Serolimus-Induced Secondary Pulmonary Alveolar Proteinosis
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Imaging findings
Serial chest CTs in a young female with graft-versus-host disease (GVHD) following a stem cell transplant show the development and progressive worsening of diffuse, discrete centrilobular nodules, mild bronchial wall thickening, and expiratory air trapping (mosaic perfusion). Over time, subtle septal thickening also becomes visible. Biopsy of the lung nodules confirmed pulmonary alveolar proteinosis (PAP), which resolved following the discontinuation of her serolimus therapy.
Key takeaways
Pulmonary alveolar proteinosis (PAP) is characterized by the intra-alveolar accumulation of surfactant-like phospholipid-rich material. While often idiopathic, secondary PAP can be triggered by immunosuppressive therapies such as serolimus (an mTOR inhibitor), which impairs alveolar macrophage function. Uniquely, early or drug-induced PAP can present on CT as a predominantly centrilobular nodular or tree-in-bud pattern rather than classic geographic "crazy-paving," and can improve or resolve completely upon cessation of the offending drug.
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