Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An autopsy case of cemented tungsten carbide pneumoconiosis, the first lethal case in our country, is presented. A 28-year-old woman, who had been engaged in grinding presintered metallic matrix for four years, developed respiratory symptoms. X-ray examinations were indicative of interstitial pulmonary fibrosis. Corticosteroid therapy revealed only little effect. She expired five years after the onset of the symptoms. Postmortem examination showed nonspecific interstitial pneumonitis resulting in marked lung fibrosis. Ultrastructurally, crystals were observed in cytoplasm of presumable macrophages in the fibrotic lung tissue. Electron probe microanalysis of the lung tissue showed the presence of tungsten and other constituents of tungsten carbide except for cobalt. Metal analysis demonstrated a large amount of tungsten in the lung. Cobalt was detected tenfold of the normal value in the bone. In pathogenesis of the pneumoconiosis in the cemented tungsten carbide workers, toxicity of cobalt is most suspectable, and in addition, individual susceptibility may be also important.
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PMID:Cemented tungsten carbide pneumoconiosis. 73 23

Hard metal pneumopathy and hard metal asthma are two separate forms of hard metal lung disease. Cobalt is the probable causal agent involved. Bronchial provocation with hard metal powder induces obstruction within 2 hours of the challenge. Suspected hard metal pneumopathy, however, should be confirmed or excluded by a period of non-exposure followed by re-exposure, since the long-term exposure in patients suffering from hard-metal pneumopathy leads to pulmonary fibrosis.
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PMID:[Hard metal-induced lung changes. Hard metal asthma--interstitial hard metal pneumopathy]. 239 30

Cobalt is a relatively rare magnetic element with properties similar to iron and nickel. The two valance states are cobaltous (II) and cobaltic (III) and the former is the most common valance used in the chemical industry. Cobalt occurs in nature primarily as arsenides, oxides, and sulfides. Most of the production of cobalt involves the metallic form used in the formation of cobalt superalloys. The term "hard metal" refers to compounds containing tungsten carbide (80-95%) combined with matrices formed from cobalt (5-20%) and nickel (0-5%). For the general population, the diet is the main source of exposure to cobalt. In the occupational setting, exposure to cobalt alone occurs primarily during the production of cobalt powders. In other industrial exposures (e.g., hard metal, diamond polishing), additional agents (tungsten) modulate the toxicity of cobalt. Cobalt is an essential element necessary for the formation of vitamin B12 (hydroxocobalamin); however, excessive administration of this trace element produces goiter and reduced thyroid activity. In 1966, the syndrome "beer drinker's cardiomyopathy" appeared in Quebec City, Canada, and was characterized by pericardial effusion, elevated hemoglobin concentrations, and congestive heart failure. An interstitial pulmonary fibrosis has been associated with industrial exposure to hard metal dust (tungsten and cobalt), but not to cobalt alone. Exposure to cobalt alone produces an allergic contact dermatitis and occupational asthma. Treatment of cobalt toxicity is primarily supportive.
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PMID:Cobalt. 1038 56

Metal dust inhalation induces an interstitial lung disease which may progress to pulmonary fibrosis (hard metal disease, HMD). Cobalt is believed to be the pathogenic agent of HMD. A strong genetic association of HMD with some HLA-DP alleles has been reported although the role of these molecules in the occurrence of the fibrotic disorder remains unclear. A possible explanation of these findings is that HLA-DP but not other HLA class II molecules can bind cobalt. This could have as a consequence an HLA-DP-mediated specific activation of the immune system. To test this hypothesis, we have set up an in vitro binding assay using 57Co and purified HLA-DP and -DR molecules. The results indicate that HLA-DP but not HLA-DR molecules bind cobalt. Moreover, the presence of HLA-DP Glu beta69, which is associated with susceptibility to HMD, determines a higher metal uptake. Molecular modelling of HLA-DP2 molecules places the Glu beta69 residue in a position relevant in determining peptide specificity. The possibility that binding of cobalt by HLA-DP molecules can interfere with their antigen presenting functions is discussed.
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PMID:HLA-DP molecules bind cobalt: a possible explanation for the genetic association with hard metal disease. 1042 76

Cobalt alone and in combination with tungsten carbide known as hard metal is capable of causing lung damage. This may vary from development of pulmonary oedema to asthma and fibrosing alveolitis. We report a case of giant cell interstitial pneumonitis caused by exposure to cobalt dust which was not identified as the etiological agent initially and hence led to progression of the disease. The patient subsequently improved following cessation of exposure and treatment with oral corticosteriods, thereby stressing the importance of occupational history in all cases of interstitial pulmonary fibrosis.
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PMID:Giant cell pneumonitis induced by cobalt. 1137 May 7

Hard metal lung disease is a rare form of occupational lung disease that can occur in workers engaged in the manufacture, utilization, or maintenance of tools composed of hard metal [a material composed mainly of tungsten carbide (WC) and cobalt] or diamond-cobalt. Clinically, the condition resembles hypersensitivity pneumonitis, with subacute presentations and possible evolution to pulmonary fibrosis. However, this interstitial lung disease is uniquely characterized by the presence of bizarre ;;cannibalistic'' multinucleated giant cells in the alveoli and the bronchoalveolar lavage. A pathological diagnosis of giant cell interstitial pneumonitis (GIP) is, therefore, specific for hard metal lung disease, even though not all affected subjects exhibit this pathognomonic feature. Cobalt is the critical toxic component causing hard metal lung disease, hence also the term cobalt-lung. Hard metal lung disease is more likely to occur in poorly regulated workplaces, but its occurrence depends mainly on individual susceptibility, rather than on cumulative exposure, so that even young subjects may be affected.
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PMID:Giant cell interstitial pneumonia (hard metal lung disease, cobalt lung). 1608 91

Cobalt is an essential heavy metal that is necessary for the formation of vitamin B12 (hydroxocobalamin). However, exposure to excess cobalt for a prolonged period can harm the human body, causing pulmonary fibrosis, blindness, deafness, and peripheral neuropathy. 3-Aminotriazole (3-AT) is a catalase inhibitor that is often used to investigate the physiological effects of catalase. The present study found that injection of 3-AT in mice significantly reduced CoCl2-induced hearing impairment. In cultured organ of Corti explants from rats, 3-AT treatment protected hair cells from CoCl2-induced cytotoxicity. To determine the mechanism by which 3-AT protected from CoCl2-induced ototoxicity, we used the HEI-OC1 auditory cell line. Pretreatment with 10 mM 3-AT attenuated CoCl2-induced accumulation of ROS and induction of proinflammatory cytokine expression. Interestingly, these protective effects of 3-AT did not require catalase activity, as demonstrated by a series of experiments using RNA interference-mediated catalase knockdown in HEI-OC1 cells and using catalase-deficient mouse embryonic fibroblasts. Our results demonstrated the mechanisms of CoCl2-induced ototoxicity that may provide better ways to prevent the ototoxic effect of cobalt exposure.
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PMID:3-Aminotriazole protects from CoCl2-induced ototoxicity by inhibiting the generation of reactive oxygen species and proinflammatory cytokines in mice. 2582 Sep 16