Luke D. Matar1,
H. Page McAdams1 and
Thomas A. Sporn2
1
Department of Radiology, Duke University Medical Center, Box 3808, Durham, NC
27710. 2
Department of Pathology, Duke University Medical Center, Durham, NC
27710.
Fig. 1A. Microscopic features of hypersensitivity pneumonitis. Low-power
photomicrograph of histopathologic specimen shows diffuse uniform expansion of
pulmonary interstitium by mononuclear inflammatory cells with accentuation of
distribution around small airways. (H and E, x52)
Fig. 1B. Microscopic features of hypersensitivity pneumonitis. High-power
photomicrograph of histopathologic specimen shows interstitial inflammation
accompanied by organizing pneumonia (thick arrow) and multinucleate
giant cell (thin arrow) typical of hypersensitivity pneumonitis. (H
and E, x130)
Fig. 2A. Acute hypersensitivity pneumonitis in 25-year-old man with severe
dyspnea after attic renovation. Chest radiographs (not shown) were normal.
Thin-section CT (1.0-mm collimation), initially interpreted as normal, shows,
in retrospect, subtle centrilobular nodules (arrowhead).
Fig. 2B. Acute hypersensitivity pneumonitis in 25-year-old man with severe
dyspnea after attic renovation. Chest radiographs (not shown) were normal.
Cone-down view of chest CT shows centrilobular nodule in left lower lobe
(arrowhead) more clearly than A. Thoracoscopic lung biopsy
revealed hypersensitivity pneumonitis. Offending antigen was never
identified.
Fig. 3B. Acute hypersensitivity pneumonitis (bird fancier's lung) in
34-year-old man with severe dyspnea. CT scan (1.0-mm collimation) shows
scattered ground-glass opacities. Radiologic and clinical findings resolved
within 5 days of removal of antigen and institution of corticosteroid
therapy.
Fig. 4A. Acute hypersensitivity pneumonitis in 38-year-old woman with acute
dyspnea, hypoxemia, and chills. Chest radiograph shows focal area of
homogeneous opacity (arrows) in right lower lung. Note subtle
heterogeneous opacities in left lower lobe.
Fig. 4B. Acute hypersensitivity pneumonitis in 38-year-old woman with acute
dyspnea, hypoxemia, and chills. CT scan (1.0-mm collimation) shows scattered
areas of consolidation and ground-glass opacities in centrilobular and
bronchovascular distribution. Thoracoscopic lung biopsy revealed
hypersensitivity pneumonitis. Offending antigen was never identified. Clinical
and radiographic findings resolved after institution of corticosteroid
therapy.
Fig. 5A. Acute and subacute hypersensitivity pneumonitis in 36-year-old
woman. (Reprinted from [10])
Chest radiograph at patient's initial presentation with severe dyspnea and
hypoxemia shows bilateral scattered heterogeneous opacities with more focal
homogeneous opacity in lung bases. During patient's hospitalization, all
radiographic and clinical manifestations resolved in several days and patient
was discharged.
Fig. 5B. Acute and subacute hypersensitivity pneumonitis in 36-year-old
woman. (Reprinted from [10])
Full (B) and coned (C) chest radiographs obtained 9 months after
A show diffuse small nodules (arrows) and normal lung volumes.
Patient complained of mild dyspnea at this time.
Fig. 5C. Acute and subacute hypersensitivity pneumonitis in 36-year-old
woman. (Reprinted from [10])
Full (B) and coned (C) chest radiographs obtained 9 months after
A show diffuse small nodules (arrows) and normal lung volumes.
Patient complained of mild dyspnea at this time.
Fig. 5D. Acute and subacute hypersensitivity pneumonitis in 36-year-old
woman. (Reprinted from [10])
CT scan (1.5-mm collimation) obtained at same time as B and C
predominantly shows poorly defined centrilobular nodules (arrows).
Note peripheral well-defined nodule in right upper lobe (arrowhead).
Thoracoscopic lung biopsy revealed hypersensitivity pneumonitis. Offending
antigen was never identified.
Fig. 6A. Subacute hypersensitivity pneumonitis in 22-year-old woman with
progressive dyspnea. Full (A) and coned (B) chest radiographs
show bilateral, diffusely distributed, well-defined small lung nodules. No
adenopathy or pleural fluid is seen. Thoracoscopic lung biopsy found
hypersensitivity pneumonitis. Offending antigen was never identified.
Fig. 6B. Subacute hypersensitivity pneumonitis in 22-year-old woman with
progressive dyspnea. Full (A) and coned (B) chest radiographs
show bilateral, diffusely distributed, well-defined small lung nodules. No
adenopathy or pleural fluid is seen. Thoracoscopic lung biopsy found
hypersensitivity pneumonitis. Offending antigen was never identified.
Fig. 8. Subacute hypersensitivity pneumonitis (bird fancier's lung) in
40-year-old woman with dyspnea. Patient kept more than 200 parakeets. Chest
radiographs (not shown) were normal. CT scan (1.5-mm collimation) shows
scattered ground-glass opacities. Note more well-defined centrilobular nodules
in dependent right lung (arrowhead). These findings suggest diagnosis
of hypersensitivity pneumonitis, which was confirmed at thoracoscopic lung
biopsy.
Fig. 9. Chronic hypersensitivity pneumonitis (bird fancier's lung) in
29-year-old woman with progressive dyspnea. Chest radiograph shows coarse
reticulonodular opacities and volume loss in both upper lobes. Thoracoscopic
lung biopsy revealed hypersensitivity pneumonitis and fibrosis.
Fig. 10A. Chronic hypersensitivity pneumonitis in 61-year-old woman with
progressive dyspnea. Chest radiograph shows bilateral reticulonodular
opacities in mid lung zones and mild loss of lung volume.
Fig. 11A. Chronic hypersensitivity pneumonitis (bird fancier's lung) in
70-year-old man with progressive dyspnea. Patient kept three cockatiels. Serum
antibodies to avian proteins were positive at greater than 1:20,000 dilution.
Chest radiograph shows bilateral coarse reticulonodular opacities,
honeycombing, and volume loss. Note small right pneumothorax after
transbronchial lung biopsy (arrows).
Fig. 11B. Chronic hypersensitivity pneumonitis (bird fancier's lung) in
70-year-old man with progressive dyspnea. Patient kept three cockatiels. Serum
antibodies to avian proteins were positive at greater than 1:20,000 dilution.
CT scan (1.5-mm collimation) with patient prone shows basal honeycombing,
traction bronchiectasis, and architectural distortion. CT findings are
indistinguishable from those of idiopathic pulmonary fibrosis.