-positive pulmonary silicosis in tunnel workers. 1474 92

A 68-year-old man, who had worked for processing quartz-containing stones for more than 50 years, complained of low-grade fever and arthralgia. Mediastinal lymph nodes were markedly swollen on chest computed tomography. Pathological findings of the lymph node were compatible with silicosis, with a high titer of myeloperoxidase anti-neutrophil cytoplasmic antibody (MPO-ANCA). During follow-up with prednisolone treatment, pleuritis and uveitis developed as manifestations of vasculitis. Thus, he was diagnosed with MPO-ANCA-associated vasculitis with occupational silica exposure, possibly microscopic polyangiitis (MPA). This case is rare, because pleuritis was the only pulmonary manifestation, without interstitial pneumonia, alveolar hemorrhage or glomerulonephritis.
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PMID:Microscopic polyangiitis accompanied by pleuritis as the only pulmonary manifestation of occupational silica exposure. 2046 78


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