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Pulmonary anatomy and physiology and the effects of COPD.

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States, yet it has received relatively little attention in the literature compared with other leading killers such as cancer and heart disease. To identify, assess, intervene, and care for patients with COPD in the home, a comprehensive understanding of this disease and its effects is imperative. This article discusses the epidemiology of COPD, reviews normal pulmonary anatomy and physiology, and explains the physiological changes to the pulmonary system caused by COPD.

Acute Disease↗

High resolution CT in respiratory bronchiolitis-associated interstitial lung disease.

High-resolution CT findings have been described for several diffuse lung diseases. Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD) is an inflammatory lung disorder associated with cigarette smoking. This condition has only recently been described and distinguished from desquamative interstitial pneumonitis, which it closely resembles. We describe high-resolution CT findings in five cases of biopsy-proven RB-ILD. The findings are variable and range from no detectable abnormality to atelectasis, ground-glass opacities, emphysema, and linear and reticular interstitial abnormalities.

Adult↗

Pulmonary manifestations of systemic lupus erythematosus: review of twelve cases of acute lupus pneumonitis.

Acute lupus pneumonitis was the presenting manifestation of systemic lupus erythematosus in six of 12 cases in this series. The clinical picture was characterized by severe dyspnea, tachypnea, fever and arterial hypoxemia. Radiographic findings included an acinar filling pattern which was invariably found in the lower lobes and was bilateral in 10 of the cases. Studies failed to reveal evidence of infection as a cause of the acute pulmonary infiltrates. All patients were treated with oxygen and corticosteroids; seven received azathioprine. Six patients survived and are clinically well 14 months to four years following their acute illness. Three of these patients have residual interstitial infiltrates with persistent pulmonary function test abnormalities indicating progression to chronic interstitial pneumonitis. Histologic sections of the lungs available from four patients revealed hyaline membranes and interstitial edema (four cases), acute alveolitis (two cases), arteriolar thrombosis (one case) and a prominent lymphocytic interstitial pneumonitis with organizing bronchiolitis (one case).

Acute Disease↗

Coal workers' pneumoconiosis.

Pathologic features and pathogenesis of coal workers' pneumoconiosis are reviewed. Roentenographic aspects of CWP have been examined; it is concluded that there is little or no correlation with physiologic abnormalities, and no abnormality is pathognomonic of this condition. It is suggested that coal workers who are physiologically disabled by any condition, usually heart disease or chronic obstructive pulmonary disease or both, be retired via an industry-government compensation plan. Chest roentgenograms should serve only to identify and retire those miners who have progressive massive fibrosis, and to identify those who have simple CWP; thus they may be moved to jobs in areas of the mine where dust concentrations are lower.

Chronic Disease↗

Autoimmunity and interstitial lung disease.

PURPOSE OF REVIEW: The pathogenesis of idiopathic pulmonary fibrosis as well as that of several other interstitial lung diseases is poorly understood. The role of autoimmunity in interstitial lung diseases associated with connective tissue disorders such as systemic sclerosis, systemic lupus erythematosus, and rheumatoid arthritis as well as the vasculitides is well established. There is at least some evidence in the literature that supports the role of autoimmunity as one of the mechanisms of alveolar injury responsible for idiopathic pulmonary fibrosis. This review is an attempt to summarize the studies on this subject. RECENT FINDINGS: Repeated extraneous insults and exposures are considered to be responsible for recurrent alveolar injury, inflammation, dysregulated tissue repair, and fibroproliferation resulting in pulmonary fibrosis. The presence of autoantibodies in the sera of patients with idiopathic pulmonary fibrosis has been demonstrated in a few studies. Several autoantibodies, including anti-Sm antibodies, antibodies to U1 ribonucleoproteins, and antibodies to U3 ribonucleoproteins, have been demonstrated in connective tissue disorders, many of which are associated with interstitial lung involvement. Autoimmunity has been also suggested as a possible mechanism of rejection caused by bronchiolitis obliterans after lung transplantation. SUMMARY: It might seem that the role of autoimmunity in interstitial lung disease has been underestimated or even underinvestigated. The subject requires further investigation, especially with regard to the problems of lung allograft rejection due to bronchiolitis obliterans of nonalloimmunity origin and the failure of patients with idiopathic pulmonary fibrosis to respond to most forms of currently available therapy.

Antirheumatic Agents↗

Chip pile workers and mould exposure. A preliminary clinical and hygienic survey.

Chip pile workers are exposed to high concentrations of airborne mould spores. Few sporadic cases of allergic alveolitis have been reported in Finland. Eight non-smoking workers, six on chip piles and two on bark piles, were examined to study the immunological and clinical response to continuous mould spore exposure. The spore exposure ranged between 10(4) and 10(5) spores/m3. Three of the six chip pile workers had precipitating serum antibodies against Aspergillus fumigatus. The three antibody-positive workers had a tendency to decreased total pulmonary diffusion capacity and vital capacity. Significant respiratory symptoms were not noted. Long-term spore exposure may include an occupational health risk to chip pile workers.

Adult↗