Abstract
To date, α1-;antitrypsin (α1-;AT) deficiency remains the only proven genetic risk factor for COPD. The homozygous-deficient phenotype is rare (1-;AT it is a genetically complex disease 8. This is as expected given that the pathogenesis of COPD probably involves several cell types, enzymes and inflammatory mediators interacting in an intricate manner to influence the development of airways inflammation and parenchymal destruction.