Panlobular emphysema is characterized by uniform destruction and
enlargement of the alveoli throughout the entire acinus, affecting all
parts of the lobule equally. It is typically associated with alpha-1
antitrypsin deficiency, a genetic disorder that leads to a lack of
protection against enzymes that break down lung tissue. Unlike
centrilobular emphysema, which predominantly affects the upper
lobes, panlobular emphysema usually involves the lower lobes of
the lungs. The pathogenesis involves chronic enzyme activity that
damages the alveolar walls, leading to loss of elastic recoil,
hyperinflation, and impaired gas exchange. Patients often present
with progressive shortness of breath, exercise intolerance, and
sometimes cough with minimal sputum production. Diagnosis is
made through pulmonary function tests (PFTs) showing airflow
obstruction, and high-resolution CT (HRCT) scans that reveal
widespread, low-density areas due to the loss of lung tissue.
Identifying the underlying cause, such as alpha-1 antitrypsin (Etesami)
