RHEUMATOID PLEURISY ANDPERICARDITIS · Ann. rheum. Dis. (1968), 27, 521 RHEUMATOIDPLEURISY ANDPERICARDITIS BY G. D. CHAMPION,* M. R. ROBERTSON,t AND R. G. ROBINSON Arthritis Unit,

Ann. rheum. Dis. (1968), 27, 521

RHEUMATOID PLEURISY AND PERICARDITISBY

G. D. CHAMPION,* M. R. ROBERTSON,t AND R. G. ROBINSONArthritis Unit, the Royal North Shore Hospital of Sydney, Australia

Pleurisy and pericarditis occurring in rheumatoidarthritis are generally held to have non-specifichistological characteristics, except where rheumatoidnodules are demonstrated. This view was empha-sized in the Symposium on "The RheumatoidLung" at the 1966 Annual General Meeting of theHeberden Society in London (Leading Article, Brit.med. J., 1967):

"The experts at the meeting were, however, at painsto point out that there is nothing specific about thehistology of the pleura in rheumatoid pleurisy; usuallynothing more than a simple fibrous thickening withchronic inflammatory changes can be found".

However, Gruenwald (1948) in a case report ofconsiderable interest stated that:

"There are indications that a type of growth similarto that of the nodules may also occur in a continuouslayer spread out over large areas of serous surfaces.In that event the various layers of the granuloma arearranged roughly parallel to the surface of the organrather than concentrically".

Sporadic reports of similar pathology of pleuraand pericardium have appeared in the literature, buthave received little attention in review articles(Bevans, Nadell, Demartini, and Ragan, 1954;Heller, Kellow, and Chomet, 1956; Horler andThompson, 1959; Schools and Mikkelsen, 1962;Lassiter and Tassy, 1965; Portner and Gracie, 1966;Sutton, 1967).Three further cases with serous membrane involve-

ment, as described by Gruenwald, are presentedbelow. The appearance may be likened to that of

Spurway Fellow in Rheumatology, Royal North Shore Hospital,Sydney, Australia.

tMedical Registrar, Prince Henry Hospital, Sydney, Australia.

a rheumatoid nodule opened out, exposing thefibrinoid zone to the serous cavity, a feature whichis seen not uncommonly in rheumatoid synovitis(Sokoloff, 1961, 1966). The analogy between thepleurisy and synovitis may be carried further byconsideration of biochemical and cytological studieson the effusions from these and other cases reportedin the literature.

Case 1. A fitter aged 60 years was admitted to hospitalin January, 1956, with a history of breathlessness of 3 to4 weeks' duration. In the same period he developedpolyarthritis involving the cervical spine, knees, shoul-ders, elbows, and hands.Examination.-Signs of a pleural effusion were

detected at the right base. There was active arthritis ofthe right knee with effusion, restriction of cervical andelbow movement, and right olecranon bursitis.Laboratory Investigations.-3 1. fluid were aspirated

from the right pleural space. Specific gravity was 1020,and protein 4-7 g. per cent. The fluid was sterile, andcontained no visible carcinoma cells on cytologicalexamination.Haemoglobin 15 g. per cent.; white cell count 8,800/

cu. mm.; ESR 7 mm. in one hour; no LE-cells.Repeated x rays revealed no abnormality in the chest

apart from the right pleural effusion. Needle biopsyof the pleura provided an inadequate specimen. Sputumwas negative for acid-fast bacilli.Progress.-The arthritis increased in severity, requiring

cortisone 200 mg./day for symptomatic relief. Thedyspnoea worsened, and the patient was noted to haveatrial fibrillation and congestive cardiac failure. Hypo-tension and mental confusion followed a few days later.An electrocardiograph showed flattening of T wavesrelative to previous tracings. Repeated pleural aspira-tions assisted the dyspnoea but he remained confused.Deterioration was progressive and was associated withfever, anaemia, and impaired renal function.

Termination.-Death ensued in April, 1956, 14 weeksafter the onset of symptoms.

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ANNALS OF THE RHEUMATIC DISEASES

Autopsy.-The pleural cavities contained a smallquantity of blood-stained fluid, and were partlyobliterated by fibrinous and fibrous adhesions. Theleft lung showed evidence of septic inhalationalpneumonia. The pericardial cavity contained a

small quantity of blood-stained fluid, and was alsopartly obliterated by fibrinous adhesions. Theright ventricle was slightly dilated. The endo-cardium was a little thickened, and adhesions werenoted between two of the aortic valve cusps nearthe commissure. Widespread atherosclerosis andcongestive changes were observed. The spleniccapsule appeared thickened and inflamed.

Microscopic ExaminationLUNG.-The pleura (Fig. 1) was markedly

thickened. On the surface was a zone of fibrinoidin which necrotic nuclear debris could be seen. Apalisaded zone of histiocytes separated this from adeeper zone of inflammatory granulation tissue inwhich occasional giant cells were present. Thispathological change was widespread throughoutthe pleura.A similar appearance was noted in the pericardium

(Fig. 2) where, however, the surface fibrin was

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Fig. 1.-Case 1. Rheumatoid pleurisy with superficial fibrinoidand necrotic nuclear debris, subjacent palisade layer, and thick zoneof granulation tissue with lymphocytes, plasma cells, and occasional

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RHEUMATOID PLEURISY AND PERICARDITIS

Patchy myocardial fibrosis and infective andcongestive pulmonary changes were seen.

KNEE.-Synovitis consistent with rheumatoidarthritis was observed in a section taken from theright knee.

ELBOW.-A subcutaneous rheumatoid nodulewas found adjacent to the right elbow, and necroti-zing arteritis was noted in the adjacent connectivetissue.

GUT.-Necrotizing arteritis was seen in the sub-serosal region.

In summary, the arthritis, subcutaneous nodule,arteritis, pleurisy, and pericarditis were all consi-dered to be manifestations of rheumatoid disease.

Case 2. A 42-year-old housewife first came to the out-patient department in February, 1965, with a 2-year his-tory of mild rheumatoid arthritis. There were nosubcutaneous nodules. Chest x ray showed ill-definedopacities in the right mid-zone-a small round lesionand a ring shadow (Fig. 3). Tomography demonstratedthese to be situated in the pleura.A policy of observation was indicated, and she was

treated with aspirin.In September, 1965, a right pleural effusion developed

(Fig. 4), coincident with an exacerbation of arthritis,and admission to hospital was advised.

Laboratory Investigations.-Waaler-Rose test positive(1:1028); ESR 57 mm. in one hour; haemoglobin con-centration and white cell count normal; no LE-cells.Mantoux test was negative. Aspiration of the right

Fig. 3.-Case 2. Tomogram, demonstrating pleural ring shadowand poorly-defined nodular lesion.

Fig. 4.-Case 2. Chest x ray, showing right pleural effusion.

pleural space produced 180 ml. of turbid green-greyfluid, in which the protein was 5 4 g. per cent., glucose35 mg. per cent., and the lactic acid dehydrogenase3,900 I.U./l. (serum 165 I.U./l.). The fluid was sterileand negative for acid-fast bacilli. No malignant cellswere seen on cytological examination.At this stage the possibility of rheumatoid pleurisy

was considered. The arthritis settled with rest andaspirin.Progress.-18 months later (February, 1967) a diag-

nostic right thoracotomy was advised because of therecurrent nature of the effusion, and because cytologicalexamination of the fluid at this stage revealed abnormalcells which raised the possibility of carcinoma. Thepleural lesions previously seen in the right mid-zone wereno longer apparent.Thoracotomy.-The visceral and parietal pleura were

white, glistening, and thickened. In the right upperlobe there was an area 1 *5 cm. in diameter which macro-scopically resembled an abscess. This lesion wasremoved and total pleurectomy performed. Post-operatively the arthritis has been inactive, there havebeen no complications and the chest x ray is clear.

Microscopic Examination.-The visceral and pari-etal pleura (Figs 5 and 6, overleaf) showed markedfibrous thickening deep to a surface layer of cells,sometimes in palisade formation, which werepresumably of the serosa. The fibrous tissue washyaline and relatively acellular superficially, butnearer to the underlying lung there were largecollections of lymphocytes and macrophages. In

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Fig. 5.-Case 2. Thick fibrous pleurawith a superficial proliferation of cells,presumably derived from the serosa.The appearance was not regarded asspecific. Haematoxylin and eosin. x

125.

Fig. 6.-Case 2. In this section thepleura, which is tliickened and redun-dant, is folded on itself. The central slit

is the serosal surface. Superficial necrosis,underlying palisaded layer, and thickfibrous inflammatory zone in this foldedsection illustrate the striking similarity tothe typical rheumatoid nodule. Haema-

toxylin and eosin. x 75.

one section a typical rheumatoid nodule was seen.The edge of what was thought, at operation, to be anabscess showed central fibrinoid necrosis with a wallformed by the relatively acellular fibrous tissue whichwas part of the thickened pleura. In the sub-pleural zone of the lung in this region there wasquite extensive fibrous thickening of interalveolarsepta, and marked lymphocytic and plasma cellinfiltration. Neighbouring blood vessels showedintimal thickening and cellular infiltration of theirwalls.

Case 3. A 55-year-old storeman developed polyarthritisin June, 1966, which involved the small joints of the handsand feet, the wrists, knees, elbows, and shoulders. Hisgeneral practitioner prescribed prednisone 15 mg. perday to minimize the loss of working hours.

In January, 1967, he was recalled from a routine yearlychest x ray because of a right-sided pleural effusionand referred to hospital for investigation. Respiratorysymptoms were specifically denied, and there was nofever. The arthritis was quiescent despite the recentwithdrawal of prednisone.

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RHEUMATOID PLEURISY AND PERICARDITIS52

Examination.-MetacarpophalangeaI and proximalinterphalangeal joint swelling and stiffness, and a sub-cutaneous nodule and bursitis in relation to the left elbow,enabled a clinical diagnosis of rheumatoid arthritis tobe made. Signs of a pleural effusion were evident at theright base.

Laboratory Investigations.-The Mantoux test waspositive. Sputum was negative for acid-fast bacilli ondirect examination and culture on two occasions. Chestx ray revealed no abnormality other than the effusion.Haemoglobin 12-2 g. per cent., white cell count 8,500/cu. mm.; ESR 65 mm. in one hour (Westergren); noL.E.-cells. The RA latex test was positive and the Waa-ler-Rose titre 1:64. Total serum protein was 7-8 g.per cent., albumin 4-5 g. per cent.; globulin 3 -3 g. percent. Electrophoretic pattern showed a slight rise ina2 and y globulins. Joint x rays were consistent withearly rheumatoid arthritis, erosions being present onlyin the hands.

1,500 ml. of turbid yellow fluid was aspirated from theright pleural space. The fluid contained red cells,polymorphs, and lymphocytes, was sterile, negative foracid-fast bacilli on direct examination and culture, andcontained no visible malignant cells on cytological exam-ination. The RA latex test was positive, and the Waaler-Rose titre 1: 4. The total protein was 7 -8 g. per cent.,identical with the serum, but the distribution of theproteins was markedly dissimilar, the albumin being3-4 g. per cent. and the total globulin 4 -4 g. per cent.Electrophoretic analysis of these proteins revealed a highconcentration of yglobulin (approximately 3-9 g. per

cent. compared with 1 - 3 g. per cent. in the serum,bearing in mind the considerable inaccuracies ofquantitation by these means).

Needle biopsy failed to provide sufficient pleura fordiagnosis. Bronchoscopy, normal.

Pleural Biopsy.-The visceral pleura was thickenedand was studded with multiple pleural and subpleuralnodules, some approaching 1 cm. in diameter, particu-larly over the right upper lobe.

Progress.-The postoperative course was complicatedby empyema, and also by pericarditis which may havebeen of rheumatoid aetiology. The patient was dis-charged from hospital in July, 1967, the arthritis beingadequately controlled by aspirin and phenylbutazone.

Microscopic Examination.-Sections of the nodu-lar lesions showed the three zones characteristic ofrheumatoid nodules (Fig. 7). Ziehl-Neelsen stainrevealed no acid-fast bacilli. The remainder ofthe sections of pleura were all of similar appearance(Figs 8, 9, and 10, overleaf). On the surface was athin layer of fibrin which had been separated in somesections.Deep to this was a continuous layer of palisaded

cells with their long axes orientated perpendicularlyto the surface. These cells were indistinguishableby light microscopy from the palisaded histiocytesof the pleural nodules. Between the palisaded layer

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Fig. 8.-Case 3. Low-power view of thickened pleura. NoteHaematoxylin a

and the normal underlying lung was a broad zoneof relatively vascular fibrous tissue, infiltrated byplasma cells and lymphocytes, in which occasionalgiant cells and lymphoid follicles were also seen.

DiscussionThe discrete nodules situated in the pleura in

Cases 2 and 3 were sufficiently characteristic toenable a diagnosis of rheumatoid pleurisy to bemade. The remainder of the sectioned pleura inthese two cases, and the pleura and pericardium ofCase 1 had a similar histological picture, in whichthree layers or zones were readily discerned. Onthe surface was a layer either of fibrin or of fibrinoidnecrosis with necrotic nuclear debris, of varyingthickness, which in some sections had been partlyshed during preparation. The subjacent cells werearranged in a palisaded fashion with their long axesperpendicular to the surface. Between the palisadedlayer and the underlying lung (and myocardium inCase 1) was a thick layer of vascular fibrous tissue(granulation), infiltrated by lymphocytes and plasma

surface palisade of cells, and focalnd eosin. x 60.

cells, in which giant cells and lymphoid follicles werealso seen.The surface fibrinoid necrosis may be compared

with the central zone of a rheumatoid nodule. Thepalisaded cells, which may be derived, at least inpart, from the pleural mesothelium, are indistin-guishable by light microscopy from the elongatedconnective tissue cells arranged radially around thecentral zone of the subcutaneous nodules. Theunderlying granulation tissue on the pleura is alsoakin to the equivalent zone of the nodule. Thisresemblance is even more striking when one com-pares the pleural reaction with the wall of a nodulewhich, as not uncommonly happens, had under-gone central softening and developed a buirsa-likecavity.We have observed a very close similarity of this

pleural pathology to the very early lesions ofrheumatoid synovitis as described by Kulka,Bocking, Ropes, and Bauer (1955). In this study,biopsies were taken from the knee joint within weeksor months of the onset of disease in that joint. A

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RHEUMATOID PLEURISY AND PERICARDITIS 527

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generalized proliferative synovitis was the dominant-feature. In this reaction stratification of the syno-viocytes was frequent, the more superficial cellsoften becoming arranged in a palisade formation,so resembling the proliferative zone of rheumatoidnodules. Summarizing, they state that the relativelyearly and active articular lesions differed from theclassic descriptions of the permanently-deformingstage of rheumatoid arthritis in showing a closerresemblance to the type of tissue reaction charac-terizing the subcutaneous nodules and othersystemic lesions of the disease. It is apparent thatthe early changes of rheumatoid pleurisy and peri-carditis may simulate the earliest lesions in thesynovium, and that it is in the later stages of thedisease, as exemplified by Case 2, that the appear-ances are more fibrotic and less distinctive.

In more recent reviews of the pathology ofrheumatoid arthritis, Sokoloff (1961, 1966), com-menting on the occasional similarity of the synovitis

to the rheumatoid nodule reaction, suggested thatthe necrotic material, unlike that in the subcutan-eous nodule which is circumscribed by firm cicatrix,tends to be cast off into the joint space, leaving asuperficial palisade of elongated connective tissuecells. Grimley and Sokoloff (1966) suggested thatin this situation the synovial lining layers might beconceived as an advancing front of granulationtissue, with macrophage-like cells selectively migra-ting to, or proliferating at, the surface. Kulka(1966), however, from studies of the microcircula-tory derangement in rheumatoid arthritis, attributedthis appearance to terminal vascular thrombosisand ischaemia in the synovial villis, with selectivesurvival of synoviocytes. The latter may satisfytheir metabolic requirements by interchange withthe synovial fluid.Although early rheumatoid synovitis is not

usually diagnostic microscopically, pleurisy andpericarditis with the histological features of these



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Fig. 10.-Case 3. High-power view of palisaded cell layer shown in Fig. 7. Haematoxylin and eosin. x 400.

three cases may be specific or at least stronglysuggestive of rheumatoid disease. We have beenunable to find similar histological changes in pleurisyand pericarditis due to other diseases either in theliterature or in pathological material from this hos-pital. However, it is appreciated that pleuralmesothelium is capable, in the presence of certainirritants, of undergoing metaplasia and assumingthe characteristics of columnar epithelium.A review of the literature of rheumatoid arthritis

with involvement of serous membranes has revealedseveral examples of the same pathological process,the references having been listed in the introductoryparagraphs. Gruenwald's case was of particularinterest in that not only were the pleura and peri-cardium involved but also the splenic capsule.Furthermore, typical rheumatoid nodules were alsofound on the serous membranes. The authors ofthe more recent reports have given no indication ofawareness of the previous similar findings.

Linear or band-like fibrinoid necrosis and cellularinfiltration, of the same type as found in the nodule,have also been described in mitral and aortic valvesand adjacent endocardium (Bevans and others,1954; Waaler, 1967).Needle biopsy of the parietal pleura has not, in

the past, been a fruitful source of material ofdiagnostic value. But more recent reports of needlebiopsy material showing typical rheumatoid nodules(Schools and Mikkelsen, 1962; Berger and Seckler,1966), and the pathology described above (Schoolsand Mikkelsen, 1962; Portner and Gracie, 1966)indicate the possible usefulness of this procedure.

If indeed the pathology of the pleurisy and peri-carditis is analogous to the synovitis, then onewould anticipate similar findings in their respectiveeffusions. Recent reports of investigations inrheumatoid pleural and pericardial effusions tendto support this concept. Low glucose concentra-tion, positive tests for rheumatoid factor, poly-

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morphs with inclusions containing rheumatoidfactor-IgG complexes, very high lactic aciddehydrogenase levels, high lipid concentrations, andcholesterol crystals, all of which may be seen insynovial effusions have been found in rheumatoidpleural and pericardial effusions (Ball and Whitfield,1966; Berger and Seckler, 1966; Carmichael andGolding, 1967; Dodson and Hollingsworth, 1966;Lassiter and Tassy, 1965; Schools and Mikkelsen,1962; Stengel, Watson, and Darling, 1966; Walkerand Wright, 1967). Further studies are requiredto assess the diagnostic significance of all thesefindings. It is not known whether such a series ofinvestigations can differentiate rheumatoid pleuraleffusions from effusions of other aetlology occurringin rheumatoid patients.The investigations on the pleural fluid in the cases

presented were incomplete, serving mainly toexclude tuberculosis, pyogenic infection and malig-nancy. The high pleural fluid concentration ofyglobulin in Case 3 is interesting in view of thecommonly-held concept that the yglobulin con-centration of exudative pleural effusions remainsless than in the serum (Zinneman, Johnson, andLyon, 1957). Although the literature includes oneor two instances in which the yglobulin concentra-tion appears to be high (Lassiter and Tassy, 1965),the possible value of this investigation has not beenstudied.The three cases illustrate several of the well-known

clinical features of rheumatoid pleurisy which haverecently been reviewed by Walker and Wright(1967). Cases 1 and 3 were males in the sixthdecade with rheumatoid subcutaneous nodules,who developed pleurisy at or shortly after the onsetof the disease. This is the most characteristicstory. The woman (Case 2) was younger and didnot have subcutaneous nodules. The relationshipof the pleurisy with age, and with the duration andnature of the rheumatoid arthritis, is more variablein women.

Coexistent with the pleurisy in Case 1 was peri-carditis; in Case 2 pleuropulmonary nodules andlocalized interstitial fibrosis: and in Case 3 pleuralnodules, and pericarditis which may also be of

rheumatoid origin. When rheumatoid pleurisy issuspected, a careful search for pleuropulmonarynodules and early interstitial pneumonia or fibrosison chest x ray, and for pericarditis, may assist thediagnosis. Review of the literature indicates thatsuch coexistence of manifestations is more frequentthan is generally appreciated. Of the patients withrheumatoid pleural effusions reported by Walkerand Wright (1967), three of the eleven men alsodeveloped pericarditis.

SummaryThree cases of rheumatoid pleurisy, one also with

pericarditis, are presented, in which the pathologywas of distinctive appearance, resembling a rheuma-toid nodule but with the various layers of thegranuloma arranged parallel with the surface of theorgan rather than concentrically. The second andthird cases also had typical rheumatoid nodules inthe pleura.

Similar histopathology has been reported inseveral other cases, not only in the pleura andpericardium, but also involving the splenic capsule,but there is no general awareness of this change,and of the assistance it may render in the inter-pretation of pleural needle biopsy findings. Theresemblance to rheumatoid synovitis, particularlyin the early stages, is emphasized.The third case is of further interest in that a high

concentration of yglobulin was present in the pleuralfluid.

We wish to acknowledge the advice and assistance ofDr. K. Viner-Smith, Director of Clinical Pathology andSenior Morbid Anatomist, and Dr. W. H. Payne,Morbid Anatomist, of the Royal North Shore Hospitalof Sydney; of Dr. V. J. McGovern, Director of the Fair-fax Institute of Pathology, Royal Prince Alfred Hospitalof Sydney; and of Dr. A. Tait Smith, Morbid Anatomistand Histopathologist, Prince Henry Hospital, Sydney.We should also like to thank Dr. M. Elliott, Dr. M.

Owen, and Dr. J. Schneeweiss, and Dr. D. Child, GeneralMedical Superintendent of the Royal Prince AlfredHospital, Sydney, for permission to report the cases.Thanks are also due to Miss M. Simpson and Mr. K.Deason for preparation of the photomicrographs.

REFERENCESBall, G. V., and Whitfield, C. L. (1966). Arthr. and Rheum., 9, 846 (Studies on rheumatoid disease

pleural fluid).Berger, H. W., and Seckler, S. G. (1966). Ann. intern. Med., 64, 1291 (Pleural and pericardial effu-

sions in rheumatoid disease).Bevans, M., Nadell, J., Demartini, F., and Ragan, C. (1954). Amer. J. Med., 16, 197 (The systemic

lesions of malignant rheumatoid arthritis).Carmichael, D. S., and Golding, D. N. (1967). Brit. med. J., 2, 814 (Rheumatoid pleural effusion

with "RA cells" in the pleural fluid).

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Dodson, W. H., and Hollingsworth, J. W. (1966). New Engl. J. Med., 275, 1337 (Pleural effusion inrheumatoid arthritis. Impaired transport of glucose).

Grimley, P. M., and Sokoloff, L. (1966). Amer. J. Path., 49, 931 (Synovial giant cells in rheumatoidarthritis).

Gruenwald, P. (1948). Arch. Path., 46, 59 (Visceral lesions in a case of rheumatoid arthritis).Heller, P., Kellow, W. F., and Chomet, B. (1956). New Engl. J. Med., 255, 684 (Needle biopsy of

the parietal pleura).Horler, A. R., and Thompson, M. (1959). Ann. intern. Med., 51, 1179 (The pleural and pulmonary

complications of rheumatoid arthritis).Kulka, J. P. (1966). In "Modern Trends in Rheumatology", 1st ed., ed. A. G. S. Hill, p. 49. Butter-

worths, London.Bocking, D., Ropes, M. W., and Bauer, W. (1955). A.M.A. Arch. Path., 59, 129 (Early jointlesions of rheumatoid arthritis).

Lassiter, G. S., and Tassy, F. T. (1965). Arch. intern. Med., 116, 930 (Malignant rheumatoiddisease with aortic stenosis).

Leading article (1967). Brit. med. J., 1, 186 (Rheumatoid lungs and rheumatoid piles).Portner, M. M., and Gracie, W. A. Jr. (1966). New Engl. J. Med., 275,697 (Rheumatoid lung disease

with cavitary nodules, pneumothorax and eosinophilia).Rubin, E. H., Gordon, M., and Thelmo, W. L. (1967). Amer. J. Med., 42, 567 (Nodular pleuro-

pulmonary rheumatoid disease).Schools, G. S., and Mikkelsen, W. M. (1962). Arthr. and Rheum., 5, 369 (Rheumatoid pleuritis).Sokoloff, L. (1961). In "Inflammation and Diseases of Connective Tissue: a Hahnemann Sym-

posium", ed. L. C. Mills, and J. H. Moyer, p. 146, Saunders, Philadelphia and London.(1966). In "Arthritis and Allied Conditions", 7th edition, ed. J. L. Hollander, p. 187. Leaand Febiger, Philadelphia.

Stengel, B. F., Watson, R. R., and Darling, R. J. (1966). J. Amer. med. Ass., 198, 1263 (Pulmonaryrheumatoid nodule with cavitation and chronic lipid effusion).

Sutton, R. A. L. (1967). Proc. roy. Soc. Med., 60, 339 (Rheumatoid pericarditis).Waaler, E. (1967). Acta rheum. rcand., 13, 20 (The visceral lesions in rheumatoid arthritis).Walker, W. C., and Wright, V. (1967). Ann. rheum. Dis., 26, 467 (Rheumatoid pleuritis).Zinneman, H. H., Johnson, J. J., and Lyon, R. H. (1957). Amer. Rev. Tuberc., 76, 247 (Proteins and

mucoproteins in pleural effusions).

Pleuresie et pericardite rhumatoldes

RisuMiOn rapporte sur trois cas de pleuresie rhumatoide, y

compris une pericardite chez un malade. L'aspectanatomopathologique y etait distinctif, revetant la formede nodules rhumatoides, mais les difftrentes couches dugranulome etaient alignees parallelement a la surface del'organe et non pas d'une maniere centripete. Ledeuxieme et le troisieme cas avaient aussi des nodulesrhumatoides typiques dans la plevre.Une image histopathologique similaire avait ete

rapportee dans plusieurs autres cas, non seulement dansla plevre et le pericarde, mais aussi dans la capsule de larate; toutefois ces alt6rations et leur valeur pour l'inter-pr6tation des resultats de la biopsie pleurale ne sont pasg6neralement connues. On souligne la ressemblance &

la synovite rhumatoide, particulierement a la periode dedebut.Le troisieme cas presente un interet additionnel du

fait qu'on y a trouve une forte concentration de gamma-globuline dans le liquide pleural.

Pleuresia y pericarditis reumatoides

SUMARIOSe relatan tres casos de pleuresia reumatoide, com-

prendiendo uno de pericarditis asociada. El aspectoanatomopatol6gico fue distintivo en forma de n6dulosreumatoides, pero las diferentes capas del granuloma sealineaban paralelmente a la superficie del 6rgano y node la manera concentrica. El segundo y el tercer-casotuvieron tambien n6dulos reumatoides tipicos en lapleura.Un cuadro histopatologico similar habia sido relatado

en varios otros casos, no s6lo en la pleura y en el peri-cardio, sino tambien en la capsula esplenica, sin embargoestas alteraciones y su valor para la interpretaci6n de losresultados de biopsia de la pleura no se conocen exten-samente. Se subraya la similaridad a la sinovitis reuma-toide, en particular en el periodo inicial.

El interes adicional del tercer caso reside en el hallazgode una fuerte concentraci6n de gammaglobulina en elliquido pleural.

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RHEUMATOID PLEURISY ANDPERICARDITIS · Ann. rheum. Dis. (1968), 27, 521 RHEUMATOIDPLEURISY ANDPERICARDITIS BY G. D. CHAMPION,* M. R. ROBERTSON,t AND R. G. ROBINSON Arthritis Unit,