Abnormalities of lung function have previously been described in patients with impaired αrprotease inhibitor (α1-PI) function and more recently in insulin-dependent diabetic subjects. This study was undertaken to test the hypothesis that impaired α1-PI activity may be implicated in the pathogenesis of lung function abnormalities in young insulin-dependent diabetic patients. Twelve young (16.23 ± 4.51 years), non-smoking insulin-dependent diabetic subjects and 12 reference subjects were evaluated in respect of lung mechanics, absolute serum α1-PI levels and the functional ability of .αi-PI to inhibit elastase. Results of the ventilatory mechanics showed that the mean value for the volume-independent index of lung elasticity Kst(L) was significantly greater in the diabetic group (0.149 ± 0.05 vs. 0.116 ± 0.03; p < 0.05). The absolute serum α1-PI levels in the insulin-dependent diabetic subjects was significantly lower than in reference subjects (1.74 ± 0.11 vs. 2.06 ± 0.09 g/l; p < 0.05). While the specific α1-PI activity of the diabetic sera showed no significant difference from that of the reference sera, the total α1-PI inhibitory activity in the diabetic sera was significantly lower than reference values (201.9 ± 9.7 vs. 246.9 ± 13.5 U/L; p < 0.02). Although these findings indicate impairment of both ventilatory mechanics and α1-PI activity in the insulin-dependent diabetic subjects, the pathogenesis of these findings and their functional implications are at present unknown

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