Alpha-1 Antitrypsin Deficiency — A Missed Opportunity in COPD?

Alpha-1 Antitrypsin Deficiency — A Missed Opportunity in COPD? 


http://cdn.intechopen.com/pdfs-wm/46784.pdf

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Pathogenesis of COPD in MZ heterozygotes. A normal protease/antiprotease balance exists in MM individuals (left panel). Non-smoking MZ individuals have intermediate levels of AAT and increased sputum IL-8 levels and neutrophil counts (middle panel). Reactive oxygen species in cigarette smoke inactivate AAT resulting in a protease/antiprotease imbalance with increased amounts of neutrophil elastase. Polymerisation of Z AAT protein and increased amounts of IL-8 increase neutrophil influx into the MZ lung. An overwhelmed anti-protease defence contributes to the development of COPD (right panel).

Smoking and Alpha-1 Antitrypsin Deficiency

Smoking and Alpha-1 Antitrypsin Deficiency (AATD) 


"If you have AATD, you can develop COPD early in your life and it might progress more rapidly than usual, especially if you smoke. People with AATD who smoke might develop COPD symptoms in their 20s, while people with AATD who have never smoked are more likely to have symptoms over the age of 40. Without AATD, COPD symptoms don’t normally develop until you are over 50."

https://www.blf.org.uk/Page/Alpha-1-antitrypsin-deficiency-A1A
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