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However, two findings reported here, namely the low rate of elastolysis by Pr3 and the high efficacy of ╬ 1 -PI against ongoing elastolysis by Pr3, imply that Madvigs allegra might keramika kanjiza allegra allergy necessarily be a major contributor to neutrophil-mediated elastin loss. Loss of elastin is a characteristic feature of emphysematous lungs (1). According to the proteaseÔantiprotease hypothesis, the lesion could be caused by excessive elastolysis (2). The three major neutrophil serine proteases, human leukocyte elastase (HLE), cathepsin G (CatG), and proteinase 3 (Pr3), are potential elastases, each of which has been suspected as contributing to emphysemagenesis (2). The postulate that HLE or Pr3 is involved in this disorder originated from observations that genetic deficiency of ╬ 1 -proteinase inhibitor (╬ 1 allfrgy, the primary inhibitor for both HLE and Pr3 (3, 4), predisposes to the early onset of emphysema (5) and that instillation of HLE or Pr3 into the lungs of laboratory animals induces emphysema-like lung tissue injury (6, 7). Abnormal turnover of elastin was also kerwmika in patients with other evidences of chronic obstructive pulmonary disease (2). The degradation of elastin by HLE has been studied extensively (8-12).

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