Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High resolution computed tomography (HRCT) findings were correlated with pathologic features of 14 inflation-fixed postmortem lungs with pneumoconiosis to evaluate the ability of HRCT to depict pneumoconiotic changes. The results are as follows: 1) Irregular peribronchiolar and interlobular fibrosis was the most constant pathologic feature in all lungs. This pathologic finding corresponded to an area of hazy increased density or reticular density on HRCT. The reticular density on HRCT became coarser with the progression of fibrosis. Mild fibrosis, confirmed by histologic procedures, could not be detected with HRCT. 2) Subpleural curvilinear line seen on HRCT in 5 lungs corresponded to band-like zone of fibrosis containing bronchioles or zone of collapsed alveoli with fibrotic thickening on histologic sections. A subpleural band-like zone of organized pneumonia was recognized in 2 cases. Subpleural patchy density was seen on HRCT in 8 cases. Five of them were histologically a focus of fibrosis and the other 3 were localized pulmonary edema, organized pneumonia, or atelectasis without fibrosis. 3) Pneumoconiotic nodules were located at centrilobular portion or along interlobular septa on histologic sections. These location were correspond to HRCT findings. They were round with irregular borders and were surrounded by a zone of enlarged air space. Overall 71% (182/256) of pathologically proved nodules were seen on HRCT, but 63% (52/83) of small "p" type nodules (smaller than 1.5 mm) could not be detected. Enlarged air space at the periphery of the nodules was seen on HRCT in 78% (122/156) of those pathologically proved. 4) A total of 12 lesions of progressive massive fibrosis was found in 5 lungs. An irregular border, seen on HRCT in all lesions, was pathologically based on the fibrosis extending into the surrounding alveoli and partially confluencing pneumoconiotic micronodules. Pleural indentation was seen in 8 lesions. Patent residual bronchi, spared from destructive fibrotic change, were seen as strand-like air density on HRCT in 4 of 6 lesions. 5) Focal emphysema was found pathologically in 9 of the 14 lungs. They appeared as non-peripheral, small low-attenuation area with a central dot on HRCT. The dot histologically corresponded to fibrosis around centriacinar bronchovascular bundle. The limit of visibility of this form of emphysema on HRCT was 2.0 mm in size. When emphysema was complicated by pneumonia, some showed honeycomb appearance on HRCT. 6) It is concluded that HRCT can detect and quantify the various pneumoconiotic changes of the lung and the HRCT-pathological correlation data presented here will be useful for the interpretation of the findings in clinical cases of pneumoconiosis.
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PMID:[Pathologic-HRCT correlation of pneumoconiosis--a study on inflation-fixed lungs]. 154 47

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

Current topics for occupational and environmental medicine and physiology in the U.S.A., especially in the National Institute for Occupational Safety and Health (NIOSH), and the University of California, San Francisco, are reviewed. Reduction of the rate for occupational lung diseases is one of the national objectives for occupational safety and health in the U.S.A., and NIOSH has rated it as the top disease of ten-leading work-related diseases and injuries. Current topics for occupational lung diseases--asbestosis, byssinosis, silicosis, coal worker's pneumoconiosis, lung cancer, and occupational asthma & hyperreactivity, and for pathophysiology of airway hyperreactiveness and pulmonary edema are discussed.
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PMID:[Current topics for occupational and environmental medicine and physiology in the U.S.A.--with special reference to occupational lung diseases]. 352 79

Ladakh is a sparsely populated area of Indian Himalaya lying at 3-4500 m altitude mainly consisting of arid desert. This paper will discuss high altitude health problems in Ladakh under the following headings. 1. Acute altitude illness: acute mountain sickness (AMS), high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). 2. Effects of prolonged and permanent exposure to high altitude: (subacute and chronic mountain sickness). 3. Environmental dust and domestic fire pollution resulting in non-occupational pneumoconiosis and high prevalence of respiratory morbidity.
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PMID:Mini review of high altitude health problems in Ladakh. 1518 46

This study was carried out with the aim of identifying types of gross and histopathological lesions in lungs of camels slaughtered between October 2009 and April 2010 at Addis Ababa abattoir enterprise, Ethiopia. All camels were originated from Borana and Kereyu areas. A total of 387 slaughtered camel lungs were inspected during the study period. Of which, one or more gross lesions were encountered on 300 lungs. Lesions were further subjected for detail gross and histopathological examinations. The occurrence of pulmonary lesions was 77.5%. The gross and histopathological examination of these lesions had revealed 60.2% emphysema, 21.2% hydatidosis, 18.6% pneumonia, 10.6% atelectasis, 4.9% aspiration of blood, 3.9% pneumoconiosis, 2.6% pulmonary edema and congestion, 1.6% abscess, 1% pleurisy, and 0.8% granulomatous pneumonia. Most camels had one or more pulmonary lesions on postmortem examination, but they were apparently healthy during antemortem inspection. Therefore, the prevailing stressful environmental condition coupled with the existing poor level of veterinary service in camel-rearing areas of the country might reverse these hidden inactive lesions and thereby contributed for the higher occurrence of respiratory diseases in camels.
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PMID:Gross and histopathological studies on pulmonary lesions of camel (Camelus dromedarius) slaughtered at Addis Ababa abattoir, Ethiopia. 2190 67

Methamphetamine is a substance of abuse that is most commonly smoked. Both regular and non-regular use can cause toxic injury to the lung parenchyma, the signs and symptoms of which are non-specific. Clinical scenarios include non-cardiac pulmonary oedema, acute respiratory distress syndrome, alveolar haemorrhage, pneumonia and pneumoconiosis. As radiological imaging is often non-specific, a positive history of methamphetamine use is the only way to reach a definite diagnosis. The use of methamphetamine is now increasing in Europe, so it is important as physicians to be aware of this differential diagnosis in patients in respiratory distress with risk factors for illicit drug use.
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PMID:Methamphetamine-Induced Lung Injury. 3129 88