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

The impact, time trends and potential for prevention of premature deaths in Canada were assessed. There were almost 100,000 deaths before age 75 in Canada during 1986 resulting in over 1.7 million potential years of life lost (PYLL). The three leading broad disease categories responsible for PYLL were cancer, injuries/violence and cardiovascular disease. In both sexes, coronary heart disease, car accidents, lung cancer and perinatal conditions ranked in the top 5 specific diseases responsible for PYLL; breast cancer (females) and suicide (males) also ranked in the top 5 conditions. Over the period 1969 to 1986, death rates among persons less than age 75 increased for 3 conditions among females and 11 conditions among males. Lung cancer and brain cancer death rates increased in both sexes, chronic obstructive pulmonary disease death rates increased among females only and death rates for suicide and 8 types of cancer increased among males only. Over the same period, death rates declined for 37 discrete disease categories among both females and males including particularly large improvements for coronary heart disease, stroke, car accidents and perinatal conditions. An estimated 50,000 or over 50% of all premature deaths per year are preventable through control of smoking, hypertension, elevated serum cholesterol, diabetes and alcohol abuse. About 6,000 premature deaths are avoidable through improvements in medical care.
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PMID:Premature deaths in Canada: impact, trends and opportunities for prevention. 225 55

A group of patients with serious chronic diseases of the chest (n = 18) travelled from northern Norway to Yugoslavia for treatment (approximately four hours air travel and 16 hours total travel). The group included patients with asthma, chronic obstructive pulmonary disease, sequelas after tuberculous disease and resections for lung cancer. Minute lung function tests were performed before departure. SaO2 was monitored by pulsoximetri during the flight. All patients experienced a fall in SaO2 during the flight. Patients with restrictive pulmonary disease or combined restrictive/obstructive disease fell significantly lower than the rest of the group (p less than 0.001), and they experienced serious discomfort. Recommendations for minimum lung functions are FEV1 greater than 1.0 liter, PaOa greater than 9.3 kPa and PCO2 less than 7.0 kPa.
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PMID:[Experiences of pulmonary disease on jet planes]. 233 47

In a case-control study, we tested the hypothesis that the genetically determined ability to metabolize debrisoquine is related to risk of lung cancer. Overall, individuals who were extensive metabolizers of debrisoquine were at significantly greater risk of lung cancer than those who were poor or intermediate metabolizers (odds ratio = 6.1; 95% confidence interval = 2.2-17.1). In this study, case patients had lung cancer, and control subjects had either chronic obstructive pulmonary disease or cancers other than lung cancer. Results were adjusted for age, race, asbestos exposure, and smoking. Both black and white individuals who were extensive metabolizers of debrisoquine were at significantly increased risk after similar adjustment (for blacks, odds ratio = 4.5, 95% confidence interval = 1.1-18.1; for whites, odds ratio = 10.2, 95% confidence interval = 2.0-51.4). Significantly increased risk of lung cancer was also present for individuals who were extensive metabolizers when subjects with chronic obstructive pulmonary disease or other cancers were considered separately. These data confirm that the ability to metabolize debrisoquine is a major determinant of susceptibility to lung cancer. Evaluation of the marker in other case-control settings, further exploration of racial differences, and the prospective evaluation of this marker in subgroups at high risk of lung cancer are areas worthy of further study.
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PMID:Lung cancer and the debrisoquine metabolic phenotype. 237 72

Extravascular coagulation and fibrinolysis is an integral part of inflammatory reactions. Disordered expression of procoagulant and profibrinolytic factors by mononuclear phagocytes of the lung (i.e. lung alveolar macrophages (LAM) and interstitial macrophages) may have important bearings on inflammatory lung tissue destruction and repair. Based on this hypothesis we have measured the presence of trigger molecules and activation products of the coagulation and fibrinolytic system in cell-free bronchoalveolar lavage fluid and in bronchoalveolar cells. Patient groups with chronic obstructive disease (COLD) (n = 76), idiopathic pulmonary fibrosis (IPF) (n = 29), sarcoidosis (n = 22), lung cancer (n = 36), pneumonia (n = 39), acquired immunodeficiency syndrome (AIDS) (n = 17) and a control group (n = 60) were studied by bronchoalveolar lavage (BAL). In all patient groups tissue thromboplastin (TPL) and fibrinopeptide A (FPA) were significantly increased compared to controls. Plasminogen activator (PA) activity was significantly lower in patients than in normals, and usually associated with high levels of antifibrinolytic activity. The level of PA inhibitor (PAI-2) was not significantly higher in any patient group compared to controls. The sensitivity of the method for fibrin degradation products (FDP) analysis was not high enough to detect FDP in BAL fluid of control individuals, whereas such products could be demonstrated in 25-53% of patients in various categories. We conclude that disordered expression of procoagulant and plasminogen activator activities in bronchoalveolar lavage fluid may reflect a milieu that favours accumulation of fibrin in inflammatory lung tissue and form the basis for the development of pulmonary fibrosis.
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PMID:Local activation of the coagulation and fibrinolysis systems in lung disease. 238 54

The hypothesis that rare variable nucleotide tandem repeat alleles of the Ha-ras-1 polymorphism are an inherited predisposing factor in human lung carcinogenesis has been evaluated in an age, race, and smoking matched case-control study. Twenty-three different alleles were identified by their restriction fragment length in DNA isolated from peripheral blood lymphocytes and were categorized into three groups: common; intermediate; and rare. The frequencies of rare alleles in blacks with either squamous cell carcinoma, large cell carcinoma, or small cell carcinoma were found to be significantly higher than those among groups of control subjects that were comprised of chronic obstructive pulmonary disease patients and patients with cancer at sites other than the lung. A similar trend which did not reach statistical significance was observed in whites. These data are consistent with the hypothesis that inheritance of Ha-ras-1 rare restriction fragment length alleles represents a genetic risk factor for some human lung cancers. The biological basis of this observation remains to be clarified, and it is possible that ethnic variations in rare allele frequencies are responsible for the differences noted. However, the data suggest that further evaluation of the Ha-ras-1 polymorphism as a marker of individual lung cancer susceptibility is warranted.
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PMID:Association of rare alleles of the Harvey ras protooncogene locus with lung cancer. 240 46

A computerized tube LAI assay was used to determine the antitumor immune response in lung cancer patients. A standardized assay was established by the use of tumor antigen recovered from the spent medium of lung and colon adenocarcinoma cell lines. Furthermore, modulation of the assay by prostaglandin E2 (PGE2) was used to increase its sensitivity. Of 65 patients with epidermoid lung cancer, 34 (52.3%) had a positive nonadherence index (NAI). The NAI was inversely related to tumor burden, with 31 of 44 (70.6%) patients with lung cancer stages I and II and only 3 of 21 (14%.2%) patients with stage III having positive assays (greater than 30%). Addition of PGE2 to the as say increased the overall sensitivity so that a positive NAI was obtained in 88.6% of patients with lung cancer stages I and II, and 88.6% with stage III, respectively. Of 174 individuals from the control group, positive NAI was found in only 9 and 3.8% of patients with chronic obstructive pulmonary disease and normal controls, respectively. These results support previous observations on the specificity and sensitivity of the LAI assay in the diagnosis and study of human cancer.
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PMID:A computerized tube leukocyte adherence inhibition assay in the diagnosis of human lung cancer. 241 75

This report forms a background paper for a World Health Organization document on "Assessment of the role of lifestyles in influencing workers' health risks". It identifies occupational and non-occupational factors which contribute to occupational mortality and morbidity. Eight categories of mortality and morbidity are identified as priorities for discussion, based on UK data. These are cardiovascular disease; lung cancer; chronic obstructive pulmonary disease; occupational deafness; dermatitis; vibration white finger; tenosynovitis; and suicide. Non-occupational factors associated with these include age, sex, race, smoking, social class, alcohol consumption, diet, exposures in leisure time, exercise, atopy, heredity, personal hygiene, personality type, stress, past or predisposing illness or injury, weather/climate and air pollution. Smoking is identified as the most widely studied non-occupational factor in occupational disease. Smoking interacts with some occupational exposures to produce more disease than the sum of both agents separately. Smoking and asbestos interact multiplicatively in lung cancer causation. The ability to quantify interactions between occupational and non-occupational factors in disease etiology is important in assessing priorities for preventive action. Despite this, only the interactions of smoking have begun to be defined. The many other non-occupational factors mentioned above have each been studied individually but their interactions with occupational factors have not been assessed. This report describes models of quantifying interactions and recommends that further work is carried out to assess the interactions of non-occupational factors other than smoking in disease causation.
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PMID:Non-occupational factors in occupational morbidity and mortality. 248 18

This multicentre, randomized, double-blind study evaluated the effectiveness and safety of cefixime versus amoxicillin. Patients were admitted if they had lower respiratory tract infection with a bacterial pathogen susceptible to both study drugs. Diagnoses included acute respiratory tract infections with no underlying pulmonary pathology (cefixime 21, amoxicillin 27), acute exacerbation of chronic obstructive lung disease (cefixime 32, amoxicillin 42), superinfection of viral bronchitis or lung cancer, and pleuritis (cefixime 10, amoxicillin 6). Patients were treated for at least 10 days with either cefixime 200 mg b.d. or amoxicillin 1 g b.d. A clinical success rate of 80.7 per cent (50/62) in the cefixime group and 82.2 per cent (60/73) in the amoxicillin group was achieved in infections due to susceptible organisms. In acute infections with no underlying pathology, the clinical success rate was 90.5 per cent with cefixime and 81.5 per cent with amoxicillin. Twenty-three cefixime patients and 20 amoxicillin patients were seen 2 to 6 weeks after treatment: there were 2 and 1 clinical recurrences, respectively. All 3 patients were suffering from chronic obstructive lung disease. The bacteriological eradication rate at the end of treatment in assessable patients was 94.7 per cent (17/18) with cefixime and 80 per cent (16/20) with amoxicillin. Six and 11 new organisms appeared, responsible for 2 superinfections under cefixime and 7 under amoxicillin. Treatment was well tolerated by 96.4 per cent of cefixime patients and 90 per cent of amoxicillin patients. This study confirms the value of cefixime as a new oral antibiotic in the treatment of lower respiratory tract infections in adults.
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PMID:[Controlled multicentric study comparing cefixime and amoxicillin in the treatment of lower respiratory tract infections in adults]. 253 May 42

The value of mucus hypersecretion as a predictor of mortality and hospitalization was studied in a random population sample of 876 men, aged 46-69 years. The cohort was examined in 1974 with the British Medical Research Council questionnaire and lung function tests. A total of 219 men had died between 1974 and 1985. Twenty-seven men died from lung cancer and 14 died from other respiratory diseases. Mucus hypersection was not found to be significantly related to overall mortality after controlling for age, smoking and FEV1. Similarly, mucus hypersection was not a predictor of lung cancer mortality after controlling for age and smoking habits. The predictive value concerning death due to respiratory disease could not be examined because of the limited number of deaths in the cohort from these diseases. Mucus hypersecretion was not significantly related to hospitalization in general. Mucus hypersecretion had a significant predictive value concerning hospitalization due to respiratory disease in general, but the value was insignificant after controlling for FEV1. In contrast to this, mucus hypersecretion was a significant predictor of hospitalization due to COPD, even after controlling for FEV1. We conclude that the predictive value of mucus hypersecretion concerning mortality is of no value. Concerning morbidity, our results show that, although secondary to airflow obstruction, mucus hypersecretion must be viewed as an indicator of severity of COPD.
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PMID:The value of mucus hypersecretion as a predictor of mortality and hospitalization. An 11-year register based follow-up study of a random population sample of 876 men. 259 38

The purpose of this ongoing study is to determine whether thoracic radiotherapy for lung cancer produces an early increase in serum copper (Cu) concentration, an increase which might predict clinical outcome. Copper and iron concentrations were measured in serum obtained from nonsmall cell lung cancer patients at 0, 1, 2, 4, and 6 weeks after the start of radiotherapy. Control groups included patients irradiated for breast cancer (low dose of radiation to the lung), for endometrial, cervical or prostatic cancer (no dose to lung), and patients with congestive heart failure, pulmonary hypertension, chronic obstructive pulmonary disease (COPD), and cutaneous burns with or without smoke inhalation (no irradiation). Serum Cu concentration increased at least 10 micrograms/dl from the pretreatment level in approximately 75% of the adenocarcinoma and squamous cell lung cancer patients, but in only 1 of 4 undifferentiated lung cancer cases. In virtually all of these responders, serum Cu increased to a maximum at 2 weeks after the start of therapy, then plateaued or decreased slightly despite continuing irradiation. Within the subset of squamous cell lung cancers, there was a direct correlation between the degree of histologic differentiation and both baseline serum Cu concentration and the probability of an early increase therein. In contrast, only 33% of breast cancer patients and 15% of endometrial, cervical and prostate cancer patients exhibited an increase in serum Cu concentration at 2 weeks after the start of radiotherapy. Serum Cu concentration was within normal limits in virtually all patients with congestive heart failure, pulmonary hypertension, and COPD. Burn patients exhibited a significant reduction in serum Cu, although concomitant smoke inhalation increased serum Cu back to low-normal levels. Serum iron concentration did not change significantly in any category of patients. These data suggest that thoracic radiotherapy for well differentiated non-small cell lung cancer is accompanied by an early increase in serum Cu concentration. This increase is partly but not wholly related to lung dose in particular rather than tissue dose in general, and specifically reflects radiation-induced lung injury rather than pneumopathy in general. In lung cancer patients, the change in serum Cu concentration during the first 2 weeks of radiotherapy exhibits a sufficiently broad range (+60 to -13 micrograms/dl) to permit testing this parameter as a predictor of tumor response and pulmonary complications.
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PMID:Serum copper concentration as an index of clinical lung injury. 262 91


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