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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1982 and 1989, three women and seven men older than 70 years of age underwent elective free-tissue transfer. Nonhealing wounds of 1 scalp, 2 upper extremities, and 7 lower extremities were covered with 3 serratus anterior, 3 latissimus dorsi, 2 gracilis, and 2 lateral arm flaps. Major coincidental medical problems included hypertension, congestive heart failure, chronic obstructive pulmonary disease, coronary artery disease, diabetes mellitus, metastatic lung cancer, tachyarrhythmias, syncope, elevated liver function tests, and previous arterial bypass in the affected lower extremity. One flap failed and 2 others were compromised by venous thromboses but salvaged by reoperation. There were no major anesthetic complications. This series demonstrates that elective free-tissue transfers can be safely performed in patients older than 70 years of age.
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PMID:Microsurgical tissue transfer in patients more than 70 years of age. 200 39

A group of 2,065 gold miners surveyed between 1968 and 1970 was followed to 31 December 1986, at which date 859 were known to be dead. The relationship between airways obstruction and mucus hypersecretion to causes of mortality was analyzed. Airways obstruction was strongly related to mortality from chronic obstructive pulmonary disease (COPD), lung cancer, coronary heart disease and other causes. After standardization for airways obstruction, mucus hypersecretion was not related to mortality from COPD but remained related to mortality from ischaemic heart disease (IDH) and other causes, even after adjustment for tobacco smoking and dust exposure. Mucus hypersecretion was not related to mortality from lung cancer when standardized for airways obstruction.
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PMID:Relevance of airflow obstruction and mucus hypersecretion to mortality. 201 56

Pulmonary alveolar macrophages (PAM) obtained by bronchoalveolar lavage in 13 normal individuals, 17 lung cancer patients and 10 patients with chronic obstructive pulmonary disease (COPD) were incubated in vitro for 24 hours. Every specimen was divided into two portions and lipopolysaccharides were used to stimulate PAMs to produce interleukin-1 (1L-1) in one. The levels of 1L-1 in normal subjects were 5547.65 +/- 2420.42 cpm/10(6) cells (stimulated) and 718.46 +/- 472.25 (unstimulated), which were higher than the 2733.20 +/- 1611.17 (stimulated, P less than 0.01) and 327.57 +/- 226.86 (unstimulated, P less than 0.05) in lung cancer patients, but lower than that of 8716.26 +/- 2977.66 (stimulated, P less than 0.05) in COPD patients. The enhanced 1L-1 activity in COPD patients might contributed to the active inflammatory process and tissue destruction of COPD. Our findings that 1L-1 activity in patients with bronchogenic carcinoma was decreased may reflect the local immune deficiency in malignant disease. The release of 1L-1 by PAMs stimulated by smoking was suggested to be associated with the development of COPD, but its role in immune response has to be determined.
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PMID:[A preliminary study on the role of interleukin-1 in chronic lung disease]. 209 Mar 52

Pulmonary ventilation and perfusion on regional level was measured by determining the distribution and elimination of introduced by inhalation 133He-gas, accordingly of intravenously injected 133He-solution. Fifty seven patients 7 to 60 years of age were included in the study, distributed by diagnoses, as follows: pulmonary thromboembolism 24 patients, 16 children with recurrent bronchopneumonia, pneumonia 10, central lung cancer 4, lung echinococcus 2 and one patient with LTE associated with chronic obstructive lung disease. All had ventilatory and subsequent perfusion dynamic scintigraphy. Ventilation was measured by the single breath technique. Perfusion scintigraphy was performed by the foregoing scheme, but by intravenous injection of 133He-solution. The entry, distribution and elimination of 133He-solution. The entry, distribution and elimination of 133He-gas and accordingly 133He-solution were followed up on gamma-camera display, and the time of radioactive gas elimination from the lungs was determined. Being practicable and nontraumatic, ventilation and perfusion scintigraphy may be repeated several times. This fact helps to follow up the evolution of the disease and the effect of conservative or surgical treatment. The results give an idea of the topographic and functional diagnosis of lung diseases.
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PMID:[133Xe (xenon) study of pulmonary ventilation and perfusion with a gamma camera]. 210 2

Forty-two lung cancer patients with COPD (7.9% of 534 lung cancers), and 84 age- and sex-ratio-matched controls who were randomly selected from lung cancer patients without COPD were examined. Lung cancers with COPD consisted of 25 cases of squamous call carcinoma (59.5%), 11 of adenocarcinoma (26.2%), 2 of small-cell carcinoma (4.8%), and 4 of large-cell carcinoma (9.5%). Squamous cell carcinoma occurred more in patients with COPD than in controls (35.7%) (p less than 0.01). In squamous cell tumors with COPD, 12 cases (48.0%) were centrally located and 13 cases (52.0%) were peripherally located. Squamous cell carcinoma of peripheral origin occurred more in patients with predominant emphysema (76.9%) than controls (36.7%) (p less than 0.05). Our results suggest that the COPD patients with predominant emphysema may be at greater risk for squamous cell tumors of peripheral origin.
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PMID:[Clinical and pathological characteristics of lung cancer with chronic obstructive pulmonary disease]. 217 Jul 29

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

Although much of the evidence in environmental lung disease remains equivocal, some environmental exposures are known to be clinically relevant. Ambient air pollution remains of concern as a source of morbidity, particularly for susceptible populations such as persons with asthma, chronic obstructive pulmonary disease, or cardiac disease and the elderly. The adverse effects of several components of indoor air pollution have been established. Environmental tobacco smoke contributes to lower-respiratory illness in infants; office workers exposed to thermophilic actinomycetes contaminating ventilation systems have developed hypersensitivity pneumonitis; and in the home, components of house dust and fungus spores may provoke asthma via immediate hypersensitivity. The evidence is less compelling for a link between other exposures and disorders of the respiratory tract. For example, formaldehyde may be responsible for provoking vague respiratory symptoms and even nasal cancers; however, the associations are unproved. Likewise, the relation between low-level exposure to asbestos and the development of lung cancer, although a concern, is not conclusively established. The clinician should be aware of practical measures for patients who inquire about air cleaning. Often, relatively simple solutions are effective. A knowledge of sources and exposures as well as an understanding of the principles of inhalation lung injury should prove useful in directing patient care.
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PMID:Environmentally mediated disorders of the respiratory tract. 218 Dec 9

Trends in smoking associated respiratory diseases in England and Wales during 1941-85 have been studied, with careful attention to problems caused by changes in classification of cause of death. Three diseases were selected for analysis: lung cancer, emphysema, and chronic obstructive lung disease. During 1971-85 deaths that would previously have been certified under chronic bronchitis have increasingly tended to be classified under chronic airways obstruction. The definition of chronic obstructive lung disease that was used includes both terms to avoid the artificial decline caused by consideration of chronic bronchitis in isolation. Age specific rates for all three diseases show a pronounced cohort (period of birth) pattern, rates for men rising up to the rates for those born shortly after the turn of the century and then declining, and rates for women peaking in the cohort born 20-25 years later. For chronic obstructive lung disease, but not for lung cancer and emphysema, the cohort peak is superimposed on a sharply declining downward trend. In both sexes cohort patterns of cumulative cigarette consumption peak at a time broadly similar to those seen for the three diseases. Trends in cigarette consumption, however, cannot explain the underlying steeply declining rate of chronic obstructive lung disease. Nor can they fully explain the declining trends in lung cancer and emphysema rates in younger men and women.
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PMID:Trends in lung cancer, chronic obstructive lung disease, and emphysema death rates for England and Wales 1941-85 and their relation to trends in cigarette smoking. 834 7

Of the four principal categories of indoor pollution (combustion products, chemicals, radon and biologicals), research in developing countries has focused on combustion-generated pollutants, and principally those from solid-fuel-fired cooking and heating stoves. Such stoves are used in more than half the world's households and have been shown in many locations to produce high indoor concentrations of particulates, carbon monoxide and other combustion-related pollutants. Although the proportion of all such household stoves that are used in poorly ventilated situations is uncertain, the total population exposed to excessive concentrations is potentially high, probably several hundred million. A number of studies were carried out in the 1980s to discover the health effects of such stove exposures. The majority of such studies were done in South Asia in homes burning biomass fuels or in China with coal-burning homes, although a sprinkling of studies examining biomass-burning have been done in Oceania, Latin America and Africa. Of the health effects that might be expected from such exposures, little, if any, work seems to have been done on low birthweight and eye problems, although there are anecdotal accounts making the connection. Decreased lung function has been noted in Nepali women reporting more time spent near the stove as it has for Chinese women using coal stoves as compared to those using gas stoves. Respiratory distress symptoms have been associated with use of smoky fuels in West India, Ladakh and in several Chinese studies among different age groups, some with large population samples. Acute respiratory infection in children, one of the chief causes of infant and childhood mortality, has been associated with Nepali household-smoke exposures. Studies of chronic disease endpoints are difficult because of the need to construct exposure histories over long periods. Nevertheless, chronic obstructive lung disease has been associated with the daily time spent near the stove for Nepali women and found to be elevated among coal-stove users compared to gas-stove users in Shanghai. In contrast to early reports, there seems to be little or no risk of nasopharyngeal cancer from cookstove smoke. Several studies in China, however, have found smoke to be a strong risk factor for lung cancer among non-smoking women. In addition, severe fluorosis has been observed in several parts of China where coal fluoride levels are high.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Indoor air pollution in developing countries. 223 93

Differential cell counts and fibronectin levels were recorded in bronchoalveolar lavage fluids (BALF) from patients with lung cancer, idiopathic pulmonary fibrosis (IPF), sarcoidosis, pneumonia, acquired immunodeficiency syndrome (AIDS), and chronic obstructive lung disease (COLD). In all groups fibronectin levels were significantly higher than in the control group; patients with sarcoidosis had a six-fold higher fibronectin level (mean values), AIDS 5.4-fold, pneumonia 4.4-fold, lung cancer, IPF and COLD 2.4-3.0-fold. In control smokers the fibronectin level was significantly higher compared to healthy nonsmokers (p less than 0.002). The increased fibronectin levels could not be explained by contamination of BALF with blood or leakage of plasma proteins. Thus, increased fibronectin levels probably reflect local (e.g. macrophage/fibroblast) synthesis.
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PMID:Distribution of bronchoalveolar cells and fibronectin levels in bronchoalveolar lavage fluids from patients with lung disorders. 224 65


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