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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to work out the simplified standard for distinguishing COPD from bronchial asthma. An overall sample of 150 individuals was used for statistical analysis. Sixty one were diagnosed as having COPD and 89 as suffering from asthma. For each patient the modified ATS-DLD-75-C questionnaire was filled out, and laboratory tests results were collected. Laboratory findings included: basic spirometry and flow-volume curve parameters, diurnal PEF variation, tests with bronchodilators (salbutamol, ipratropium bromide and corticosteroids), challenges with histamine and exercise, blood gas analysis, skin tests, chest X-ray, ECG, blood cell count, blood and sputum eosinophilia. Continuous variables were transformed into discrete (dichotomous) ones using commonly accepted threshold values. Then, sensitivity, specificity and accuracy indexes were calculated for each variable and for all possible sets of 2, 3 and 4 variables. Finally, 2 sets of 4 signs and symptoms were selected as the most characteristic of the diseases of interest. Asthma was diagnosed if 3 out of 4 following conditions were present: 1) episodes of shortness of breath and wheezing, 2) smoking index (cigarettes number per day x years of smoking) < or = 200, 3) PC20 < or = 8 mg/ml or delta FEV1 after bronchodilator > or = 15% predicted, 4) diurnal PEF variation > or = 20% predicted. COPD was recognised in the same way on the basis of: 1) productive cough, 2) smoking index > 200, 3) signs of emphysema on the chest X-ray, 4) maximal FEV1 < 80% predicted (after treatment). Diagnosis established using this model was correct in 76% and false (what was very important) in only 2.6% of cases. In the remaining 21% of patients it was uncertain (e.g. both of the diseases confirmed).
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PMID:[Diagnostic standard for differentiation between bronchial asthma and chronic obstructive pulmonary disease]. 1035 85

COPD is a disease manifested by a combination of chronic bronchitis and pulmonary emphysema. The main risk factors of COPD are chronic smoking and genetic dispositions. The current definition of COPD was established in Western countries in the late 1960s and 1970s, but in Japan COPD has long been used as a term for a physiological syndrome showing chronic obstructive airway symptoms including not only chronic bronchitis and pulmonary emphysema, but also asthma, diffuse panbronchiolitis, and even lymphangioleiomyomatosis. This difference in understanding between the West and Japan is probably due to the markedly lower incidence of COPD in Japan. However, increases in the number of patients with pulmonary emphysema from the late 1980s in Japan have been gathering new concern about COPD. In the governmental statistics for 1995, the term COPD was used for the same entity it is used in the West. Also, the Japanese COPD guideline, the definition of COPD is the same as that in the West.
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PMID:[Definition of chronic obstructive pulmonary disease]. 1049 86

Elastase anti-elastase imbalance theory is most important in the pathogenesis of COPD (pulmonary emphysema). Proteolytic activity of neutrophil elastase (NE) plays an important role because of the detachment of cells through proteolysis of extracellular matrix. In addition to proteolytic activity of NE, NE-induced activation of intracellular signaling (MAPK(Erk), Rho and MLCK) participates in NE-induced morphological changes in airway epithelial cells.
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PMID:[Elastase anti-elastase imbalance in the pathogenesis of COPD]. 1049 94

Pulmonary rehabilitation is comprehensive and multidimensional care for patients with COPD and their families. The aim of pulmonary rehabilitation is for patients to achieve and maintain the individual's maximum level of independence and functioning in the communities. Recent investigation of well-designed studies confirmed the efficacy of lower extremity training, upper extremity training, and ventilatory muscle training in some selected patients. Patient education is a essential component. Pulmonary rehabilitation improves exercise tolerance, the symptoms of dyspnea and health-related QOL, and reduce the frequency and period of hospitalizations. Pulmonary rehabilitation programs include assessment and education of patient, exercise training, and chest physical therapy techniques. In our follow-up study in 100 patients with chronic pulmonary emphysema who participated in pulmonary rehabilitation programs, groups that continued exercise more than 30 minutes a day at home, had tendency to escape from progression of dyspnea after 19 months (mean).
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PMID:[Efficacy of pulmonary rehabilitation]. 1049 8

1. The number of heart transplant operations performed in the US decreased by 52 procedures between 1996 (2,344) and 1997 (2,292). The number of lung transplants increased by 118 in 1997 (928). 2. The most frequently reported indication for heart transplantation in the US was coronary artery disease (44.9%). For other thoracic transplants, the most frequently reported indications included cystic fibrosis (36.8%) for double-lung, emphysema/COPD (53.8%) for single-lung and congenital disease (33.9%) for heart-lung transplants. The most frequently reported diagnoses for thoracic transplantation outside the US included cardiomyopathy (50.4%) for heart, cystic fibrosis (31.3%) for double-lung, idiopathic pulmonary fibrosis (32.4%) for single-lung and primary pulmonary hypertension (23.3%) for heart-lung transplants. 3. US heart transplant recipients were predominately male (77.4%), over age 50 (55.9%) and white (82.1%). In contrast, US lung transplant recipients were predominantly female (51.9%), between ages 35-64 (73.4%) and white (89.5%). No meaningful variance from the US recipient demographic profile was noted for the non-US recipients during the same time period. 4. Mean ischemic time showed minimal change for hearts (2 minutes), a sharp increase for heart-lungs (29.5 minutes) and a decrease for lungs (11 minutes) from 1997-1998. 5. The one-year survival rates for thoracic transplants performed in the US were 83.2% for heart, 75.7% for lung and 34.1% for heart-lung in 1997. Five-year survival rates for US thoracic transplants were 66% for heart and 46.4% for lung for transplants performed in 1993. 6. Long-term patient survival rates were: 29.5% at 14 years for heart, 19.4% at 9 years for lung and 26.2% at 11 years for heart-lung recipients. 7. The most important risk factor for mortality of US heart recipients at one month, one year and conditionally at 5 years after transplantation was receipt of a previous heart transplant. Significant short-term risk factors included recipient age and ischemic time. Substantial long-term risk factors included older donor age and donor race. 8. The factors having the most significant impact on lung mortality at all time points were related to either the patient's medical condition (e.g.x, in the ICU prior to transplant, requiring mechanical ventilation) or diagnosis. 9. Mechanical ventilation and previous transplant had the largest impact on heart-lung mortality. 10. For heart and lung recipients, the major cause of rehospitalization during the first year after transplantation was infection alone.
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PMID:Worldwide thoracic organ transplantation: a report from the UNOS/ISHLT International Registry for Thoracic Organ Transplantation. 1050 84

Macrophages are the predominant defense cell in the normal lung and during conditions associated with chronic inflammation such as COPD. However, the role of the macrophage in the development of COPD has been controversial. Scientific evidence from a variety of sources is emerging that supports a primary role for the macrophage in regulating the inflammatory response and tissue destruction associated with COPD. The role of macrophage proteinases in the development of emphysema, a major component of COPD, will be discussed. Shapiro SD. The macrophage in chronic obstructive pulmonary disease.
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PMID:The macrophage in chronic obstructive pulmonary disease. 1055 66

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
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PMID:Lung disease at high altitude. 1063 92

Smoking is overwhelmingly the major cause of chronic bronchitis and emphysema worldwide. Additional risk factors for developing COPD are presented, along with the variables that govern cigarette smoke deposition in the lung. Major paradigms for the pathogenesis of COPD, including the protease-antiprotease and oxidant-antioxidant theories are described, and evidence for impaired reparative mechanisms in the causation of emphysema is noted. A description of the natural history of declining lung function in smokers and in the susceptible subset of smokers that ultimately develop smoking-induced COPD is accompanied by a discussion of the effects of smoking cessation on preservation of lung health. The disordered ventilation and gas-exchange physiology in the cigarette smoke-damaged lung is explained on the basis of the observed morphological changes.
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PMID:Smoking and chronic obstructive pulmonary disease. 1076 90

Chronic obstructive pulmonary disease is a syndrome including illnesses such as asthma, chronic bronchitis, and emphysema. Although these diseases share a common obstructive component, their optimal treatment and prognosis differ. This article examines the salient features of the history, physical exam, pulmonary function tests, and radiological evaluation which may allow the clinician to differentiate the various diseases that make up COPD; thus allowing the clinician to better target the multiple therapeutic modalities available.
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PMID:Differential diagnosis of chronic airflow obstruction. 1083 Nov 46

At least three conditions contribute to COPD. (1) Chronic bronchitis (mucous hypersecretion) is an inflammatory condition in which CD8+ T-lymphocytes, neutrophils, and CD68+ monocytes/macrophages predominate. The condition is defined clinically by the presence of chronic cough and recurrent increases in bronchial secretions sufficient to cause expectoration. There is enlargement of mucus-secreting glands and goblet cell hyperplasia, which can occur in the absence of airflow limitation. (2) Adult chronic bronchiolitis (small or peripheral airways disease) is an inflammatory condition of small bronchi and bronchioli in which there are predominantly CD8+ and pigmented macrophages. The functional defect is difficult to detect clinically but may be recognized by sophisticated tests of small airway function. There is mucous metaplasia, enlargement of the mass of bronchiolar smooth muscle, and loss of alveolar attachments. (3) Emphysema is an inflammatory condition of the alveoli in which T-lymphocytes, neutrophils, and pigmented alveolar macrophages are involved, associated with the release of excessive amounts of elastases. It is defined anatomically by permanent, destructive enlargement of airspaces distal to terminal bronchioli without obvious fibrosis. In contrast, asthma is a clinical syndrome characterized by allergic inflammation of bronchi and bronchioli in which CD4+ (helper) T-lymphocytes and eosinophils predominate. There is increased production and release of interleukin (IL)-4 and IL-5, which is referred to as a Th2-type response. There is usually increased tracheobronchial responsiveness to a variety of stimuli, and the condition is usually manifest as variable airflow obstruction. While differences between COPD and asthma have been highlighted, new data are emerging that indicate there may also be similarities.
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PMID:Comparison of the structural and inflammatory features of COPD and asthma. Giles F. Filley Lecture. 1084 39


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