Alpha 1 Antitrypsin

Alpha 1 antitrypsin (AAT) deficiency leads to lung destruction and the formation of emphysema by uncontrolled neutrophil elastase. Replacement of AAT by recombinant AAT (rAAT) given intravenously (IV) is the currently accepted treatment. Early evaluation of aerosolized AAT documented adequate alveolar fluid AAT and penetration into the lung interstitum [145]. A neutrophil elastase inhibitor, secretory leukocyte protease inhibitor, has also been considered for protection against elastase in CF and patients with AAT deficiency. Delivery to CF patients showed good penetration to well-ventilated areas but little to poorly ventilated areas, a finding that is not surprising [146]. In normal volunteers studied 36 hours after AAT inhalation, the half-life of AAT in bronchoalveolar fluid was 69 hr, the level was twice baseline, and the half-life of antineutrophil elastase activity was 53 hr [147]. It would also be useful to know the level achieved in AAT-deficient individuals. Patients with severe AAT deficiency but with milder pulmonary impairment have been studied by isotope scanning methods and have been found to retain sufficient inhaled AAT in the lung periphery [148]. Eventual clinical application of an aerosol approach to treatment of AAT deficiency will depend upon documentation of efficacy. In rare and slowly progressive disorders, documenting the outcome of any therapy will be a great challenge.

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