COPD
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Exercise intolerance is a hallmark of chronic obstructive pulmonary disease (COPD) and forced expiratory volume in one second (FEV1) is the traditional metric used to define the severity of COPD. However, there is dissociation between FEV1 and exercise capacity in a large proportion of subjects with COPD. The aim of this study was to investigate whether other lung function parameters have an additive, predictive value for exercise capacity and whether this differs according to the COPD stage. ⋯ Diffusing capacity was the strongest predictor of exercise capacity in all subjects. In addition to FEV1, DLCO and IC provided a significantly higher predictive value regarding exercise capacity in COPD patients. This suggests that it is beneficial to add measurements of diffusing capacity and inspiratory capacity when clinically monitoring COPD patients.
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Microalbuminuria is an important risk factor for cardiovascular diseases. Microalbuminuria may be seen due to hypoxemia in patients with chronic obstructive pulmonary disease (COPD). ⋯ Microalbuminuria may be seen in patients with COPD, depending on the severity of disease and hypoxemia. Microalbuminuria in patients with severe COPD should be examined in regular periods for risk of cardiovascular morbidity or mortality.
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Although less well appreciated than pulmonary emphysema, inflammation of the airways is an early and important finding in alpha-1 antitrypsin deficiency (AATD). The spectrum of clinical presentations of airways disease includes cough and wheezing that is frequently diagnosed as asthma. Study of the airways inflammation in sputum or the proximal airways usually reveals neutrophilic inflammation. ⋯ Other phenotypes of varicose and saccular bronchiectasis have been described. Since AAT may impact the course of bacterial, mycobacterial and viral clearance, future studies of the airway microbiota will inform whether airway pathogens are responsible for some pulmonary AATD phenotypes. Whether airways disease improves with AAT augmentation therapy remains unknown.
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Elastases of both the neutrophil and macrophage have been implicated in lung disease initiation and progression. Although it is unlikely that these proteases evolved for the purpose of injuring lung tissue, the elastin-rich connective tissue framework of the lungs appears to be particularly susceptible to the action of elastolytic proteases. Assuming that neutrophil elastase most likely plays a role in the migration of neutrophils toward a site of inflammation and degradation of proteins from invading organisms or other products of the inflammatory response, it is the role of inhibitors of this protease to protect normal tissues from its effects. In alpha-1 antitrypsin deficiency we find an experiment of nature that disrupts this protease-anti-protease balance, resulting in an increased risk of destructive lung disease.
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Biography Historical Article Classical Article
The electrophoretic α1-globulin pattern of serum in α1-antitrypsin deficiency. 1963.