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)

Silicosis is a serious occupational lung disease associated with irreversible pulmonary fibrosis. The interaction between inhaled crystalline silica and the alveolar macrophage (AM) is thought to be a key event in the development of silicosis and fibrosis. Silica can cause direct injury to AMs and can induce AMs to release various inflammatory mediators. Acute silicosis is also characterized by a marked elevation in surfactant apoprotein A (SP-A); however, the role of SP-A in silicosis is unknown. We investigated whether SP-A directly affects the response of AMs to silica. In this study, the degree of silica toxicity to cultured rat AMs as assessed by a (51)Cr cytotoxicity assay was shown to be dependent on the time of exposure and the concentration and size of the silica particles. Silica directly injured rat AMs as evidenced by a cytotoxic index of 32.9 +/- 2.5, whereas the addition of rat SP-A (5 microg/ml) significantly reduced the cytotoxic index to 16.6 +/- 1.2 (P < 0. 001). This effect was reversed when SP-A was incubated with either polyclonal rabbit anti-rat SP-A antibody or D-mannose. These data indicate that SP-A mitigates the effect of silica on AM viability, and this effect may involve the carbohydrate recognition domain of SP-A. The elevation of SP-A in acute silicosis may serve as a normal host response to prevent lung cell injury after exposure to silica.
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PMID:Surfactant protein A prevents silica-mediated toxicity to rat alveolar macrophages. 1074 48

A 21-year-old male having a history of 4 years of working at a denim factory as a sandblaster was diagnosed with pulmonary silicosis and he was also an active smoker. Productive cough, dyspnea on effort, night sweats, and weight loss in a short period of time were his complaints. Chronic occupational exposure to tiny particles of silicon dioxide can stimulate parenchymal inflammation, collagen synthesis and, ultimately pulmonary fibrosis called silicosis. A typical history of exposure and chest X-ray is usually enough for diagnosis. No effective treatment exists except supportive care. Although chest X-ray of the patient revealed bilateral disseminated micronodular densities, a peripherally diffuse prominent FDG [(F-18)-2-fluoro-2-deoxy-D-glucose] uptake in both lungs and faint FDG uptake in mediastinal lymph nodes demonstrating active inflammation regions were noted on PET (Positron Emission Tomography) scan. This case was presented to show the active disease discriminated by FDG PET from chronic changes detected by radiological studies. FDG PET can provide additional information to CT regarding the diagnosis of acute silicosis and the rare accelerated silicosis.
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PMID:FDG PET findings in a case with acute pulmonary silicosis. 1986 35