Table 1 Summary of metabolic lung diseases

Pulmonary calcification

Dystrophic or metastatic mechanisms

Deposition of calcium in the alveolar septa

Often asymptomatic

Usually non-diagnostic

Numerous subcentimetre calcified nodules

 Nodular form

Chronic passive congestion

Calcified/ossified intra-alveolar masses

Often asymptomatic

Usually non-diagnostic

Mid to lower lung predominant 1-5 mm calcified nodules

 Dendriform form

Unclear, occurs in areas of chronic lung insult

Branching calcifications affecting the interstitium

Often asymptomatic

Serpentine opacities

Characteristic lower lobe predominant branching delicate calcifications, often in areas of fibrosis

  Pulmonary alveolar microlithiasis

Unclear, association with SLC34A2 gene

Intra-alveolar deposition of microliths

Often asymptomatic, occurs in all age groups

Diffuse small calcified nodules, giving a “sandstorm” appearance. Lucent subpleural line

Diffuse uniform calcified micronodules with a lower lung predominance

  Pulmonary amyloidosis

Extracellular deposition of insoluble beta pleated proteins

All age groups

 Tracheobronchial form

Involvement of trachea and airways

Upper airway obstruction, stridor, dyspnea

Narrowing of the tracheal lumen

Nodules, plaques or wall thickening of the subepithelial trachea, which may be calcified

 Nodular parenchymal form

Lung nodule/mass

Asymptomatic

Peripheral solitary or multiple nodules

Peripheral well circumscribed nodule/s which may be calcified

 Diffuse interstitial form

Amyloid infiltration of pulmonary interstitium

Dyspnea

Reticular markings

Interlobular septal thickening, which may be nodular; calcifications may be seen

  Pulmonary alveolar proteinosis

Mutations in surfactant protein or GM-CSF genes

Intra-alveolar accumulation of surfactant like material

Young to middle aged men, modest clinical symptoms

Drastic appearance with bilateral perihilar airspace disease

Interlobular septal thickening with ground-glass opacities giving a “crazy paving” appearance