Emphysema: new concepts

Pathophysiologic and therapeutic concepts concerning lung emphysema are evo lving. The old pathophysiologic concept is based upon the hypothesis that e mphysema is the consequence of an imbalance between the proteases released by neutrophils and the antiproteases shield in the alveolar space that allo ws the destruction of elastin fibers. Recent data suggest (1) that protease s secreted by alveolar. macrophages might be more relevant to the pathogene sis of the disease than that released by neutrophils (2) that collagenolyti c enzymes might participate to the destruction process within the lung as w ell as elastolytic protease, (3) that the repair of elastin and collagen fi bersoccurs in the lung simultaneously to their destruction, at least in ani mal models of emphysema, and (4) that repair is possible in a rat model of elastase-induced emphysema using all trans-retinoic acid. Therapeutic optio ns in human emphysema are also evolving. Increasing the antiprotease alveol ar shield through the intravenous or inhaled administration of alpha-1-anti trypsin in selected patients with genetical alpha-1-antitrypsin deficiency is used worldwide in selected patients despite the lack of scientific evide nce of efficacy. Surgical treatments have been developed in the past 10 yea rs and are currently under investigation. Lung transplantation is used in p atients with severe airway obstruction on lung function tests and functiona lly disabled. Its beneficial effect in terms of survival is not prove but q uality of life is improved with the technique. Lung volume reduction surger y improves dyspnea, lung function and gas exchange in most patients, but lo ng term beneficial effects, selection criteria of die patients are currentl y unknown.