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

The aim of this study was to evaluate the causes of prolonged cough in a patient population referred to a chest clinic during a single year. One hundred and ninety-eight patients (11%) of the total yearly 1745 adult admissions fulfilled our criteria of prolonged cough. Asthma, suspicion of asthma and postnasal drip were the commonest causes of prolonged cough in 147 patients with normal chest roentgenograms (26%, 9% and 16%, respectively), and in 45% the cough was of unexplained origin. Nonspecific bronchial hyperreactivity was common in this latter group of patients probably due to a previous respiratory infection. Lung cancer (37%), tuberculosis (16%), sarcoidosis (16%), and allergic alveolitis (9%) were the most important findings in patients with abnormal chest roentgenograms.
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PMID:Causes of prolonged cough in patients referred to a chest clinic. 260 35

Asthma is a common chronic childhood disease yet not much is known about factors that determine its outcome. Cigarette smoke has been associated with lung cancer in adults but its effects on children has hitherto been underestimated and not well studied. Cigarette smoke has been noted through various research studies to influence the development and or the exacerbation of asthma in childhood. Furthermore the prevalence of childhood asthma is higher among the children of smoking parents, more so when both parents are smokers as compared to those of non-smoking parents. Corroborative evidence indicates elevated urine cotinine levels amongst children of smoking parents than those of non-smoking parents. There is a corresponding increase in prevalence and exacerbation of asthma symptoms among children with raised urine cotinine levels than those with low levels. The presence of other risk factors increases the risk of development and exacerbation of bronchial asthma in children exposed to tobacco smoke than those not exposed. Cigarette smoking is on the increase, especially in developing countries due to aggressive advertising and exportation by the tobacco industry from developed countries. International legislation is needed to regulate the production and exportation of tobacco products. However, this may be resisted by the influential tobacco industry and may not get the support from the developing countries due to economic gains from the sale of tobacco products. This scenario poses major health problems for the developing countries in the future.
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PMID:Relationship between exposure to tobacco smoke and bronchial asthma in children: a review. 960 35

The 'Sendzimir' Steel Mill, Cracow, Poland, gives employment to approximately 17,000 workers. During the years 1994-98, 1396 compensation claims for diseases related to occupational hazards were registered. After a scrupulous investigation, 851 cases were certified as occupation-related diseases. Of this number, 481 cases (56.5%) were diagnosed as pulmonary diseases, including silicosis (n = 225, 46.7%); chronic bronchitis (n = 138, 28.7%); lung carcinoma (n = 59, 12.3%); epithelial cancer (n = 42); adenocarcinoma (n = 12); microcellular carcinoma (n = 5); asthma, 12 atopic and 24 non-atopic (n = 36, 7.5%); and asbestosis (n = 23, 4.8%). Chronic bronchitis was diagnosed in patients exposed to industrial dusts, containing SiO2, NOx, and SO2. Asthma occurred most frequently among those exposed mainly to Cr+6, Co and Ni containing dusts, and lung carcinoma in those exposed to policyclic aromatic hydrocarbons, including benz(a)pyren, asbestos, chromium, vapours of oils and lubricants. In 1994-96, chronic bronchitis and silicosis, and in 1997-98, lung carcinoma and asthma were most frequently diagnosed in the workers under study. It is likely that the diminishing frequency of chronic bronchitis and silicosis was the consequence of technological progress, and greater concern for hygiene standards. Increasing incidence of lung cancer reflects long latency characteristic of this illness.
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PMID:Occurrence of pulmonary diseases in steel mill workers. 1096 40

Asthma is common among older persons, affecting approximately 4 to 8% of those above the age of 65 years. Despite its prevalence, late onset asthma may be misdiagnosed and inadequately treated, with important negative consequences for the patient's health. The histopathology of late onset disease appears to be similar to that of asthma in general, with persistent airway inflammation a characteristic feature. It is less clear, however, that allergic exposure and sensitisation play the same role in the development of disease in adults as they do in children. Atopy is less common among those with late onset asthma, and the prevalence of elevated immunoglobulin E levels is lower among those aged over 55 years of age than younger patients. Occupational asthma is an aetiological consideration unique to adult onset disease, with important implications for treatment. The differential diagnosis for cough, wheeze, and dyspnoea in the elderly is broad, and includes chronic obstructive bronchitis, bronchiectasis, congestive heart failure, lung cancer with endobronchial lesion and vocal cord dysfunction. Keys to accurate diagnosis include a good history and physical examination, the demonstration of reversible airways obstruction on pulmonary function tests and a favorable response to treatment. Inhaled corticosteroid therapy is recommended for patients with persistent disease, and careful instruction in the use of metered-dose inhalers is particularly important for the elderly.
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PMID:Late onset asthma: epidemiology, diagnosis and treatment. 1119 Apr 18

Acetaldehyde, a metabolite of alcohol and primary mediator of alcohol-induced asthma, causes bronchoconstriction via histamine release from airway mast cells. Acetaldehyde also is found in cigarette smoke and may cause airway inflammation. The purpose of this study was to determine the effect of acetaldehyde on cytokine production and nuclear factor kappa B (NF-kappa B) activation in human bronchial tissues. Human bronchi were prepared from normal parts of lung tissues resected for lung cancer (n = 11). The bronchi were cultured in the presence of 5 x 10(-4) M of acetaldehyde for 24 hours and the concentrations of eotaxin, granulocyte macrophage colony-stimulating factor (GM-CSF), interleukin-5, interleukin-8, and regulated on activation, normal T cells expressed and secreted in cultured supernatants were determined by enzyme-linked immunosorbent assay. Tissues also were immunohistochemically stained for NF-kappa Bp65. Acetaldehyde significantly increased GM-CSF production from human bronchi and nuclear translocation of NF-kappa Bp65 in airway epithelium but had no effects on other cytokines. Our findings suggest that acetaldehyde potentially causes airway inflammation via increased GM-CSF production through nuclear translocation of NF-kappa B.
Allergy Asthma Proc
PMID:Acetaldehyde induces granulocyte macrophage colony-stimulating factor production in human bronchi through activation of nuclear factor-kappa B. 1461 38

Using data from 8,896 men and women aged 50-89 years from the Adverse Childhood Experiences Study who were free of a self-reported history of lung cancer or any cancer at baseline, we examined the association between self-reported asthma and incident lung cancer. The prevalence of smoking was 33% among those who developed lung cancer (n = 52) and 7% among those who did not. Asthma was reported by 17% of adults who developed lung cancer and by 9% of those who did not. After adjustment for age, gender, race/ethnicity, educational attainment, smoking status, number of cigarettes smoked per day, and growing up with a parent who smoked the risk of lung cancer was 2.1 (95% CI: 1.0, 4.4) times greater among adults with a history of asthma compared to those without. Among nonsmokers, a similar result was observed, although it did not attain statistical significance (RR: 2.1; 95% CI: 0.9, 5.1). Smoking-attributable lung cancer incidence and mortality are in part a function of the prevalence of smoking in the population. Thus, decreases in the prevalence of smoking in the United States that have occurred since its peak in the 1960s will inevitably result in a decline in the proportion of lung cancer in the population caused by smoking. We hope that our findings and those of others will stimulate research of the biologic mechanism(s) underlying the occurrence of lung cancer among nonsmokers so that possible treatments and prevention strategies may be developed.
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PMID:Re: asthma and the risk of lung cancer. findings from the Adverse Childhood Experiences (ACE). 1284 63

Environmental factors play a major role in a majority of lung diseases. Asthma, chronic obstructive pulmonary disease (COPD), lung cancer, and many interstitial lung diseases are influenced or caused by environmental factors. Animals and humans may respond differently to the same agent, and a study of the comparative pathology between the two is useful for optimizing animal models of environmental lung disease and for evaluating their predictive value in carcinogenicity studies. This overview describes the most common nonneoplastic pathologic pulmonary responses to inhaled environmental agents in the human and contrasts them with the responses observed in rats exposed to the same agents. We show both similarities and difference in response to the same agents; furthermore, both species have unique responses to some agents (for example, progressive massive fibrosis in the human and proliferative squamous lesions in the rat). Quantitative analysis of the grades of response to three environmental particulate dusts revealed differences between the 2 species at the cellular level. Specifically, acute intra-alveolar inflammation, alveolar epithelial hyperplasia, and alveolar lipoproteinosis were all greater in rats than in humans exposed to the same agents. These differences may account for differences between the 2 species in carcinogenic response to nonfibrous particulates.
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PMID:Comparative pathology of environmental lung disease: an overview. 1732 82

The lung offers a rich opportunity for development of therapeutic strategies focused on isozymes of protein kinase C (PKCs). PKCs are important in many cellular responses in the lung, and existing therapies for pulmonary disorders are inadequate. The lung poses unique challenges as it interfaces with air and blood, contains a pulmonary and systemic circulation, and consists of many cell types. Key structures are bronchial and pulmonary vessels, branching airways, and distal air sacs defined by alveolar walls containing capillaries and interstitial space. The cellular composition of each vessel, airway, and alveolar wall is heterogeneous. Injurious environmental stimuli signal through PKCs and cause a variety of disorders. Edema formation and pulmonary hypertension (PHTN) result from derangements in endothelial, smooth muscle (SM), and/or adventitial fibroblast cell phenotype. Asthma, chronic obstructive pulmonary disease (COPD), and lung cancer are characterized by distinctive pathological changes in airway epithelial, SM, and mucous-generating cells. Acute and chronic pneumonitis and fibrosis occur in the alveolar space and interstitium with type 2 pneumocytes and interstitial fibroblasts/myofibroblasts playing a prominent role. At each site, inflammatory, immune, and vascular progenitor cells contribute to the injury and repair process. Many strategies have been used to investigate PKCs in lung injury. Isolated organ preparations and whole animal studies are powerful approaches especially when genetically engineered mice are used. More analysis of PKC isozymes in normal and diseased human lung tissue and cells is needed to complement this work. Since opposing or counter-regulatory effects of selected PKCs in the same cell or tissue have been found, it may be desirable to target more than one PKC isozyme and potentially in different directions. Because multiple signaling pathways contribute to the key cellular responses important in lung biology, therapeutic strategies targeting PKCs may be more effective if combined with inhibitors of other pathways for additive or synergistic effect. Mechanisms that regulate PKC activity, including phosphorylation and interaction with isozyme-specific binding proteins, are also potential therapeutic targets. Key isotypes of PKC involved in lung pathophysiology are summarized and current and evolving therapeutic approaches to target them are identified.
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PMID:Lung disease and PKCs. 1758 82

Chronic cough is a common and frequently disruptive symptom which can be difficult to treat with currently available medicines. Asthma/eosinophilic airway disease and gastro-oesophageal reflux disease are most commonly associated with chronic cough but it may also trouble patients with chronic obstructive pulmonary disease, pulmonary fibrosis and lung cancer. Over the last three decades there have been a number of key advances in the clinical approach to cough and a number of international guidelines on the management of cough have been developed. Despite the undoubted benefit of such initiatives, more effective treatments for cough are urgently needed. The precise pathophysiological mechanisms of chronic cough are unknown but central to the process is sensitization (upregulation) of the cough reflex. One well-recognized clinical consequence of this hypersensitive state is bouts of coughing triggered by apparently trivial provocation such as scents and odours and changes in air temperature. The main objective of new treatments for cough would be to identify ways to downregulate this heightened cough reflex but yet preserve its crucial role in protecting the airway. The combined efforts of clinicians, scientists and the pharmaceutical industry offer most hope for such a treatment breakthrough. The aim of this chapter is to provide some rationale for the current treatment recommendations and to offer some reflections on the management of patients with chronic cough.
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PMID:Clinical cough II: therapeutic treatments and management of chronic cough. 1882 46

During the first half of its 100-year history, tuberculosis was predominant in the German Society of Pneumology (DGP). This led largely to the separation of pneumology from internal medicine, particularly in the universities. Since the 1960s, the spectrum of respiratory diseases has changed considerably. Asthma, COPD, lung cancer, and pneumonia today rank among the most widespread diseases. Numerous new diagnostic and therapeutic methods have induced dramatic changes in the field of pneumology. Today, pneumology, together with cardiology and gastroenterology, belongs to the major specialties of internal medicine. One of the most urgent tasks of the DGP is to improve the insufficient representation at German universities, and thus promote teaching and research in respiratory medicine.
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PMID:[100 years DGP -100 years of pneumology in Germany]. 2009 40


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