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Some Connective Tissue Disorders of the Lung Margaret Turner-Warwick Cardiothoracic Institute, University of London, Fulham Road, London SW3 6HP, UK

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Some Connective Tissue Disorders of the Lung Margaret Turner-Warwick Cardiothoracic Institute, University of London, Fulham Road, London SW3 6HP, UK Postgrad Med J: first published as 10.1136/pgmj.64.753.497 on 1 July 1988. Downloaded from Postgraduate Medical Journal (1988) 64, 497-504 Some connective tissue disorders of the lung Margaret Turner-Warwick Cardiothoracic Institute, University of London, Fulham Road, London SW3 6HP, UK. Summary: Many connective tissue disorders involve the lungs. The same clinical syndrome may be associated with several distinctive types of pathology in different patients. Fibrosing alveolitis is a common feature of a number of different syndromes. An hypothesis is set out in schematic form which may help to account for some of these differences and emphasizes the potential importance of the pulmonary vasculature in pathogenesis. Introduction The tissues of the lung alone receive virtually the necrotic nodules, pleural effusions, alveolitis or entire venous circulating blood volume coming rarely pulmonary hypertension may each be the from other organs of the body. It is not therefore predominating lesion in different patients. surprising that the lungs are affected in a wide Another current unresolved argument centres on variety of multisystem disorders. In particular it is whether 'cryptogenic' fibrosing alveolitis (CFA) not suprising that an inflammatory response and occurring in association with connective tissue dis- fibrotic reaction in the lung is common to several orders differs from 'lone' CFA (i.e. that condition different connective tissue syndromes including sys- apparently affecting the lungs only) either in its temic rheumatoid arth- natural history or in its response to treatment. lupus erythematosus (SLE), copyright. ritis and systemic sclerosis as well as occurring The question has been considered in a large occasionally in a number of other conditions such retrospective series of 139 patients with 'lone' CFA, as primary biliary cirrhosis, chronic active hepatitis, comparing them to 66 patients with associated ulcerative colitis, Sj6gren's syndrome, autoimmune connective tissue diseases and followed during treat- thyroiditis and ill defined digital vasculitides. A ment over a similar period of time.1 The clinical central unresolved question is why lung involve- features at presentation were found to be very ment is very common in certain syndromes such as similar although there was a trend towards a sclerosis and much less male in those with 'lone' systemic apparently very greater predominance http://pmj.bmj.com/ common in others such as ulcerative colitis and CFA. In particular, the severity of symptoms was perhaps chronic hepatic disease. Another unex- notably similar. From this series about two thirds plained fact is that a number of different types of of each group was selected on clinical grounds for pathology may be found in the lungs of different treatment with corticosteroids and a similar propor- patients with the same connective tissue syndrome tion showed a subjective improvement when (Table I). For example, in rheumatoid arthritis, assessed after 4 to 8 weeks, although there was a trend towards a better response in those with associated disease. Overall, however, the survival on September 28, 2021 by guest. Protected Table I The overlap of pulmonary pathology in various curves were almost superimposable even in those different connective tissue disorders patients who had been followed for up to 15 years Systemic Rheumatoid (Figure 1). SLE sclerosis arthritis In spite of the many clinical similarities shown between CFA with and without associated dis- Pulmonary haemorrhage + - - orders, some of the immunological characteristics Acute alveolitis + - + differ. Circulating non-organ specific autoantibodies Pleural effusions + + - + are increased in both groups but the frequency is Fibrosing alveolitis + + + + ++ in those with associated disease. Some differ- Necrobiotic nodules - - + higher Obliterative ences are also found in the type of nuclear anti- bronchiolitis - - + bodies demonstrated. For example Chapman and colleagues2 showed that extractable anti-ribonuclear protein antibody was found in only 4% of 689 Correspondence: Professor M. Turner-Warwick, Ph.D., patients with 'lone' CFA but in 12 (22%) of 54 D.Sc.(Hon), D.M., F.R.C.P., F.R.A.C.P., F.A.C.P.(Hon). patients with associated connective tissue disorders. © The Fellowship of Postgraduate Medicine, 1988 Postgrad Med J: first published as 10.1136/pgmj.64.753.497 on 1 July 1988. Downloaded from 498 M. TURNER-WARWICK 100- antibody-dependent lymphocyte cytoxicity shows greater impairment in CFA with associated dis- 80- C orders than in those with 'lone' disease. When 0 fibrosing alveolitis is also present, deposits of ° 60 immune complexes in the pulmonary capillaries have been shown occasionally both in SLE where 0.4040- With complement can also be found (Figure 3) and in -00- associated CV disease rheumatoid arthritis where it is sometimes 20- absent.5 6 Deposits in the media of larger pulmon- 0 P=Not significant 'Lone' CFA ary arteries are very occasionally seen (Figure 4).7 0 ~ 1 1 1 i Electron microscopic evidence of immune com- 1 2 3 4 5 6 7 8 10 11 12 13 14 15 16 plexes is almost always negative although occasio- Years nally tubular reticular structures as previously Figure 1 Log rank survival curves for cryptogenic described by Yeo and colleagues8 are found (Figure fibrosing alveolitis (CFA) with and without associated 5). collagen vascular (CV) disease. The fact that when CFA with and without asso- ciated disorders are compared, several immunologi- 100- P<005=.05 cal features differ (at least in intensity) while the clinical features are similar, suggests that these - P<0.01 80 immunological markers may have relatively little influence on the pathogenesis of disease in the lung. 60- 0 * 0 0 c 0 C-0 40 NS NS Pathogenesis To explain the similar as well as distinctive patholo-copyright. 20 0 0 0~~~~ -8- gies found in the lungs in different connective tissue disorders, we have explored the hypothesis repre- 0- sented schematically in Figure 6. In this it is I~~~~~~I suggested that the type of lesion found is at least in , part due to the size of the pulmonary vessels ( C>, bearing the brunt of damage as well as the modu- lating influence of the secondary circulation of the lung (bronchial circulation), 'protecting' tissue oxy- http://pmj.bmj.com/ C3A genation. The larger the vessels affected the greater Figure 2 Clq binding studies in 77 patients with the chances of ischaemic necrosis or infarction. cryptogenic fibrosing alveolitis. 0, Positive rheuma- Microscopic areas of increased metabolism due to toid factor; 0, negative rheumatoid factor. concomitant inflammatory infiltrates may be par- ticularly vulnerable. In passing, it should be noted that in this series The hypothesis goes some way to explain why a extractable nuclear in antigen (ENA) was found similar pathological process in the lung may be on September 28, 2021 by guest. Protected association with a variety of clinical syndromes and found in a range of disorders limited to the lung, the clinical features of 'mixed connective tissue such as 'lone' CFA, pulmonary hypertension, idio- disease', as described by Sharpe and colleagues3 pathic pulmonary haemosiderosis (IPH) and hae- was found in only two patients. morrhage or veno-occlusive disease. It may also As expected rheumatoid factor is raised more explain why an identical pathology is also found in frequently and found in higher titres in those with the lungs of patients with a variety of associated associated disorders because this group includes all connective tissue disorders. For example CFA, pul- patients with rheumatoid arthritis. However, raised monary hypertension and a pulmonary haemosider- titres of rheumatoid factor are found more fre- osis and haemorrhage have also all been found in quently in patients with 'lone' CFA compared with patients with SLE. Evidence supporting the import- normal controls.I0 ance of pulmonary capillary damage in fibrosing Circulating immune complexes are commonly alveolitis with and without associated connective found in CFA but the prevalence as well as the tissue disease is to be found in the marked increase titres are often higher in those with associated in lung permeability measurements observed in disorders (Figure 2). Probably associated with this, these conditions (Figure 7). Permeability is even Postgrad Med J: first published as 10.1136/pgmj.64.753.497 on 1 July 1988. Downloaded from CONNECTIVE TISSUE DISORDERS OF THE LUNG 499 Figure 3 Lung biopsy for a patient with SLE and fibrosing alveolitis. Fluorescein labelled antibody to complement C3 showing granular deposits in the alveolar walls. Dense white areas on the right hand side of the photograph are autofluorescent elastin. copyright. http://pmj.bmj.com/ on September 28, 2021 by guest. Protected Figure 4 A pulmonary artery from the same preparation as Figure 3 showing complement deposits between the internal and external elastic laminae. more rapid in cases of IPH and pulmonary hae- digital vasculitis, eyes and kidneys. The question as morrhage where evidence for pulmonary endothelial to whether the pulmonary capillaries are a primary damage on electron microscopy has been reported.9 target or are involved as a secondary manifestation Alveolitis is also found in 'hypersensitivity' drug of an inflammatory response is not of course reactions and these too may affect other systems resolved, but in view of the clinical patterns of commonly involved in connective tissue disorders disease, the hypothesis that the primary damage is including joints,
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