Revue des maladies respiratoires
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Computed tomography, and particularly high-resolution computed tomography, allows a detailed exploration of the pulmonary parenchyma. We discuss here work on the use of this technique in the diagnosis and quantification of pulmonary emphysema. ⋯ We summarize our work which has demonstrated. 1) that the relative surface with density below -950 Hounsfield units and measured on millimetric tomographic slices obtained at the end of maximal inspiration is a valuable measurement of the extent of the macroscopic emphysema and reflects the microscopic emphysema; 2) that subjective quantification overestimates minimally extensive emphysema and shows important intra- and inter-operator variability; 3) that indexes derived from computed tomographic images acquired at the end of expiration reflect more the obstructive syndrome than emphysematous destruction; 4) that age and the size of the lungs influence computed tomographic measurements while hyperinflation appears to have no effect. Finally, we present an example of recent work applying the computed tomographic technique.
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We describe the relationships in Switzerland between two medical specialties, critical, or intensive, care and the respiratory medicine. To date, there are only few direct relationships between these medical fields, and very rarely a respirologist becomes the head of a critical, or an intensive care unit. There are two main reasons explaining this situation. ⋯ Second, intensive care medicine is a full specialty, distinct from anaesthesiology, with a strong structure. However, things are moving, and the general tendency now is to reduce the total number of beds in the Swiss hospitals, and to open some specialised wards under the direct supervision of specialists, including pneumologists. Nevetherless, due to the small size of the country and the important number of decentralised hospital structures, specialised intensive care units, as respiratory intensive care units, are unlikely to be open in the future.
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Cystic fibrosis is a common genetic disorder caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Although the link between the mutations of the CFTR gene and the progressive lung disease is not completely understood, noteworthy advances have been made in the understanding of the mechanisms underlying lung injury in CF. The pathophysiologic cascade starts with CFTR dysfunction resulting from mutations of the CFTR gene, and leading to abnormal ion and water transport across airway epithelia. ⋯ Each of these steps has been elucidated in more detail in the recent years. This is of relevance from a therapeutic viewpoint. New therapeutic interventions include gene therapy, agents that may circumvent the defect in intracellular processing of mutated CFTR, agents that may modulate defects in epithelial ion transport, and anti-inflammatory agents.