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

A total of 4,604 men who were interviewed in Finland in 1962 in connection with the Finnish-Norwegian lung-cancer study were followed-up for lung cancer during 1963-87 to establish why urbanized (via migration) men who smoked had a greater lung-cancer risk than native urban smokers. Exposure to occupational carcinogens was inferred from the title of the longest job held. A clear dose-response relation between occupational exposure and lung cancer was found in the urbanized but not among the native urban dwellers. The extra risk associated with migration to towns and smoking was found especially by those urbanized subjects who worked in heavily exposed industries: their lung cancer risk was more than twice that of native urban men in similar jobs, while those urbanized subjects in academic or clerical jobs showed no increased risk when compared with native urban men in corresponding work. Cardiorespiratory symptoms had a prognostic value in every residential group, but especially among the urbanized. Urbanized men who smoked and worked in heavily exposed industries, and suffered from shortness of breath, had a fourfold risk of lung cancer when compared with native urban smokers without this symptom. We conclude that although the joint effect of smoking and occupational exposure is the main explanatory factor for high risk of lung cancer in urbanized males, environmental and psychosocial factors also may have a contributory effect.
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PMID:Migration to towns, occupation, smoking, and lung cancer: experience from the Finnish-Norwegian lung cancer study. 848 92

During the last 25 years, several hundred papers have been published on the respiratory health effects of environmental tobacco smoke (ETS). Various independent assessments have concluded that ETS causes lung cancer in adult nonsmokers and increases the risk of various noncancer effects, principally in children. The effects on children include pneumonia, bronchitis and bronchiolitis in young children; chronic middle ear effusion; increased frequency and severity of attacks among asthmatics; possible induction of asthma in previously asymptomatic individuals; small reductions in lung function; and symptoms of upper respiratory tract irritation. In nonsmoking adults, ETS exposure is associated with irritation of the eyes, nose, and throat, and with wheezing, symptoms of bronchitis, shortness of breath, and decreased lung function. The results of recent studies not only confirm and strengthen the above findings but also provide strong suggestive evidence that ETS causes sinonasal cancer and is a risk factor for sudden infant death syndrome. To mitigate such a preventable environmental health impact, public health measures to reduce involuntary ETS exposure are warranted.
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PMID:Respiratory health effects of exposure to environmental tobacco smoke. 900 Mar 1

To assess the efficacy and toxicity of an outpatient combination chemotherapy in small-cell lung cancer (SCLC), we treated 70 consecutive patients with epirubicin 80 mg m(-2) i.v. on day 1 and etoposide 200 mg o.d. p.o. on days 1-4 (EE) at 3-weekly intervals. The median age of patients was 64 years (range 39-84). The male-female ratio was 42:28 and 35 (50%) had metastatic disease. Fifty-seven patients were evaluable for response. The overall response rate was 64.4%, including 14 (23.7%) complete responses and 24 (40.7%) partial responses. Median time to progression was 7 months in responders and 8 months in patients with limited disease. The median survival in patients with limited disease was 10.5 months (range 0.5-70 +) and 7 months (range 0.5-24) in those with extensive disease. Improvement of symptoms occurred in 79% of patients with shortness of breath, 80% with cough, 81% with haemoptysis and 68% with pain. In 19 patients an increase in body weight was noted. Major (WHO grade 3/4) toxicities were neutropenia in 13 (18.5%) patients, alopecia in 33 (47.1%) patients, mucositis in 15 (21.4%) patients, anorexia in eight patients (11.4%), nausea and vomiting in six patients (8.5%) and diarrhoea in 4 (5.7%) patients. In conclusion, EE is an active and well-tolerated outpatient regimen in the treatment of SCLC. The survival data in this unselected group of patients were disappointing and the possible explanations for this are discussed.
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PMID:Outpatient treatment with epirubicin and oral etoposide in patients with small-cell lung cancer. 930 64

Whatever facts we gather and no matter how many we have, you and I must eventually put the journal down and pick up our stethoscope, pen, and prescription pad and go to work. Hopefully we can do better than, "Therapy is not uniform and specific antibiotic regimens are usually selected based on local tribal custom." We can discard an old paradigm, "The absence of data bears no relation to the strength of opinion." Personally, I have used these new scientific data before I reached my conclusion. I have developed 10 points to structure my new approach. I invite you to compare my conclusions to yours. 1. In acute bronchitis, in otherwise healthy adults, my preference is to not prescribe an antibiotic. If I do, it is not over the phone. You should want to see and examine the patient. If there are no helpful hints to etiology, I choose a newer macrolide for those under age 50 and use a short course, five-seven days. For patients over age 50, especially if they are "healthy smokers," consider a short course of cefuroxime. (You can see, even in these acute bronchitis patients, you want an antibiotic effective against today's pathogens.) 2. In all chronic bronchitis patients, prevention of further damage to the airways should be attempted by instituting a program of smoking cessation and appropriate immunizations against influenza and pneumococcus. 3. Treatment outcomes will also improve if we recognize that in some patients the progressing SOB, cough, and increasing sputum production are due to congestive heart failure and not due to infection. I try to think about congestive heart failure in all of my patients, but especially in those with known heart disease and cardiomegaly on their chest x-ray. 4. Routine pulmonary function testing is important in smoking patients. Physicians underestimate the degree of obstruction present when they rely on physical exam alone. Hopefully long before the patient's acute illness you have established whether or not obstruction is present. This information helps identify the high risk patient for not only recurrent bouts of infection but also those at increased risk for lung cancer. 5. We will have more success in treating AECB when we elect to use an antibiotic only for patients with at least two of the following three cardinal symptoms: increased dyspnea, increased sputum production, and increased purulent sputum. COPD patients have many days when they feel more SOB. To use this or any one sign as the sole indication for starting an antibiotic has been proven not to make a statistically significant difference in outcome in most patients. Also, the value of prophylactic antibiotic therapy has not been established. 6. When airflow obstruction is moderately severe or more pronounced, AECB should usually be treated with oral steroids. Other measures such as chronic bronchodilator therapy, supplemental and home oxygen use, and pulmonary rehabilitation have been extensively reviewed elsewhere.
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PMID:Challenging questions in treating bronchitis. 979 74

Optimal management of dyspnea in terminal cancer patients requires an understanding of the responsible pathophysiological mechanisms. This prospective study assessed visual analogue scales (VAS) of shortness of breath (SOB) and anxiety, bedside spirometry, maximum inspiratory pressure (MIP), chest radiography, arterial blood gases, hemoglobin, and electrocardiogram, if indicated, in 100 terminally ill cancer patients. Forty-nine percent of the patients had lung cancer. The median VAS scores for SOB and anxiety were 53 mm and 29 mm, respectively. Spirometry was abnormal in 93% of patients, with 5% having obstructive, 41% restrictive, and 47% mixed patterns. The median MIP was 16 cm H2O. Sixty-five percent of the patients had parenchymal or pleural involvement on chest radiograph. Twenty-nine percent had evidence of cardiac ischemia, recent or current myocardial infarction or atrial fibrillation. Patients had a median of five different abnormalities that could have contributed to their shortness of breath. Only anxiety (p = 0.001), a history of smoking (p = 0.02), and pCO2 levels were statistically significantly correlated with SOB VAS scores. The potentially correctable causes of dyspnea included hypoxia (40%), anemia (20%), and bronchospasm (52%). The finding of very low MIPs suggests severe respiratory muscle weakness may contribute significantly to dyspnea in this patient population. Further studies are needed to confirm this finding and characterize the underlying pathophysiology.
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PMID:Dyspnea in the advanced cancer patient. 1058 52

A 56-year-old woman who had been given oral prednisolone for iridocyclitis by an ophthalmologist received a diagnosis of pulmonary sarcoidosis on the basis of transbronchial lung biopsy findings, and began receiving therapy at our hospital on an outpatient basis. Chest X-ray films disclosed hilar lymphadenopathy in both lungs. In addition, Holter electrocardiograms detected ventricular premature beat (Lown 4B) and echocardiograms detected reduced left ventricular wall motion with dilatation of the left ventricular chamber. Cardiac sarcoidosis developed in the patient. She was admitted to our hospital because of shortness of breath on exertion. Chest X-ray films on admission disclosed a large nodular heterogeneous mass in the right upper lobe. Histologically, transbronchial lung biopsy specimens of the mass disclosed an adenocarcinoma. Although lung cancer and sarcoidosis are common, their coexistence in the same patient is not. Furthermore, the coexistence of lung cancer with cardiac sarcoidosis, as in this case, is very rare.
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PMID:[Primary lung cancer (adenocarcinoma) associated with cardiac sarcoidosis]. 1043 50

A 67-year-old male underwent a right upper lung lobectomy for lung cancer in January 1993. Follow-up chest X-rays revealed a progressive and rapidly growing intrathoracic mass in the right thorax. The mass, however, did not resemble a tumor recurrence, and the patient complained only of shortness of breath. Computerized tomography and magnetic resonance imaging confirmed the presence of the intrathoracic mass and its associated compression of the residual lung. A right thoracotomy was performed in January 1998, and a mass found arising from the sympathetic nerve trunk was resected. Microscopic examination revealed stellate or spindle-shaped cells in myxoid stroma with sparsely distributed collagen fibers. Immunohistochemically, the cells were positive for neuron-specific enolase, and the tumor was identified as neurofibroma. The patient did not suffer from von Recklinghausen's disease, and there was no family history of the disease. After resection of the neurofibroma, the compressed lung was able to re-expand, and the patient's shortness of breath disappeared. At one year postoperative, the patient remains well, and there is no evidence of recurrence.
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PMID:A rapidly growing benign intrathoracic neurofibroma after lung lobectomy. 1093 32

The objectives of this study were to determine the prevalence of dyspnea in the general cancer population, the intensity of the symptom as perceived by the patient, and the patient characteristics associated with the presence of dyspnea. Nine hundred and twenty-three cancer outpatients completed visual analogue scales (VAS) and verbal rating scales (VRS-D) to assess the intensity of their dyspnea. Baseline data included variables that were known covariates of dyspnea. Forty-six percent of the patients had some shortness of breath. Only 4% had a diagnosis of lung cancer and 5.4% lung metastases. Risk factors found to be significantly related to the presence of dyspnea were history of smoking; asthma or chronic obstructive pulmonary disease (COPD); lung irradiation; or a history of exposure to asbestos, coal dust, cotton dust or grain dust (P values from 0.001 to 0.038). The prevalence of dyspnea was strongly related to the number of risk factors a patient had (P < 0.0001). The VAS and VRS-D were significantly correlated, establishing concurrent validity for the VRS-D.
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PMID:Dyspnea in cancer patients: prevalence and associated factors. 1122 61

A 68-year-old woman was admitted to our hospital in 1998 with shortness of breath on exertion. On the first admission, chest radiography revealed multiple nodular shadows and areas of ground-glass appearance mainly in the basal lung fields, and chest CT scans showed multiple thin-walled cystic lesions in both lung fields. Bronchioloalveolar carcinoma was diagnosed by transbronchial lung biopsy. The CA 19-9 level in the serum was abnormally high. The disease progressed, and the patient died 7 months after diagnosis. We report this case because CT scans showed multiple cystic lesions, which is very rare. The mechanism of cystic formation in this case of lung cancer may have involved disruption of the alveolar structure and enlargement of disrupted spaces or of the check valve mechanism.
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PMID:[A case of bronchioloalveolar carcinoma with multiple cystic shadows on chest CT]. 1143 12

Classical radiation pneumonitis has been described after single dose whole lung irradiation in experimental animals where above a threshold dose of irradiation, there is a sigmoid dose response curve with increasing morbidity and mortality. After clinical fractionated irradiation, however, acute radiation pneumonitis consisting of cough shortness of breath and patchy radiological changes, occurs in <10% of patients, has dyspnoea out of proportion to the volume of lung irradiated and usually resolves completely without long-term effects. There is increasing evidence that this represents a bilateral lymphocytic alveolitis or hypersensitivity pneumonitis and has been termed sporadic pneumonitis. Late radiation toxicity results in pulmonary fibrosis. This is a consequence of repair, which is initiated by tissue injury within the radiation portal. It follows release of chemotactic factors for fibroblasts including transforming growth factor-beta, fibronectin and platelet derived growth factor. Radiation fibrosis is the clinically more significant syndrome for patients. It may result in progressive dyspnoea and mortality in patients. The most predictable change in laboratory lung function tests is a decrease in transfer factor due to damage at the capillary-alveolar level. It also results in decreased lung compliance, which will affect the total lung capacity and the forced vital capacity. The forced expiratory volume in 1 s is less affected, although this seems to depend on the volume of lung irradiated. There is also a decrease in perfusion in the irradiated lung. Radiation fibrosis seems to depend, amongst other factors, on the volume of lung, which is irradiated above a threshold of 20-30 Gy. The morbidity of radiation fibrosis may therefore be minimized by the use of dose volume histogram to minimize the volume of normal lung irradiated in patients at high risk, e.g., patients with who present with poor lung function. The importance of the baseline perfusion in the irradiated areas continues to be studied.
Lung Cancer 2002 Feb
PMID:Lung toxicity following chest irradiation in patients with lung cancer. 1180 81


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