AIMS: The histopathology of the Sauropus androgynus (SA)-constrictive bronchiolitis obliterans (BO) is still controversial. A recent report using pneumonectomy specimens showed that the major histopathology was obliterative arteriopathy with segmental necrosis of small bronchi instead of constrictive BO as previously described. METHODS AND RESULTS: We analysed semiquantitatively and immunohistochemically the histopathology of one pneumonectomy and four biopsies specimens of SA-associated lung disease. We found a significant number of constrictive and obliterative bronchioles 1 mm or less in diameter and segmental inflammatory destruction with complete luminal obliteration of the bronchi less than 3 mm in diameter in the pneumonectomy specimen (37% and 25%, respectively). Fibromuscular intimal sclerosis of the bronchial arteries was identified in 15% of the bronchi 4 mm or less in diameter. The inflammation in these airways was composed predominantly of T-lymphocytes, macrophages, mast cells and eosinophils. They were present throughout the evolutionary stages of the bronchiolitis ranging from early oedematous to the late fibrotic obliterative stage. Double immunohistochemical stains revealed negative proliferative cell nuclear antigen for most of the T-lymphocytes and macrophages but positive for fibroblasts. CONCLUSIONS: A more accurate histopathological designation of the SA-associated lung disease should be constrictive obliterative bronchitis/bronchiolitis, with the participation of T-lymphocytes, macrophages, mast cells, eosinophils and fibroblasts in its morphogenesis. The persistent accumulation of inflammatory cells was mediated predominantly by continued recruitment to the site of injury from the bloodstream, resulting eventually in the irreversible fibrosis of the bronchioles and the bronchi less than 3 mm in diameter. Obliterative arteriopathy is suspected of being only an indirect contributing factor.
AIMS: The histopathology of the Sauropus androgynus (SA)-constrictive bronchiolitis obliterans (BO) is still controversial. A recent report using pneumonectomy specimens showed that the major histopathology was obliterative arteriopathy with segmental necrosis of small bronchi instead of constrictive BO as previously described. METHODS AND RESULTS: We analysed semiquantitatively and immunohistochemically the histopathology of one pneumonectomy and four biopsies specimens of SA-associated lung disease. We found a significant number of constrictive and obliterative bronchioles 1 mm or less in diameter and segmental inflammatory destruction with complete luminal obliteration of the bronchi less than 3 mm in diameter in the pneumonectomy specimen (37% and 25%, respectively). Fibromuscular intimal sclerosis of the bronchial arteries was identified in 15% of the bronchi 4 mm or less in diameter. The inflammation in these airways was composed predominantly of T-lymphocytes, macrophages, mast cells and eosinophils. They were present throughout the evolutionary stages of the bronchiolitis ranging from early oedematous to the late fibrotic obliterative stage. Double immunohistochemical stains revealed negative proliferative cell nuclear antigen for most of the T-lymphocytes and macrophages but positive for fibroblasts. CONCLUSIONS: A more accurate histopathological designation of the SA-associated lung disease should be constrictive obliterative bronchitis/bronchiolitis, with the participation of T-lymphocytes, macrophages, mast cells, eosinophils and fibroblasts in its morphogenesis. The persistent accumulation of inflammatory cells was mediated predominantly by continued recruitment to the site of injury from the bloodstream, resulting eventually in the irreversible fibrosis of the bronchioles and the bronchi less than 3 mm in diameter. Obliterative arteriopathy is suspected of being only an indirect contributing factor.