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CT of the lungs in patients with pulmonary emphysema.

Pulmonary emphysema is a pathological diagnosis. The clinical diagnosis of emphysema can be difficult because correlations between results of lung function tests and the extent of emphysema are poor. Features of chronic bronchitis or asthma may overlap with emphysema, making the clinical diagnosis more challenging. Nonetheless, the diagnosis of pulmonary emphysema can be made with relative confidence on the basis of clinical and radiological criteria. Despite not detecting mild emphysema and underestimating the severity of disease, CT--and high-resolution CT in particular--is the best noninvasive modality for detecting or corroborating pulmonary emphysema. This review focuses on several important aspects of pulmonary emphysema: (1) the definition and pathological characterization, (2) techniques of CT imaging, (3) CT findings and their correlation with pathophysiological data, and (4) quantification with CT.

Humans↗

The vasculature as a target in the treatment of pulmonary emphysema.

Pulmonary emphysema, a major component of chronic obstructive pulmonary diseases, is a highly prevalent progressive tissue-destructive disease, with no effective treatments. The interplay between inflammation, matrix proteolysis, oxidative stress and apoptosis might account for the irreversible progression of the disease. Recent investigations have underlined the importance of the lung vasculature in the pathobiology of chronic obstructive pulmonary diseases offering new therapeutic strategies. This review will focus on the pulmonary microvessels as a target in the treatment of pulmonary emphysema.

Animals↗

How a test for elastic fiber breakdown products in sputum could speed development of a treatment for pulmonary emphysema.

Pulmonary emphysema is a devastating disease for which there is no effective treatment. The development of therapeutic agents for this disorder has been hampered by the lack of clinical or biochemical tests which can rapidly evaluate drug efficacy. Since emphysema is associated with degradation of elastic fibers, the authors propose measuring the content of the elastin-specific amino acids, desmosine and isodesmosine, in sputum as a more immediate means of monitoring therapeutic interventions. Sputum samples would be chemically degraded to separate the component amino acids of elastic fibers, then measured for the total quantity of desmosine and isodesmosine, using any one of a number of established methods for quantifying these compounds, including radioimmunoassay, chromatography, or mass spectrometry. Such techniques allow for detection of nanogram quantities of desmosine and isodesmosine, and the procurement of ample amounts of induced sputum from the lower respiratory tract should improve the chances of detecting these amino acids. If proven valid, such a test could serve as a convenient marker for assessing lung injury in pulmonary emphysema, thereby facilitating rapid evaluation of new forms of treatment for this disease. The test might also prove to be a useful screening procedure for persons who smoke or otherwise have a greater than normal risk of developing emphysema.

Desmosine↗

Defect of hepatocyte growth factor production by fibroblasts in human pulmonary emphysema.

Pulmonary emphysema results from an excessive degradation of lung parenchyma associated with a failure of alveolar repair. Secretion by pulmonary fibroblasts of hepatocyte growth factor (HGF) and keratinocyte growth factor (KGF) is crucial to an effective epithelial repair after lung injury. We hypothesized that abnormal HGF or KGF secretion by pulmonary fibroblasts could play a role in the development of emphysema. We measured in vitro production of HGF and KGF by human fibroblasts cultured from emphysematous and normal lung samples. HGF and KGF production was quantified at basal state and after stimulation. Intracellular content of HGF was lower in emphysema (1.52 pg/mug, range of 0.15-7.40 pg/mug) than in control fibroblasts (14.16 pg/mug, range of 2.50-47.62 pg/mug; P = 0.047). HGF production by emphysema fibroblasts (19.3 pg/mug protein, range of 10.4-39.2 pg/mug) was lower than that of controls at baseline (57.5 pg/mug, range of 20.4-116 pg/mug; P = 0.019) and after stimulation with interleukin-1beta or prostaglandin E(2). Neither retinoic acids (all-trans and 9-cis) nor N-acetylcysteine could reverse this abnormality. KGF production by emphysema fibroblasts (5.3 pg/mug, range of 2.2-9.3 pg/mug) was similar to that of controls at baseline (2.6 pg/mug, range of 1-6.1 pg/mug; P = 0.14) but could not be stimulated with interleukin-1beta. A decreased secretion of HGF by pulmonary fibroblasts could contribute to the insufficient alveolar repair in pulmonary emphysema.

Acetylcysteine↗

Hyperplasia of pulmonary neuroendocrine cells in a case of childhood pulmonary emphysema.

Pulmonary emphysema is very uncommon in children in the first decade of life. The few cases documented in the literature were all due to alpha1-antitrypsin deficiency. We present the case of a 6-year-old white boy with chronic cough and dyspnea on exertion. Lung biopsy showed panacinar type emphysema with patent airways and diffuse hyperplasia of pulmonary neuroendocrine cells revealed after immunostaining for bombesin, a peptide produced by these cells. We speculate that idiopathic diffuse hyperplasia of bombesin-producing pulmonary neuroendocrine cells may contribute to the pathogenesis of unusual COPD in childhood.

Bombesin↗

On defining microcardia: application in pulmonary emphysema.

Pulmonary emphysema was the disease entity from which we derived a definition for microcardia in males. After the fourth decade, a cardiothoracic ratio of 38% or less is considered to represent a small heart. Among male Veterans Hospital patients between the ages of 41 and 83, the probability of an individual without emphysema having a cardiothoracic ratio of 38% or less was under 1%. Microcardia, even as an isolated sign, should make one suspect strongly the presence of subclinical emphysema and to consider instituting a prophylactic regimen. Hearts should be measured to judge not only increased size but decreased size in both patient and examinee groups.

Adult↗

[The clinical study of pulmonary emphysema with pulmonary fibrosis].

OBJECTIVE: Emphysema and interstitial pulmonary fibrosis are two different diseases in clinical manifestation and pathology, but it was noticed that there were cases diagnosed as pulmonary emphysema and pulmonary fibrosis. It is necessary to study the relationship between the clinical aspects of these cases. METHODS: 11 patients with emphysema and pulmonary fibrosis were found in the past five years. Clinical symptoms, radiographic features, arterial blood-gas, lung function testing and computed tomography of the chest were analyzed. RESULTS: These patients had a long history of cigarette-smoking. Their clinical features are those of both emphysema and pulmonary fibrosis. CONCLUSIONS: Although emphysema and interstitial pulmonary fibrosis are two different diseases, they could coexist in some patients. Their clinical features do not like either of the two diseases. HRCT is an important method for discovering the coexistance of pulmonary emphysema and interstitial fibrosis.

Diagnosis, Differential↗

[The effects of the treatment with oxitropium bromide after one month or more in patients with pulmonary emphysema--evaluation of pulmonary function tests, exercise tests, and a questionnaire].

Chronic effects of oxitropium bromide were studied in patients with pulmonary emphysema. Pulmonary function tests, an exercise test, and a questionnaire were used. Seven subjects underwent two successive studies, including a questionnaire on QOL, pulmonary function tests, and an exercise test before and after one month or more of regular inhalation of ocitropium bromide (600 micrograms/day). The complaint of breathlessness was significantly reduced and the ability to perform activities of daily living had improved slightly after the treatment. There were no significant differences in the values of arterial oxygen pressure at rest. The VC, RV/TLC, and peak expiratory flow rate improved. A significant decrease in oxygen uptake at rest, a slight decrease in minute ventilation at rest, and a significant prolongation of exercise time were observed after the treatment. No other changes were noted. We conclude that oxitropium bromide may improve lung mechanics and reduce the work of respiratory muscles.

Administration, Inhalation↗

Subcutaneous emphysema, pneumomediastinum, and pulmonary emphysema in a young schipperke.

A 4-month-old, intact female schipperke was presented for evaluation and treatment of subcutaneous (SC) emphysema. Radiographs revealed pneumomediastinum and SC emphysema. Sequential radiographs confirmed a worsening of the SC emphysema. Extensive, nonsurgical evaluation failed to reveal the source of the air within the mediastinum. Exploratory thoracotomy revealed an emphysematous right middle lung lobe. Lobectomy of the right middle lung lobe resolved both the pneumomediastinum and SC emphysema. Histopathological evaluation confirmed pulmonary emphysema. A variation of congenital pulmonary emphysema was considered in this case.

Animals↗

Pulmonary emphysema followed by pulmonary fibrosis of undetermined cause.

Idiopathic pulmonary fibrosis (IPF) and pulmonary emphysema (PE) have distinct clinical and pathological characteristics, and have been considered to be separate disorders. However, recent animal experiments have suggested that, with regard to their pathogenesis, the diseases have some features in common. However, there are no clinical data supporting this hypothesis. We report here 9 patients (all male, 67 +/- 2 years, mean +/- SE) who had PE followed by IPF. They were found among 152 PE patients who came to Tohoku University Hospital during the past 15 years (1976-1991). All patients were male and heavy smokers and 2 patients also had prostate cancer and gastric cancer, respectively. Three patients were alive during this study and had been diagnosed as having IPF and PE by the combination of transbronchial biopsy, selective alveolobronchogram, CT examination and lung function tests. The diagnosis of IPF and PE in the other patients was based on the pathological findings of autopsied lungs in addition to clinical findings. All patients showed PE mainly in the upper lobes and IPF in the lower lobes. In all patients, in addition to all known causes of pulmonary fibrosis, the possibilities that chronic or recurrent infections in PE induced pulmonary fibrosis and that IPF produced emphysematous changes were carefully excluded by medical records and pathological findings. It is not clear whether the occurrence of emphysema and pulmonary fibrosis in these cases is coincidental, or whether the two diseases are linked by a common pathogenetic pathway.

Aged↗