[Function tests in pulmonary emphysema].
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Patients with end-stage pulmonary emphysema are usually proposed for either heart-lung or double-lung transplantation. The single-lung transplantation is reversed for patients with pulmonary fibrosis. Patients with emphysema are thought to be unsuitable for single-lung transplantation because of the ventilation-perfusion imbalance that is supposed to occur, the ventilation being preferentially distributed to the native lung when the perfusion is distributed to the transplanted lung. We now report a preliminary success with single-lung transplantation in two consecutive patients with end-stage pulmonary emphysema. Despite the persistence after transplantation of an obstructive syndrome, the clinical status was good, the blood gases were markedly improved, and ventilation-perfusion imbalance did not occur on lung scans. After discharge from the hospital, the patients could return to an almost normal life. Thus, our data support the feasibility of single-lung transplantation in patients with end-stage pulmonary emphysema, and we consider that single-lung transplantation could be the optimal form of lung transplantation in these patients.
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Pulmonary emphysema is defined as abnormal irreversible enlargement of airspaces distal to the terminal bronchioli, accompanied by destruction of their walls and without obvious fibrosis. It occurs usually as a consequence of smoking. Advanced stages of emphysema lead to dyspnea and are associated with airflow obstruction, hyperinflation and reduced diffusing capacity. Measures that have been shown to alter the course of the disease are smoking cessation and long-term oxygen administration to correct arterial hypoxemia. Antibiotics, bronchodilators, corticosteroids and rehabilitation may provide symptomatic relief. Surgery is another treatment option for selected cases. Recurrent pneumothoraces resulting from rupture of subpleural bullae may be prevented by thoracoscopic pleurodesis. Large bullae that compress adjacent lung and mediastinal structures may be resected. In selected cases of diffuse advanced emphysema associated with significant hyperinflation, volume reduction by resection of the most destroyed areas of the lungs may improve dyspnea, pulmonary function and exercise tolerance. In severely symptomatic patients with reduced life expectancy due to endstage emphysema, lung transplantation may provide with dramatic symptomatic and functional improvement. If the indications for operation are carefully considered and the intervention is performed by an experienced team, surgery is a valuable treatment modality in certain patients with pulmonary emphysema.
BACKGROUND: The purpose of the study was to determine in a prospective randomized trial the independent short-term physiologic impact of reduction pneumoplasty (RP) on respiratory rehabilitation (RR). METHODS: Sixty patients eligible for RP were randomly selected by computer to receive either RP (n = 30) or comprehensive RR (n = 30). Pulmonary function tests, analysis of blood gas levels, measurement of respiratory muscle strength (maximal inspiratory and expiratory pressures), 6-minute walk test (6MWT), and incremental treadmill test (ITT), were performed at baseline and at 3 and 6 months. RESULTS: Two treatment-related deaths occurred after RP and one after RR. At 6 months dyspnea index, maximal inspiratory pressure, 6MWT, ITT, and PaO2 were significantly improved in both groups whereas forced expiratory volume in 1 second and residual volume were significantly improved only in the surgical arm. In addition at 6 months, dyspnea index, 6MWT, maximal ITT, and PaO2 improved significantly more after RP than after RR. CONCLUSIONS: In our study short-term improvements in dyspnea index, oxygenation, inspiratory muscle strength, and exercise capacity occurred after either RP and RR. However dyspnea index, PaO2, and exercise capacity improved more after RP than after RR whereas pulmonary function improved only after RP.
Physical fitness was studied in patients with chronic pulmonary emphysema using Kraus-Weber methods in addition to pulmonary function and exercise tolerance. In Kraus-Weber tests, explosive strength of abdominal muscles in these patients were within the normal range, but both abdominal and back muscle endurance were significantly diminished compared to age-matched controls. On the other hand, flexibility was not different between the patients and the controls, although large variation was present. Exercise performance as assessed by 6 minutes' walk distance in patients was significantly correlated with FEV1.0, DLco and maximal inspiratory mouth pressure, as well as explosive strength of abdominal muscles and abdominal and back muscle endurance capacity. Treadmill walking training for 20 minutes with a load greater than 80% VO2max, twice a week for 2 months was performed in 11 patients with mild to moderate pulmonary emphysema. Six minutes' walk distance (6MD) was significantly prolonged with improvement of back muscle endurance and flexibility. Another walking training consisting of five repetitions of two minutes' near maximal walking and a two minute interval of rest was performed in 6 patients with severe pulmonary emphysema. 6MD tended to increase with improvement of both back and abdominal muscle endurance. However, pulmonary function tests and VO2max showed no significant changes after both types of training. Improved walked distance after the training was significantly correlated with improved VO2 at AT. Furthermore VO2, VE, HR and lactate production during exercise at the same load were significantly decreased compared to pre-training. Dyspnea sensation measured by modified Borg scale during exercise was improved after the training. It is concluded that a physical training program adapted to the condition of the individual patients could improve exercise performance, and should be prescribed in addition to medication.
A case of erythroleukemia coexistent with pulmonary emphysema is reported. A 67-year-old male was admitted to our hospital in May 1981, with a few year history of cough, sputum and fatigue. He had already been diagnosed as having pulmonary emphysema and moderate anemia. On physical examination, except for pallor, no other findings were remarkable. The initial hematological examination showed hemoglobin, 9.6 g/dl, red cell count, 251 x 10(4)/microliters, platelet count, 7.3 x 10(4)/microliters, white cell count, 2600/microliters with neither myeloblasts nor erythroblasts. A sternal marrow aspiration revealed 21% myeloblasts and 40% erythroblasts including 7.5% megaloblastoids. Periodic Acid Schiff staining was strongly positive for a part of erythroblasts. A chest X-P finding was typical for pulmonary emphysema. Pulmonary function was moderately damaged. He was started on chemotherapy with AAAP (ACNU 50 mg/d i.v. drip over 4 hr x 4d, adriamycin 20 mg/d i.v. push x 4d, Methotrexate 20 mg i.v. push x 4d). The first course of AAAP brought him a complete remission with both disappearance of myeloblasts and erythroid precursors with megaloblastoid nuclei in the marrow and the normalization of white cell count and platelet count in the blood. He was discharged in September 1981 after completion of a consolidation chemotherapy with AAAP. Since then, he received two courses of AAAP as an intensification chemotherapy and has been in complete remission for more than 13 months. His pulmonary function has not been affected and no myocardial damage has been seen throughout AAAP therapy. Thus, AAAP therapy seems to be an excellent chemotherapy even for an aged patient with erythroleukemia.
Chronic obstructive pulmonary disease (COPD) is characterised by chronic inflammation of the airways and progressive destruction of lung parenchyma, a process that in most cases is initiated by cigarette smoking. Several mechanisms are involved in the development of the disease: influx of inflammatory cells into the lung (leading to chronic inflammation of the airways), imbalance between proteolytic and anti-proteolytic activity (resulting in the destruction of healthy lung tissue) and oxidative stress. Recently, an increasing number of data suggest a fourth important mechanism involved in the development of COPD: apoptosis of structural cells in the lung might possibly be an important upstream event in the pathogenesis of COPD. There is an increase in apoptotic alveolar epithelial and endothelial cells in the lungs of COPD patients. Since this is not counterbalanced by an increase in proliferation of these structural cells, the net result is destruction of lung tissue and the development of emphysema. Data from animal models suggest a role for Vascular Endothelial Growth Factor (VEGF) in the induction of apoptosis of structural cells in the lung. Other mediators of apoptosis, such as caspase-3 and ceramide, could be interesting targets to prevent apoptosis and the development of emphysema. In this review, recent data on the role of apoptosis in COPD from both animal models as well as from studies on human subjects will be discussed. The aim is to provide an up to date summary on the increasing knowledge on the role of apoptosis in COPD and pulmonary emphysema.
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