By Steven D. Shapiro (auth.), Prof. Robert A. Stockley (eds.)
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Additional info for Molecular Biology of the Lung: Volume I: Emphysema and Infection
Example text
Subsequent familial studies confirmed not only that the deficiency was inherited in what appeared to be an autosomal recessive pattern, but also that this was associated with a very high incidence of emphysema (about 80%). Larger epidemiological studies confirm that subjects with ai-antitrypsin deficiency have a decreased life expectancy and that this decrease was accelerated in subjects who smoked [30]. As smoking has been a well-recognized cause of the development of emphysema, it was believed that, in subjects with ai-antitrypsin deficiency, the additional risk factor of cigarette smoking accelerated the development of lung pathology.
In about 1-2% ofpa mice of our colony, no serum levels of ai-PI could be measured (unpublished results). It would be of great interest to breed these null mutants successfully. 3. Neutrophil Lysosomal Functions and Lung Elastase Burden Similar levels of elastase specific activity were found in neutrophils from pa and control (NMRI) mice. However, when pa neutrophils were tested for their ability to release lysosomal enzymes after stimulation with FMLP/cytochalasin b, only moderate amounts of elastase, cathepsin G and ,B-glucuronidase were detected in the degranulation assay medium.
In children the usual form of presentation is with neonatal jaundice. This is associated with cholestasis that may occur between 4 days and 2 months after birth, and may last for up to 8 months [49]. Longitudinal studies of subjects with aI-antitrypsin deficiency identified at birth have indicated that abnormal lung function tests can be present in as many as 70% of neonates 6 months after birth, and this falls to less than 10% by the age of 18 [49]. The overall pattern is therefore for the liver problem to regress, although occasionally it may progress to cirrhosis and liver failure.