Emphysema and AAT Deficiency

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Emphysema is a form of chronic obstructive pulmonary disease (COPD). Emphysema is caused by destruction of alveoli, which leads to reduced surface area for gas exchange. Emphysema also involves a loss of elasticity, which results in trapping of air in the lungs.

Individuals with alpha₁-antitrypsin (AAT) deficiency* are at risk for developing emphysema because of the role that AAT plays in protecting the lungs. Neutrophil elastase (NE), an enzyme which breaks down bacteria, can become destructive of lung tissue if it is not neutralized by AAT.

*Also known as Alpha-1, AAT Deficiency, AATD, A₁-PI deficiency, alpha-1 antiprotease deficiency, A1AD, or hereditary or genetic emphysema.

Individuals with alpha₁-antitrypsin deficiency do not have enough AAT to maintain the balance between AAT and NE, and so have inadequate protection against the damaging effects of NE. This imbalance between AAT and NE can lead to AAT deficiency-related emphysema, sometimes referred to as hereditary emphysema.

AAT-related emphysema results in permanent, progressive damage to the lungs which can become fatal if the progress is not slowed.¹

Patients with AAT-related emphysema and typical emphysema often have similar clinical presentations. Key differentiating factors include age of onset, family history, and presence of extrapulmonary manifestations.

ARALAST [Alpha₁-Proteinase Inhibitor (Human)] is indicated for chronic augmentation therapy in patients having congenital deficiency of A₁-PI with clinically evident emphysema. ARALAST is not indicated as therapy for lung disease patients in whom congenital A₁-PI deficiency has not been established.

Please review the Important Safety Information and the Full Prescribing Information