Corrin B, Dewar A, Rodriguez-Roisin R, Turner-Warwick M
J Pathol. 1985 Oct;147(2):107-19. doi: 10.1002/path.1711470206.
Lung biopsies from 17 patients with cryptogenic fibrosing alveolitis of a cellular rather than fibrotic pattern were examined by transmission electron microscopy in the hope that such cases would show features of pathogenetic significance. Further selection was made by choosing minimally affected areas. There was no ultrastructural evidence of immune complex deposition but alveolar epithelial and capillary damage was frequently found (17 and 14 of the 17 cases respectively). Alveolar epithelial injury consisted of patchy necrosis and regenerative hyperplasia. Alveolar capillary injury consisted of cytoplasmic swelling and basement membrane thickening and reduplication. Many of these features have not been emphasized in previous reports and their prominence in early stages of the disease suggest that they may have pathogenetic significance, possible mechanisms of which are discussed. Similar findings identified during the course of this study in 8 asbestos workers suggest that similar pathogenetic mechanisms may operate in asbestosis.
对17例细胞型而非纤维化型隐源性纤维性肺泡炎患者的肺活检组织进行了透射电子显微镜检查，希望此类病例能显示出具有发病机制意义的特征。通过选择受影响最小的区域进行进一步筛选。没有免疫复合物沉积的超微结构证据，但经常发现肺泡上皮和毛细血管损伤（分别在17例中的17例和14例中出现）。肺泡上皮损伤包括片状坏死和再生性增生。肺泡毛细血管损伤包括细胞质肿胀、基底膜增厚和重复。这些特征中的许多在以前的报告中未被强调，它们在疾病早期的突出表现表明它们可能具有发病机制意义，并讨论了其可能的机制。在本研究过程中，8名石棉工人也有类似发现，提示石棉肺可能存在类似的发病机制。
