DIFFERENTIAL DIAGNOSIS IN THE PATHOLOGY OF ASBESTOSIS

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1 DIFFERENTIAL DIAGNOSIS IN THE PATHOLOGY OF ASBESTOSIS J. Gough Welsh National School of Medicine, Cardiff, Wales, Great Britain The differential diagnosis will be considered under three main headings : 1. The distinction between asbestosis and other forms of diffuse fibrosis : 2. The distinction between asbestosis and pneumoconiosis due to other silicates ; 3. The distinction between asbestos bodies and hemosiderosis of elastic tissue which may mimic asbestosis. The cases in this study did not include asbestos miners in whom there may be a mixture of silicosis and asbestosis. All had their experience in Britain in the manufacture or use of asbestos products. Asbestosis is most frequently found in the lower parts of the lungs but may involve the mid zones and the upper lobes. Sometimes the upper lobe involvement is predominant, the so-called inverse distribution. In such cases the possibility of more than one form of pneumoconiosis being present should be borne in mind. The distinction of asbestosis from other fortti.? of diffuse fibrosis. Asbestosis is diagnosed histologically by the association of asbestos bodies and asbestos fibers with fibrosis. The two components, however, are not necessarily coterminous. For instance, greatly thickened interlobular septa may contain no asbestos bodies or only a few and usually small ones. There is often disproportion between the amount of fibrosis and the number of asbestos bodies present. The fibrosis alone, however, is not diagnostic because histologically it is similar to that of several other diseases. Cystic (honegcoinbl varietu. Asbestosis is most frequently a diffuse fibrosis which may be associated with survival and dilatation of some of the bronchioles and bronchi. This form belongs to the group of conditions classified as honeycomb (cystic) lung. Fibrosis and dilatation of air spaces are common to various forms of honeycomb lung but the distribution of the lesions is useful in identification of different types. Honeycombing is not usually uniform throughout the lung and its distributions is often distinctive. Whole lung sections prepared by the Gough-Wentworth technique are most useful for showing the different distributions. (Gough & Wentworth, 1959 and 1960). In some instances the holes in the honeycomb in asbestosis are small, 1-3 mm. in diameter, the smaller air passages being dilated. In other instances the large bronchi are dilated and the condition may amount to gross bronchiectasis. Diffuse systemic sclerosis (Sclerodermn) is also a form of fibrosis characteristically affecting the bases of the lungs particularly the costophrenic 368

2 Gough : Differential Diagnosis 369 regions where it produces honeycombing (Gough, 1956). Solid patches of fibrosis may occur in other parts of the lungs. The lung changes may be prominent with little or no affection of the skin although in these cases Raynaud s phenomena may be present. Since scleroderma is said to be more common in goldminers (Erasmus, 1957) the possible association of scleroderma with exposure to asbestos should be borne in mind. One of Erasmus s cases had worked in an asbestos mine. Idiopathic diffuse interstitial fibrosis. The commonest form of honeycomb lung in the general population affects the peripheral parts of the lung (Gough, 1959). It involves the subpleural zone to a varying depth up to several crns. The central part of the lung is often spared, there being a sharp division between the affected and the unaffected portions. This idiopathic interstitial fibrosis is also called cirrhosis of the lung, muscular cirrhosis of the lung or chronic Hamman-Rich disease. It is sometimes thought to be related to unusual industrial exposure and the distinction, therefore, from asbestosis may be important. (Spain, 1963). Eosinophilic Xant homatous granuloma leads to honeycomb lung but is unlikely to be confused with asbestosis. It is predominantly in the upper part of the lung although it may extend throughout. If the lesion is active it has characteristic histiocytic cells and collections of eosinophiles. The active phase is most likely to be found in the zone nearest unaffected lung, i.e. at the lower margin of the honeycomb. Coexistent bone lesions or diabetes insipidus help in the diagnosis. Sarcoidosis may give rise to widespread fibrosis which in its healed stage becomes hyalin. Any dust that may have been present in the lung becomes incorporated in this fibrous tissue. Sarcoid fibrosis is known to mimic silicosis. One can imagine that similarly incorporation of asbestos bodies into sarcoid tissue may occur. Rarer forms of honeycomb lung, such as that associated with tuberose sclerosis, are very unlikely to cause difficulty. The affected persons usually have other stigmata, often being mentally deficient. There are, however, established instances in individuals with normal mentality. Solid fibrosis inasbestosis. It must be pointed out that although asbestosis frequently occurs as a diffuse interstitial fibrosis causing honeycomb appearance it may also occur as solid fibrosis and so may simulate other pneumoconioses or other conditions such as carcinoma. Solid fibrotic masses may reach several crns. in diameter and may occur in any part of the lung. As an example I quote the case of H. V. Wingfield, Tehidy Chest Hospital, Cornwall, England, of a man with a mass in the right upper lobe. Bronchoscopy showed a very narrow bronchus. A diagnosis of carcinoma was made and the lung removed. The upper lobe consisted of a mass of dense fibrous tissue and on searching, asbestos bodies were found. The bronchi were extremely thickened by hyaline fibrous tissue. The special localisation in

3 370 Annals New York Academy of Sciences this case was due to organized pneumonia associated with asbestosis. Enquiry from the man produced the information that 25 years earlier he had worked six months as a lagger, insulating pipes in a ship yard. In some cases whole lung sections show solid fibrosis in the upper part of the lung and honeycombing elsewhere, with asbestos bodies in all parts of the lung. Distinction from other forms of silicatosis. Talc, mica and kaolin pneumoconioses do not cause much difficulty. In these, the fibrosis for the most part is either nodular or massive and not of honeycomb type. The occurrence of dust fiber bodies, especially in talc lungs, may, however, lead to a wrong diagnosis, but the enormous amount of doubly refracting dust in talcosis with only few dust fiber bodies is in sharp contrast to asbestosis where there are only few or no doubly refracting fibers and most of the asbestos has been coated to form asbestos bodies. True asbestos may be a natural ingredient of talc and true asbestos bodies may be present in talcosis. In mica lungs the polarising microscope shows what appear to be numerous needle crystals but these are the plates of mica viewed edge on. Distinction from silicosis. There was no difficulty in distinguishing asbestosis from classical silicosis in these cases. There was no nodular whorled fibrosis. Diagnosis of asbestos bodies. Mineral particles of needle shape other than those of asbestos are known to give rise to structures which closely simulate asbestos bodies. They have usually been referred to as curious bodies. A more suitable generic name is desirable. I will refer to them as mineral fiber-bodies. Other than in asbestosis I have seen them most frequently formed from spicules of coal. The most important differential diagnosis is, however, from bodies having a similar appearance but formed from the elastic tissue of the lung. This condition is hemosiderosis of the elastic tissue, sometimes called simply elastosis. It is found in association with pulmonary hypertension and appears to be related to interstitial hemorrhage. It has been noted most frequently in relation to mitral stenosis but it may occur in a wide variety of chronic lung diseases, including cases of pulmonary fibrosis. Elastic tissue in blood vessels and in the framework of the lung becomes fragmented and coated with yellow material similar in appearance to that of asbestos bodies. I propose to call these elastosis bodies. Clubbing of the ends of the bodies is common. As with asbestos bodies giant cell reaction is present. These pseudo-asbestos bodies can sometimes be identified by staining the elastic tissues. When the elastic tissue bodies have been present for a considerable time the fiber loses the property of staining as elastic tissue but its outline is still visible and is then all the more likely to be mistaken for an asbestos body. Incineration and treatment with mineral acid will distinguish this condition from asbestosis. In unstained sections both asbestos bodies and

4 Gough : Differential Diagnosis 371 elastosis bodies are luminescent in dark field and phase contrast illumination. After incineration asbestos bodies still show a yellow or orange colored outer layer due to the presence of iron. Treatment with hydrochloric acid removes the iron. The bare asbestos fibers can now be seen. Dark field or phase contrast illumination facilitates finding of the fibers particularly in cases of long standing in which the fibers are fragmented (Beattie, 1960). The condition of hemosiderosis of elastic tissue has been called by Walford and Kaplan (1957) endogenous pneumoconiosis. The name is unfortunate as it implies that it is a dust disease although Walford and Kaplan recognized that it was not of that nature. Rheumatoid asbestosis. Although there are only two cases of rheumatoid asbestosis in the literature the condition is worth mentioning as it can cause a histological puzzle to anyone not knowing the association of rheumatoid disease with pneumoconiosis. The rheumatoid asbestotic nodules are rounded and unless rheumatoid disease is remembered the condition is most likely to be called tuberculosis. The histology is similar to that described by Gough et al. (1955) in coal miners except for the different nature of the dust. Rheumatoid asbestotic nodules in the lung may precede the development of rheumatoid arthritis as in Tellesson s (1961) case where the disease was diagnosed from a lung biopsy although arthritis did not commence until a year later. Summary Asbestosis occurs in two anatomical forms - diffuse and solid fibrosis. The diffuse form leads to honeycomb (cystic) lung. In the diagnosis, distinction is made from other forms of honeycomb lung. Differentiation of asbestosis from fibrosis due to other silicates is not difficult. Hemosiderosis of elastic tissue (elastosis bodies) may mimic asbestos bodies. References BEATTIE, J The Asbestos Body. Oxford Symposium on Inhaled Particles and Vapours. C. N. Davies, Ed. :434. Pergamon Press (1961). ERASMUS, L. D Scleroderma in gold miners on the Witwatersrand with particular reference to pulmonary manifestations. s. African J. Lab. Clin. Med. 3: 209. GOUGH. J Generalised and primarv fibrosis of the lungs. Brit. J. Radiol GOUGH, J Honeycomb lung. Bull. Post-Grad. Com. Med. (Univ. Sydney). 15: 277. GOUGH, J., D. RIVERS & R. M. E. SEAL Pathological studies of modified pneumoconiosis in coal-miners with rheumatoid arthritis (Caplan s syndrome). Thorax 10: 9. GOUGH, J. & J. E. WENTWORTH Correlation of roentgenological and pathological changes in some diseases of the lung. Harvey Lectures 1957/58. Series 53,171. Academic Fress. New York, N. Y. GOWGH, J. & J. E. WENTWORTH Thin sections of entire organs mounted on paper. In Recent Advances in Pathology. 7th Ed. J. & A. Churchill Ltd. London, England.

5 372 Annals New York Academy of Sciences SPAIN, D. M Atypical and newer pulmonary diseases of interest to industry. In Advances in Cardiopulmonary Diseases. Banyai, A. L. & B. L. Gordon Eds. 1: 178. Year Book Medical Publishers. Chicago, Ill. TELLESSON, W. G Rheumatoid pneumoconiosis (Caplan's syndrome) in an asbestos worker. Thorax 16: 372. WALFORD, R. L. & L. KAPLAN Pulmonary fibrosis and giant-cell reaction with altered elastic tissue. A.M.A. Archiv. Path. 63: 75.