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In order to elucidate the development of fibrosis and remodeling in the lung with sarcoidosis, we examined sixty-six autopsy lungs. The autopsy cases consisted of 20 pulmonary sarcoidosis, 31 cardiac sarcoidosis, 3 neurosarcoidosis and 12 sarcoidosis without predominant specified organ involvement. Fibrosis derived from granulomas, which was especially localized at the bronchiole and interlobular septae, developed stellate in 77% and band-like fibrosis in 42% of the 66 cases of sarcoidosis. Bronchovascular bundle fibrosis was frequently observed (58%) with accompanying peribronchial atelectasis and may play an important role in the mechanism of the upper lobe contraction. Destruction of lamina elastica of blood vessels involved by granulomata was seen in these fibrous lesions. Upper lobe contraction was seen in 65% of pulmonary sarcoidosis and 32% of cardiac sarcoidosis. Cavitation was seen in the upper lobe in 9 cases of pulmonary sarcoidosis, and aspergillosis was complicated in 8 cases among them. The main cause of cavitation and cystic lesions is considered to be stenosis of the segmental and subsegmental bronchi with granulomatous involvement and peribronchial fibrosis, and further check-valve mechanism of bronchiolar involvement of granulomata and fibrosis. Honeycomb lesion was observed in 50% of pulmonary sarcoidosis. The pathogenesis of honeycomb lesion in pulmonary sarcoidosis is considered to be developed from granuloma to fibrosis in the respiratory bronchiole and alveolar duct wall and periphery of the lobule adjacent to the interlobular spaces and fibrosing alveolitis. In conclusion, the confluence and extent of granulomata in the pulmonary parenchyma, vascular and lymphatic involvement and atelectasis may play important roles in the remodeling of pulmonary sarcoidosis.
- 日本サルコイドーシス/肉芽腫性疾患学会の論文
日本サルコイドーシス/肉芽腫性疾患学会 | 論文
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