[Pulmonary fibrosis caused by inhalation: silicosis].
Silicosis is an important disease not only for its prevalence and the degree of pulmonary insufficiency it entails but also because it provides a natural model of interstitial fibrotic disease in the lung which is of known origin. This can, in turn, help us understand the pathogenic nature of a great number of pulmonary fibroses whose cause is unknown. The fifty postmortem studies which we describe correspond to miners who had worked in underground mines in the mountainous region near Cartagena (SE Spain) for times ranging from 5 to 36 years. The autopsies showed that they had been exposed to dust containing abundant metallic particles, particularly iron oxide (mixed dust). Although the pathogenic action was related with silica, it was also clearly modified by the composition of the dust associated with it. The basic lesions which are produced in the lung after inhalation of silica (< 5 microns diameter) are coniosis, fibroconiosis and sclerohyalinosis. The sclerohyalino nodules are characterized by abundant collagenization and hyalinization, different types of which can be distinguished according to the disposition of the collagenous fibres. Nodular lesions gradually grow in size even when exposure to dust has ceased. As they grow they get nearer until they join to form conglomerate masses. When the diameter exceeds 3 cm this is called massive fibrosis. Pulmonary tuberculosis was found in 27% of cases. This took the form of lesions, which could be associated to or independent of silicotic lesions. Besides evolutive nodular lesions, a patient suffering from silicosis may show other unspecific lesions which must be correctly evaluated for a more correct clinical-pathological assessment, since, clinically, the respiratory function may be profoundly affected although such silicotic damage may be not very noticeable by radiological examination. Silicosis of the liver and spleen was not infrequent in the autopsies carried out, with basic lesions in all evolutive states being observed, the most evolved in the spleen. This means that silicosis should be considered as a systemic illness.
Ortuño Pacheco
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Cátedra de Anatomía Patológica, Universidad de Murcia.
D000818:Animals; D004195:Disease Models, Animal; D005290:Ferric Compounds; D006801:Humans; D008099:Liver / Q000473:pathology; D008173:Lung Diseases, Obstructive / Q000209:etiology; D008262:Macrophage Activation; D016676:Macrophages, Alveolar / Q000502:physiology; D008670:Metals; D009784:Occupational Diseases / Q000150:complications / Q000473:pathology; D011009:Pneumoconiosis / Q000150:complications / Q000473:pathology*; D011656:Pulmonary Emphysema / Q000209:etiology / Q000473:pathology; D011658:Pulmonary Fibrosis / Q000473:pathology; D017382:Reactive Oxygen Species; D012189:Retrospective Studies; D012829:Silicosis / Q000150:complications / Q000473:pathology; D012830:Silicotuberculosis / Q000150:complications / Q000473:pathology; D013030:Spain; D013154:Spleen / Q000473:pathology
D005290:Ferric Compounds; D008670:Metals; D017382:Reactive Oxygen Species; C000499:ferric oxide
Fibrosis pulmonares por inhalación: silicosis.