Hammar S P, Hallman K O
Diagnostic Specialties Laboratory, Bremerton, Wash. 98310.
Chest. 1993 Jun;103(6):1792-9. doi: 10.1378/chest.103.6.1792.
In reviewing pathology materials from patients occupationally exposed to asbestos, we identified eight patients with either localized nodules in their lung or unusual pathologic changes. The chest radiographs of six patients showed isolated parenchymal nodules thought to represent primary neoplasms. In three cases, pathologic examination of these nodules showed intraluminal fibrosis and inflammation of the distal airways, a pattern of change frequently referred to as "bronchiolitis obliterans organizing pneumonitis." In each instance, asbestos bodies were present in association with the fibroinflammatory tissue. In one case, the nodule showed a desquamative interstitial pneumonitis type pattern, and asbestos bodies were present admixed with the alveolar macrophages and occasionally within their cytoplasm. In one case, the nodule was composed of nonspecific inflammation and fibrosis with focal bronchiolitis obliterans and frequent asbestos bodies scattered throughout the area of inflammation and fibrosis, and in another case, necrotizing inflammation association with Aspergillus fungal organisms was identified. Granulomatous inflammation was the dominant pulmonary pathologic change in one patient, and the other patient's lung biopsy specimen showed a diffuse lymphocyte-plasma cell interstitial pneumonitis. The cases reported suggest that asbestos may cause localized lesions in the lung that clinically and radiographically are misinterpreted as cancer and that pathologically show inflammation and fibrosis of the distal airways. In addition, our observations suggest that asbestos may cause granulomatous inflammation, a desquamative interstitial type pneumonitis, and a lymphocytic interstitial pneumonitis type pattern. Our conclusions that asbestos may cause these pathologic changes are supported by case reports in the clinical and pathologic literature, clinicopathologic studies, and by experimental studies.
在回顾职业性接触石棉患者的病理资料时，我们确定了8例肺部有局灶性结节或异常病理改变的患者。6例患者的胸部X线片显示孤立的实质结节，被认为代表原发性肿瘤。在3例中，对这些结节的病理检查显示管腔内纤维化和远端气道炎症，这种改变模式常被称为“闭塞性细支气管炎机化性肺炎”。在每一病例中，石棉小体与纤维炎症组织相关存在。1例中，结节显示脱屑性间质性肺炎类型模式，石棉小体与肺泡巨噬细胞混合存在，偶尔在其胞质内。1例中，结节由非特异性炎症和纤维化组成，伴有局灶性闭塞性细支气管炎，石棉小体频繁散布于整个炎症和纤维化区域，另一例中，发现与曲霉菌属真菌生物相关的坏死性炎症。肉芽肿性炎症是1例患者的主要肺部病理改变，另一例患者的肺活检标本显示弥漫性淋巴细胞 - 浆细胞性间质性肺炎。报告的病例提示，石棉可能导致肺部局灶性病变，在临床和影像学上被误诊为癌症，而在病理上表现为远端气道的炎症和纤维化。此外，我们的观察提示，石棉可能导致肉芽肿性炎症、脱屑性间质性肺炎类型以及淋巴细胞性间质性肺炎类型模式。我们关于石棉可能导致这些病理改变的结论得到了临床和病理文献中的病例报告、临床病理研究以及实验研究的支持。
