Molecular Biology of the Lung: Volume I: Emphysema and by Steven D. Shapiro (auth.), Prof. Robert A. Stockley (eds.)

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By Steven D. Shapiro (auth.), Prof. Robert A. Stockley (eds.)

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There is a second version of the M 1 variant with valine at position 213 (50%) and both these Ml version have arginine at position 101 and glutamic acid at position 376. The common Z and S variants are derived from M 1 (Ala 213) and M 1 (Val 213) respectively. The M2 variant (19%) has two replacements with histidine at position 101 and asparagine at 376, based on the Ala 213 variant. The M3 variant (10%) is similar but with arginine at position 101. Finally, the M4 variant (1 %) is similar to the Ml (Val 213) with the exception of histidine at position 101 instead of arginine.

Emphysema At ultrastructural examination, disruption of alveolar septa was first seen at 8 months of age. At histological examination, some patchy areas of airspace enlargement with destruction of alveolar septa were seen from 12 months of age onward [36, 49] (Figure 1c). In another study, the lungs of24-month-oldpa mice showed a mild but generalized enlargement of the airspaces associated in some cases with distortion of the alveolar septa [17]. This means that, in these mice, an ai-PI deficiency may lead to both patchy and generalized changes.

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. Again there is a suggestion that a further genetic influence may play a role because the likelihood of a sibling with aI-antitrypsin deficiency developing neonatal jaundice is greatly increased when it has occurred in a first individual [50].

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