British Journal of Industrial Medicine 1985;42: 350-353

Short reports

Asymmetric rapidly progressive lung fibrosis: a cause

of pseudotumour in asbestosisW 0 C M COOKSON,' J J GLANCY,2 AND F A FROST3

From the Departments ofRespiratory Medicine, ' Diagnostic Radiology,2 and Pathology,3 Sir CharlesGairdner Hospital, Perth, Western Australia

Malignant neoplasia of the lung or pleura is a com-mon and serious complication of exposure to asbes-tos' and necessitates careful surveillance of those atrisk. The assessment of a pulmonary mass lesionafter exposure to asbestos is complicated by theoccurrence of pulmonary "pseudotumours." Theseresult from pleural fibrosis and entrapment of thelung parenchyma (Blesovsky' s syndrome.2 3) . Wereport asymmetric rapidly progressive fibrosis of theupper lobe of the lung as another cause of apparentlung malignancy after exposure to asbestos.

Case report

A 38 year old man was investigated for an enlargingopacity in the right upper lobe. Eighteen yearsbefore presentation he had worked for 12 months inthe crocidolite mill at Wittenoom Gorge in WesternAustralia. Five years before presentation, a chestradiograph first showed evidence of silicoasbestosisand he subsequently had frequent radiographicexaminations of his chest. He admitted to breath-lessness on mild exertion but had no cough orhaemoptysis. He had smoked 20 cigarettes aday from the age of 18. He had a history of renalcalculi and migraine headaches but took no medica-tion. He had worked as a barman and hotelier sinceleaving the asbestos industry. On examination hewas fit, tall, and thin. Apart from a reduced expan-sion on the right there were no abnormal physicalfindings in the chest. There was no lym-phadenopathy and no abnormalities were found onexamination of the cardiovascular system or abdo-men.The haemoglobin, white cell count, and platelet

Received 20 August 1984*Accepted 17 September 1984

count results were all normal. Results of serum elec-trolytes, serum proteins, and liver function testswere also normal. The vital capacity was 57 1 (pre-dicted 4-5 + 0-6 1) and the forced expiratory volumein one second was 3.3 1 (predicted 3-7 + 0-5 1). Thetransfer factor of the lung for carbon monoxide was16-5 ml/min/mm Hg (predicted 30*9 + 5 1 ml/min/mm Hg). The earliest abnormalities on chest radiog-raphy had been diffuse reticulonodular opacities inthe mid and upper lung fields (fig 1). An initiallysymmetric confluence of opacities in both upperlobes (fig 2) had been followed by progressive andquite asymmetrical enlargement of a mass in theright upper lobe (fig 3). Needle aspiration biopsyshowed bronchial epithelial cells, macrophages,asbestos bodies, and debris. No abnormality wasfound on rigid bronchoscopy. At thoracotomy theupper lobe was found to be shrunken, fibrotic, andcontracted to the size of a cricket ball, with the mid-dle and lower lobes correspondingly expanded. Thepleural cavity was free of adhesions. There weremultiple small white raised areas 1 mm in diameterscattered over the pleural surface of the right upperlobe. A right upper lobectomy was carried out.The resected portion of lung measured 6 5 cm in

diameter and was grey and firm. Microscopically,the normal lung architecture was effaced by nodulesand irregular bands of fibrous tissue consisting of amixture of dense collagenous hypocellular fibrosiswith other areas showing a vigorous cellular fibro-blastic proliferation. Some birefringent silica parti-cles were present in the hyaline nodules, but themost striking observation was the large number offerruginous bodies entrapped in fibrous tissue andalso located in residual alveolar spaces in associationwith numerous macrophages (fig 4). The changeswere attributed to silicoasbestosis with an exuberant

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Asymmetric rapidly progressive lung fibrosis: a cause ofpseudotumour in asbestosis

Fig 1 Fine opacities in mid and upperzones. Opacites in apices are becomingconfuent and horizontal fissure is raised alittle. Lung bases are normal.

Fig 2 Mid and upper zone opacitiesbecoming larger and denser. Appearancesare those usually associated with silicosisand early progressive massive fibrosis.

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Cookson, Glancy, and Frost

Fig 3 Clearly defined mass in right apex.Pronounced contraction ofright upperlobe evidenced by raising ofhilum andfurther raising ofhorizontal fisure.

.. a .-...-vW AFl!~., C;-'~~:

Fig 4 Complete destruction ofnormal architecture by hyaline fibrosis and cellular fibroblastic zones.Numerous ferruginous bodies occupy right halfoffield. (Haematoxylin and eosin, x 220). Inset: (a)Birefringent silica particles using polarized light (x 100), (b) ferruginous (asbestos) body (x 380).

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Asymmetric rapidly progressive lung fibrosis: a cause ofpseudotumour in asbestosis

fibrous tissue response. There was no evidence of aneoplastic process.

Discussion

The radiographic appearances of this man's lesionmimicked carcinoma of the lung, and were

sufficiently sinister to prompt thoracotomy andlobectomy. Although the radiograph suggestedsilicosis, with a predominance of small roundedopacities in an upper zone distribution, his industrialexposure was to asbestos fibre in far higher propor-tion than to -silica dust.4 The degree of deficit intransfer factor of the lung, and the histologicalappearances of the resected lobe also showed asbes-tosis to be present.

Progressive massive fibrosis of the lungs afterexposure to asbestos is uncommonS 6 and is often inassociation with some exposure to silica, as in thiscase. Upper lobe fibrosis in the absence of overtpneumoconiosis may also follow exposure to asbes-tos.78 These processes are usually bilateral andslowly progressive, by contrast with the rapidlyincreasing size of the lesion (despite the long periodsince the cessation of exposure) and the asymmetry

of the upper lobe involvement which contributed tothe suspicion of malignancy in this case.Asymmetric progressive massive fibrosis of an

upper lobe of the lung should be considered asanother cause of apparent malignancy in the dif-ferential diagnosis of large radiographic opacities inpatients with asbestos related pulmonary fibrosis,particularly if there has been concomitant exposureto silica.

References

'Doll R. Mortality from lung cancer in asbestos workers. Br J IndMed 1955;12:81-6.

2 Blesovsky A. The folded lung. Br J Dis Chest 1966;60: 19-22.3Hillerdal G, Hemmingsson A. Pulmonary pseudotumours and

asbestos. Acta Radiol [Diagn] 1980;21:615-20.McNulty JC. Asbestos mining, Wittenoom, Western Australia.

First Australian Pneumoconiosis Conference. Sydney: JointCoal Board 1968:1-10.

5 Solomon A. The radiology of asbestosis. S Afr Med J1969;43:847-51.

6 Solomon A, Goldestein B, Webester I, et al. Massive fibrosis inasbestosis. Environ Res 1971;4:430-9.

Green RA, Dimcheff DG. Massive bilateral upper lobe fibrosissecondary to asbestos exposure. Chest 1974;65:52-5.

Hillerdal G. Asbestos exposure and upper lobe involvement.AJR 1982; 139:1163-6.

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