Document n9MOGbJ0mOGyJ4MKpmkNLGYMX

FILE NAME: Philip Carey (PC) DATE: 1946 DOC#: PC077 DOCUMENT DESCRIPTION: Article from Medical Journal - Coexistent Asbestosis & Sarcoidosis THE AMERICAN JOURNAL ' OF PATHOLOGY Official Publication of The American Association oj Pathologists and Bacteriologists BOARD OF EDITORS CARL V. MALCOLM J. HAROLD AUSTIN PAUL R. CANNON HOWARD T. KARSNER W E L L E R , E ditor-in -C h iet H. SO U LE, A ssistant E ditor TR A C Y B. M ALLO R Y SHIELDS W ARREN H ARR Y M. ZIMM ERM AN VOLUME XX II (January, March, and M ay) 1946 ANN ARBOR MICHIGAN U. S, A. -V -- -'< ---"SP* asbestosis, regarded as> /`jneB^ er,1 was first described b? tibed a case in 1914, interest fom ? until the case of Cooke and MrT^taT^i^^ that time, there have appearedj^jyth upon approximately 150 necropsier op The paucity-of proved^^s^in is not due wholly to faftxre tojreport^tt*sy series {gestosis is apparently of ttd^ herare - industry. As of Octoterf 944^ <ay 1 9 ,7 0 0 1 ^ were employed in this industry in the United States.14 M u ch has been w ritten abou t th e clin ica l, roentgenologic, and biopsie aspects o f sarcoidosis. H ow ever, because o f th e in frequen cy an d relatively ben ign character o f th is disease there are o n ly isolated jd k ^ B ^ aecro p sy reports. f From th e ava ila b le literature there h a ve ` H u u u d o o ly s S se p a r tr jrf necropsies o h ca ses o f sarcoidosis.16-21 lo s t o f these w ere sum m arized b y Pinner.16 1 T h ese tw o diseases present m any clin ical and roentgeaogyaphic sim ilarities, and, also, th eir m ore frequent fa ta l co ia ^ ic stk m s ^ e alik e; pulm onary tubercu losis a n d autii?pulipc>na|y carcinom a, a frequeht asbestosis, has n ot, how ever, been d e scr ib e d a s associated , coidc^lh X ik ew ise, there h as n ot been ,a previous asbestffids w ith coexisten t sarcoidosis l t is th e purpose o i l to present the findings in su ch, a unique case, th e o n ly atnplis o f ' either pulm onary asbestosis or sarcoidosis in a series 0 / 1 8 7 0 necrop sies done a t th is hospita!. *" R e p o r t op Case The patient was a white male, 42 years of age. Subsequent to hemorrhoidectomy in December, 1943, he had noticed that slight activity produced shortness of breath. H e did not experience nocturnal dyspnea and he was able to lie flat in bed without respiratory difficulty. There was no history o f cough, hemoptysis, or cardiac embarrassment.; Notwithstanding a good appetite and the absence o f gastric Received for publication, May 9, 1945, t A sub-department of the Department of Medicine, College of Medicine, University of Cincinnati. M A* 4.94 SKAVEEM AND RITTERKOEF symptoms, there was a weight loss of 22 pounds from December, 1943, to March. 1944, at which time he presented himself for medical care. The patient had worked in an asbestos plant tor years, the Iasi ic- years i having been in a supervisory position. During this enure time he had worked in one department in which asbestos pipe was made. There was a slight but appreciable dust hazard associated with the sawing and splitting of the dried asbestos pipe, despite precautionary exhaust ventilation. The total time the patient had mem upon this final operation u[ sawing was unknown; nor was it learned wheimi he ` had been negligent in using the provided respirators. To the company's knowledge, this was their first case of asbestosis. Physical examination revealed the following findings: Temperature C ; respiration, 22 per minute; arterial blood pressure, 105/70 mm. Hg; height, 170 cm.; weight. 67 kg. The chest was of increased anteroposterior diameter. Respiratory excursions were equal but decreased. The percussion note was resonant and auscultation revealed line riles over the bases of the lungs, posteriorly. There were no evidences of cardiac enlargement, irregularity, or decompensation. Cyanosis and dubbing of the fingers were Tsent. The liver was barely palpable. Report on the roentgenogram cf the chest (Fig. r) was as follows: " The bony framework is normal. The trachea is in the midline. The hiimu shadows are moderately enlarged, bilaterally. One small calcified area is present in each hilum. There are numerous small nodular densities scattered throughout both Tog fields, especially throughout the lower lobes. There is some confluence of these honsiries in the loft iow.r lobe. Emphysema is present.' Examination of the blood showed erythrocytes, 5.5 million: leukocytes. 6.6 thousand; 75 per cent neulrocyies; 21 per cent lymphocytes; 5 per cent monocytes; r per cent ersinonhiis: sedimentation rate. 06 rr.m. No abnormality was found in the urine. The vita! oapachy. 2200 cc., was 51 per cent of normal. Tuberculin tests were not den.;. The patient was seen at regular intervals and his only complaint was increasingly severe exertion..;! dyspnea. A roentgenogram cf the chest 4 months after the initial chest film revealed no new findings. Although the patient greatly limited his activities, dyspnea became progressively more severe so that eventually, even at bed rest, there was extreme air hunger. At no time were there evidences of cardiac failure. He died approximately 11 months after the onset cf symptoms, apparently from respiratory failuie. Autopsy Findings The necropsy was performed 5 hours after death. Superficially, there was considerable decrease in the subcutaneous tissues and the body musculature. There was no clubbing of tne nail beds or dependent, edema. The mediastinum was in the midline. Each lung completely filled its hemithorax and extended far into the anterior mediastinal space. The domes cf the diaphragm, anteriority were at the level of the fourth interspace and fifth rib, right and left respectively. The lungs were encased in markedly thickened, tough, yellowish white, generally fused pleurae. The interlobar fissures were obliterated by easily broken adhesions. Lobation was normal. Hemorrhagic fi brinous n u.'t ."a* present over the pogferehrtend aspect of the left i o r r r lobe, Ion:: /;,' bound ;.he ih eT o n ed p rth rtri : h . ; u in ..he U w g in id; e r ,. COEXISTENT ASBESTOSIS AND SARCOIDOSIS 495 The frontal section of the left lung (F ig. 3) revealed coarse, lacy, tannish brown, hypercrepitant tissue throughout both lobes. Innu merable slightly elevated, grayish green, irregular, fir m nodules, 1 to 2 '/rim. in diameter, were present throughout the lung. Thin, radiating, fibrous bands surrounded and connected these nodules. Also, slightly thickened pleural septa extended into the lung substance for variable depths. In the lung tissue about the bronchi of the second and third interspaces these nodules were somewhat confluent and a similar change wa? acted in the subpleural tissues for a depth of 3 to 5 mm. Generally, these nodules, present in moderate numbers, vve;e sepa rated by wide zones cf dry emphysematous lung tissue studded by numerous minute, grayish, tubercles. Dissection of the bronchi of the lower iobe disclosed that they were moderately dilated, cylindricaliy and saccular] y, and lined b y glistening white mucosa.. In the right lung the same changes were observed as were pjesent throughout the left. However, the grayish green, irregular nodules tended to be more numerous, larger, and more confluent. This was particularly true of the anterior portions of the lower and nr'ddi lobes. Also, the nodules were connected by thicker grayish black end grayih white interlacing bands of fibrous tissue. Extending: deeply into the Iong substance, thickened pleural septa communicate4 with the fibrous tissue in and about the clusters of tubercles. Except for more pronounced dilatation and thinning of the mucosa, the bronchi of the right lung were similar to those of the left. T h e tracheobronchial lym rh nodes were moderately enlarged and on section consisted of dense, rubbery, aathracotic centers and thin rims of yellowish white tissue. Calcification was ro t grossly de monstrable. T he embalmed heart weighed 280 gra. and had the following measurements: tricuspid valve, 120 mm.; pulmonary vai^e. On nim.mitral valve, 85 nr a.; aortic valve, 65 mm.; right ventricle wall, > 1 , 8 mm.; left ventricle wall, 15 mm. The greatest transverse cardiac diameter was r.3.5 cm. (The estimated normal heart weight or- the basis of. body length Is 317 gir,.( plus 01 uihius 40,"'') T he u lc e v pid/aortic valve and pulmonic/aorlic valve ratios were 1.84 and r.2 - , actively. (These noimahy should, be -.68 and 1.05, respectively.2-''") i I-,;, right ventricle was dilated and its columnae carneae and pa<i]jjrv musek/s were more prominent than usual N e mural ibrnmbi wet* is/" -/-'able and the valvules wAomrrfinn/ was conn;;.!. ; ' s., - S . ; ! S i S i / V - y t r ' - u S S' S . y S K , , ..T.V i -g V i C ? I O C V i V : K K . ' S Y; r ; W substance was firm and purplish red with normal markings. No tubercles were seen. The liver measured 22 by 16 by 10 cm. The remaining organs showed passive hyperemia and moderate generalized arteriosclerosis. Microscopic Findings Throughout the lung there was a conspicuous linear, interlacing, peribronchial and septal pulmonary fibrosis (Fig. 2). This was par ticularly prominent in the subp?eural tissues. The intervening lung tissue was moderately emphysematous. Innumerable tubercles were present In the linear and peribronchial iibrotic areas and were present to a lesser extent in iue walls of the respiratory bronchioles and the adjacent alveolar walls. Generally, these tubercles were of two types: sarcoidal and foreign body granulomas. The former predomin at. b y approximately ten to one. Tubercles of these types were intimately ssociated and, in addition, many intermediate types were presented. The sarcoidal tubercles (Fig. 4) were free of caseation, contained no demonstrable organisms and were, ior the most, part, in the same stage of development; however, a minimal number presented some peripheral fibrosis and there was an occasional, coarse, collagenous ball. Generally, the tubercles were sharply demarcated, surrounded by delicate reticulum, and did not present peripheral rims of lympho cytes. They eonsistefPoi peripherally arranged epithelioid ceils sur rounding central, loosely arranged epithelioid and monocytic cells. Giant cells were, for the most part, centrally located and often com prised over half of the bulk of the nodule. The giant cells appeared to be of two types: Langhans' cells and foreign body giant cells,, with the former predominating. In many of the Langhans- cells .here were numerous small vacuoles, each containing a pink, round body. Other Langhans1 cells contained large, clear vacuoles; and, rarely, in those cells containing one large vacuole there was present an " asteroid'' body, an intensely eosinophilic stellate mass, i s to 20 y. it diameter (Fig. s). More frequently, the Langhans' cells contained round, oval, or suggestively budding, intracytoplasmic bodies of Schaumami,'"' 25 to 50 p. in diameter Rarely these bodies appeared tr !!? not ` ide or jpant cells, and some enclosed irregular yellowish material (Figs. 6 and 7). These bodies stained blue with hematoxylin and in ferrocyanuie preparations wer;:: strongly positive for iron. Dr. Leroy 0 . Gardner/4 who also studied this case, stated that these bodies stained `Ted with acid fuchsia of van Giesou-Weigert instead of black like elastic tissue'' * SfliLDiiiLr-. J. On i.hf liaUDT' r,i p u ib .G korh:iG"]iT "<bs(:Dr in iyDip''C::td!GjV: w-tosis twnirn;', g . g Fl\dnihK:xi:>., :'= v /. COEXISTENT APRESTOSE, A f!5 'RARCOnXc-O.S 49 anti that " von K ossa's calcium stain is nega' ive." Re-study or ap propriately stained sections revealed, ns pointed o ut b y G ardner, that the Schaumann bodies did stain red; however, a m oderate num ber abo contained calcium in variable degrees, as dem onstrated la wn R w w ( _ stain. -T:t occasional giant cell contained one or more clefts 44 gsysGv' of dholestero* crystals. 3 lore frequently, however, doubly retractile, irregular spicuies, plaques, and. conchoid:' masses were observed in giant cells. These doubl;/ retractile masse- a - - a w , c 1 the Schaumann bodies, particularly the smaller and partially caldiw d forms. The foreign body tubercles wore ind'T nilely dem arcated and con sisted of rather closely pericc b xenLch arranged, large enonocyms and one or more foreign body giant cells. These tubercles, for the most p art, were w ithin the. dense zones of fibrosis. Some, however, were presera in alveoli and respiratory bronchioles. Gulden yellow discoid, verruciform, and incompletely segmented as be si -- borne:, m any of which were in giant cells were b w n .ed In ami p '-: nooules Mbg, T Asbestos borbas. Triply or in eiwAr:: ano in eew - erate numbers, were present in the d m - - ilbretw areas ubiw p, and occasionally within alveoli (Tig. re ). Kmc jammateeb ctbdfied masses, enclosing ap p aren t asbesto- bodies ?T:g. t i l and other bodies, which appeared to be of the S r ttumaun vaaw y, wore prw ent in ine linear fibrotic bands. Asbestos bodies were also anca whored In and about the sarcoium tubercles and in die associated san ab cal giant -mbs o both varieties, b ut more frequently in those o foreign body type, Iron preparations d e a rly dainonsf' ated ihe b m trrt form.-, of the as bestos bodies. In m any areas it was ditnevk to distinguish 1.elevc-n m e two types of lesions. T ais was parbcu iarly true !lvoi:ghr-.Jt the suhplevuai rr- gioii v h w e both the melons and asbe-tos bother ware no:v rurm -erw . ciusiererb and w a b e d d rj in a dev-w e n w h w cnera-ve mas a;- of coarse elastic hbww and fine mi ledum . Tuc larger bronchi ware tamwKahlc ora: hm sliul:t chrisT , iM:h. > motion. The bronchioles a.,d :embreen y T v which:.::. embedded in cerne cn.wgen and surrounded by tabwadcs. were m 'rlcrK oiy diiaied and presented conspicuous focal squamous metaplasia and moa <te chronic tubmuCV;. indan:,,whom In the subuienrT regina.. \y;,w the ashes'"otic fbrosis and h e grunuior.,..?'as rcc lion to- riaaa. in tense, he bronchiole.. were irregularly diebed end lined by Turn el: ; 498 y^;'i^; '-- s i i ^ i 8 S ^ 'J ^ 'w r a E i t H O '''''. many contained asbestos bodies and the associated granulomatous reaction. Within the peribronchial fibrous tissue there was a moderate amount of hemosiderin in linearly disposed granules, and fine lipoid droplets. The small pulmonary arteries and arterioles presented slight iniimal thickening, and tho=e in the subpleural one /ere surrounded by thick collars of elastic fibers. The intervening alveoli were moderately dilated, the capillaries were congested, and there was a slight increase in collagen in the alveolar walls bordering the fibrous masses. Focally, dusters of alveoli con tained lipoid-laden macrophages. " Heart lesion cells1* were infrequent. Sections of the i; leura revealed dense, laminated, and oval fe- ostrated bundles of collagen. Focally. there were indefinitely demarcated nodules which consisted of circularly disposed lamellae of collagen. Superficially, the pleura presented slight fibroblastic activity and an occasional perivascular accumulation of lymphocytes and monocytes, some of the latter occasionally containing hemosiderin. No asbestos bodies were observed. The pleura over the left lower lobe, in addition, bore organizing fibrinous exudate on its visceral aspect. Sections of the tracheobronchial lymph nodes presented a repetitious pattern of sarcoidal tubercles with almost complete replacement of the lymphoid tissue. Throughout the nodes there were minimal diffuse fibrosis and several nodular masses of coarse collagen. The tubercles were similar to those in the lung as to structure and stage of develop ment. Inclusions of Schaumann were not observed and only a rare " asteroid" was present. Asbestos bodies were not identified. A mod erate number of hemosiderin-containing maciophages were present in the remaining lymphoid tissue. Similar sarcciual tubercles were present to a slight degree in the spleen and liver, and to a lesser extent la the kidneys, diaphragmatic muscle, and the right and left ventricular myocardium. These sarcoidal tubercles, however, were not as compactly arranged as those in the lung and tracheobronchial lymph nodes, and were surrounded by and permeated by lymphocytes. "Asteroid bodies" and Schaumann bodies were not present in the giant cells of these tubercles. N o asbestos bodies were found. Those in the right ventricular myocardium were associated with considerable fibrosis. The results of chemical and spectrographic analysis of lung tissue, performed under the direction ci Dr. Leroy U. Gardner,24 are pre sented in Table I. T `w final nieenow? eve' -Toder;;t>"- -''ownaxv a-btsicsk; . : wrcoidoT" o'" pviv-icrory pachvGT-':NT.k bmpl. 00 k -: markin. ch/onio w 'nv .,;y ry-,; T / T , ; . py; C O E X IS T E D ASBESTOSES AND SARCOIDOSIS 499 arteries and arterioles in (lie lungs; marked nodular obliterative pleural fibrosis; focal organizing fibrinous pleuritis; minimal sar coidosis of the bearf, iv-er, spleen, and kidneys; right ventricular cardiac dilatation and relative right ventricular hypertrophy; acate passive hv y v nia of the? viscera, slight cirrhosis of the liver; slight generalised arteriosclerosis; rmxml focal chronic adrenalitis mid nephritis; chronic posterior urethritis and interstitial prostatitis. Table I ord SpearSKpMc Amfysh nf Ash {b-y Thzus, AppraJmeUly U J * * * * * Thsue' Ask> of ** D iscussion CHmcaUv, in view of the siaifiCant history of exposure to asbestos, the possibility of sarcoidosis""^as never Pertained. Tn rrtntnpnt, the rapidly progressive, d i s a b l e d ^ p rea , unaccompanied by c a dences o f enkrvgment of the l i g ^ heart or cardiac failure, should he e aroused suspicion tiiat there ^as a concomitant pulmonary lesion, etsbestosis alone is not usually a-ceOidparui-u < .-racu piOiouna, rapichv developing, respiratory embarrassmect- Inuring case, 'ever, facto v-ere no rollatemi c u ik c l .v il y - -- : SSf;'ri:ii'r i ' ^ b ce ic m u r in ; - i i i -y ro n d y u e - *:st-ris and r-rco iy ui- v.-.-ei. A ^ v- . -fTy*** ^ ** ** w ^ ^ 500 SKAVLEM AND' RITTERHOFF -. .*- s^^ strate sarcoid lesions and the discovery of asbestos fibers in the sputum, with a history of adequate exposure to asbestos fibers and rocntgenograpbic evidences of diffuse pulmonary fibrosis. Asbestosis of the degree observed, alone should not have caused death, and sarcoidosis has generally been regarded as a benign proces". Reisner,18 however, on the basis of his observations on cases of pulmonary sar coidosis, stated " that one is not justified in assuming too confident an attitude regarding the ultimate outcome." This statement is particu larly true when, as in this case, sarcoidosis complicates pre-existing pulmonary disease. Pathologically, there were evidences of right heart strain in that there was marked dilatation of the right heart, evidenced by increased tricuspid and pulmonic/aortic valve ratios and slight passive hyperemia of the viscera. The total heart weight, however, on the basis of body lengthy- was normal. As determined b y the ratio of the left and right- ventricular weights, it has been shown that there may be considerable relative right ventricular hypertrophy without an increase in the total heart weight. However, relative right ventricular cardiac hypertrophy in Higgins' series 25 was not usually accompanied b y evidences of right ventricular failure. In view of the significant dilatation of the right side of the hbsrt and the slight sclerosis of the pulmonary arterioles, there was, in all probability, some degree of pulmonary hypertension in this case. However,' in j the absence of an increase in total hearweight and in the absence oi evidences of chronic passive hyperemia of the viscera there was probably no, or insignificant, exaggeration of air hunger due to heart failure. It has been suggested that dyspnea in the pneumoconioses is due to capillary and arterial blockage by the fibrotic process. This, in all probability, is true to a variable degree in those persons with severe fibrosis of the conglomerate type- with attendant extreme chronic emphysema. This hypothesis, however, does not explain the severe dyspnea that is seen in occasional cases of diffuse miliary studding of the framework of the lung b y silicotic, tuberculous, sarcoids1, or neoplastic tubercles. It may be that the mechanism of dyspnea in such instances is due to irritation of the vagus nerve endings with reflex stimulation of the respiratory center (Hering-Bivuer reflex). In view of the equivocal evidences of hypertrophy of the right heart in this case, mechanical obstruction to the blood now would not appear to he. the responsible factor but. more likely, because of the diffuse active du' process dwroughom. the hms-o lie Uedno-Tt.'cvvr reflex was ex-iogorateii. T v '-n c b -p ?/;<.sc ;,s Hike; 0 cm-.re so COEXISTENT ASBESTOSIS AND SARCOIDOSIS S I spiratory alkalosis or acidosis. Tissue changes sugge.si.ive of alkalosis, such as calcification of the renal tubules, were net found. Microscopically, there was some difficulty in differentiating the two types of tubercles since there were many sarcoidal tubercles which contained asbestos fibers, and tubercles of indeterminate type, not containing fibers or inclusion bodies, were sometimes seen. It wa= difficult to determine how much of the fibrosis was due to asbestosis. Morphologically, since the majority, by far, of the sarcoids) tubercles were without evidences of fibrosis and apparently of the some age, it is suggested that this process was engrafted upon an established mbestesis. Further, on the basis of Gardner and Camming ' "experi mental studies on ashestosis, the marked peribronchiolar fibrosis with sequestrated asbestos bodies, the marked pleural fibrosis and pleural septal fibrosis, and the metaplasia of the hroncbiolar epithelium in dicate that the ashestosis was well established and over 700 to 80c days old. Dr. Leroy U. Gardner, who kindly examined the mmer' d, stated: `Tn comparison with our other material the piginm wd foe' in your case seem to show more fibrosis ana less localized emphysema. Histologically, this can probably be explained by the pro-cnee sarcoid nodules within the asbestofic zones o ' reaction, I would infer that in your case the two conditions developed more or less simul taneously, but that probably the ashestosis was present to some degree before the sarcoid appeared. This opinion Is based upon use occur rence of asbestos fibers and other iron- containing part ides in Fie interior of the tubercle-like nodules and in some car-ts within the giant cells themselves. T he number of asbestos bodies Is smaller tbr-n seen in many c-ses." inclusions of the Schaumann variety, found only in the lung, oc curred in 4 per cent of the giant cells. Some of these enclosed goldenyellow, irregular bodies suggesting a5.be.-ios bodies, but similar to or ganic material previously described within such bodies. Yet thert were definite asbestos bodies enclosed by similar dark blue mr ferial. Schaumann inclusions have been described in only 4 per cent of the reported necropsies on sarcoidosis as summarized by Rubin and Pin ner,1' who did not regard these inclusions as > p t itjz saii.0Ki.'.s.:s, R ic h r7 who was impressed by the frequency of Schaumann indusior-: in sarcoidal lesion?; arid b y their absence in unequivocal tuberculeiIcsions, noted that Metchnikoff reported the presence of calcified in clusions in the hyperplastic tuberculous lesions of experimentally i 502 SKAVLEM AND RITTERHOFF sarcoidosis. Gardner ~4 pointed out that, in his sarcoid material, these bodies, regarded b y many to consist of calcium cr deified remnants of elastica, do not, by the von Kossa method, contain calcium, but, by the ferroeyanide method, give a strong reaction for iron. Only a moderate number of the Schaumann bodies observed in the present case were either wholly or partially calcified, y et ail gave a strong reaction for iron. Studies on sarcoid lesions of lymph nodes and spleen from another case revealed only a few iron-staining noncalcified Schaumann bodies. The presence of doubly retractile, nonlipoid sub stance in giant cells and frequently in close relation to Schaumann: bodies has not been emphasized in the literature on sarcoidosis. It has been noted, however, that colorless and yellowish tinged refractile material is often enclosed by the Schaumann body. The fact that these masses are frequently doubly retractile has not been stressed. It has been suggested that these enclosed masses represent disintegrat ing elastica; however, van Gieson-Weigert stains do not confirm this suggestion. The origin of this refractile and doubly refractile material is not known. Being in and about many of the small, partially calcified bodies, this doubly refractile material appears to be associated with the development of the Schaumann body. The larger and more densely- stained b od ies were not as frequently associated with visible doubly refractile substance. However, fractured and fragmented, apparently old, Schaumann bodies, as seen in control sarcoid material from lymph node and spleen, usually contained moderate amounts of doubly re fractile substance. Apparently then, the Schaumann body, which stains blue with hematoxylin and red with add fuchsin, is formed in response to doubly refractile, nonlipoid substance and initially is impiegnated by iron and later, in amounts demonstrable by von Kossa's stain, by calcium. Wolbach,21 in r q n , Jadassohn, in 1^19,'^ and Friedman,18 in 1944, have described a peculiar intracellular body in cases of sarcoidosis. This body, stellate in shape, varies in size up to 25 1, generally lies in an intracytoplasmic giant cell vacuole, and stains intensely with acidophilic stains except the central area which is basophilic. Wolbach described them as lying free in tissue spaces, in endothelial leukocytes, and in giant cells. Friedman found such bodies in only 6 to 8 per cent of the giant cells in his case. Both investigators attem pted to determine the chemical structure of this stellate bod}'- by specific stains; however, they were unsuccessful. Both considered the pos sibility of its being an extraneous o'-gainsm. although cable. COEXISTENT ASBESTOSIS AND SARCOIDOSIS 503 material and decided that they were not similar to inclusions some times seen in cases of sarcoma. Friedman regarded there hedies as nonspecific but highly characteristic of sarcoid lesions. Friedman pro posed that these bodies be called "asteroids," but perhaps it would he better, eponymically, to call them Wolfcach's asteroids. They have been described in 7 cases of sarcoidosis, and never in association with the Schaumana calcined Inclusion, body. In the present case asteroids were present in approximately 1 per cent of the giant ceils in the lungs and tracheobronchial lymph nodes. Definite transition stages of asteroid formation we e suggested by the presence of spicules on the pink, coccoid, mfravacuoiar, intracytoplasmic bodies, particularly .In those giant cells in which the small vacuoles were clustered and dis integrating. In addition, an occasional Woifaach's asteroid, instead of lying in a large, clear vacuole, was surrounded by agminated ruptured vacuoles. In view of the presence of similar pink, coccoid, inlravaeuolar bodies, similar asteroids, and the same suggestive stages of asteroid formation in the giant cells of talcum powder granuloma, ; observed in one case in this laboratory, these giant ceil cytoplasmic changes must be regarded as Woibach originally suggested, nonspecific biochemical cytoplasmic alterations. In addition, such an asteroid is depicted In the giant cells of leprous lesions b y Mallory who called them " spiculated" bodies. No transition stages between Woibachh asteroids and Schauniaim's inclusions were even remotely suggested. The pathogenetic relationships of asbestosis and sarcoidosis are dependent upon the chronologic development of the lesions and tin. nature of the causative agents. Historically and histologic >1'. 1> i l .i > case, it is most likely that; asbestos!? preceded the d"vr, 'f nr t -A -a coidcsis. The predominant localization of the sarcoioa*' *1 rc.es 1thin ssbesiolic ones of fibrosis with attendant morpbolc^-v n. *~c!r u of both lesions, as evidenced by asbestos bodies within sarcoidal tubercles and lesions of indeterminate type, would suggest an analogy to the intimate relationship existent between tubes *T - ku th : pneumoconioses. It must be remembered, though, that even in un complicated sarcoidosis the lesions occur in the framework of th-lung, and therefore the morphologic relationships of the m o may be coincidental. This would be in agreement with those who believe that morphologically sarcoid is not reconcilable with tuberculosis. How ever, to those who regard sarcoidosis as a peculiar form of tuberculous, this case then would be one of asbestosis with - nenu.y- c- 1 wnr e:wearing 1i'brr-"uIo?;?. 504 SKAVLEM AND RTTITRIIOFF REFERENCES 1. Gioyae, S. R., and Merewether. E. R. A. Asbestos. Occupation and Health Supplement. Interactional Labour Office, Geneva, 1958. (Cited by Sayers, R. Ft,, and Dreessen, W. C. Asbestosis. Am. J. Fun. Health, 1939, 29, 205-214.) 2. Murray, M. Cited bv Egbert.5 (Charing Cross Hasp. Gas.. 1900. Also: Departmental Committee on Compensation for Industrial Diseases. Minutes of Evidence. Appendices and Index, 1907. Cd. 3406, p. 127: Report, 1907. Cd. 3495. P- I4-) 3. Fafcr, T .; and Feigel. Kristallbildung in dor Lunge. Deutsche mcA. Wchnschr., 1914, 40, 1548-1549. (Cited by Egbert.5) 4. Cooke, V/. E. Pulmonary asbestosis. Brit. M . J., 1927, 2, 1024-J.025. M c Donald, S. Histology of pulmonary asbestosis. Ibid.. 192-7. 2, 1023-0026. (Cued by Egbert.5) 5. Egbert, D. S. Pulmonary asbestosis. Report of a case with necropsy findings. Am. Rev. Tuberc., 1935, 31, 25-34. 6. Shull. J. R. Asbestosis. A roentgenological review of 71 casco Radiology, 1956, 27, 279-292. 7. Lanza, A. J. Asbestosis. J. A. M . A., 1936, 106, 508-300. 8. Lynch, K. M. Pulmonary asbestosis, IV. The asbestosis body and similar objects in the lung. J. A. M. A,, 1937, 109, 1974-1978. 9. Williams. E. The presence of "curious bodies" in the lungs of South African goldminers. /. Path. & Beet., 1959, 48, 475-477. 10. Sutherland, C. L. Tuberculosis in the silica-risk industries. Lancet, 1540. 1, 893-896. 11. Hannesson, H. A case of pulmonary asbestosis accompanied by pulmonary' tuberculosis. Tubercle, 1971, 22, 40-44. 12. Hornburger, F. The co-incidence of primary carcinoma of the lungs and pulmonary asbestosis. Analysis of literature and report of three cases. Am. J. Path., 1943, to, 797- 807. _ 13. Auerbach, O. Tube pathology of the pneumoconiosis. Quart. Bull.. Sea V iev Hasp., 1936- 37, 2, 3--27 14. Monthly Labor Review, U.S. Department of Labor, Bureau of Labor Statistics, 1946, 62, p. 153, table 2. 15. Pinner, M. Noncaseating tuberculosis. An analysis of the literature. Am. Rev. Tuberc., 1938, 37, 600-728. *6. Horton, R., Lincoln, N. S., and Tanner, M. Noncaseating -ubercuiosis. Am. Rev. Tuberc., 1939, 39 186-203. 17. Rubin. E. H., and Pinner, M. Sarcoidosis. One case report end literature review of aulepsied ce.es. Am. Rev. Tuberc., 1944- 49, 14; -r 18. Reis tier, D. Boeck's sarcoid and systemic sarcoidosis (Rt snicr- iWJk-Scnaumann disease): study of 35 cases Am, Rev. Tuberc., 194^ ^ 389-307: 437-462. 19. Friedman, Ivl. Sarcoidosis of the spleen. Report of a cns,; v.i;h mmijsv ana a study of intracellular " asteroid bodies.'' Am. /. Path.. 0.,.; <,0 4->1-63; 20. Kraus, E. J. Sarcoidosis (Bocck-Besnier-Schaum..nn diser-se) -jc ;j1;, Cauwe of a pituitary syndrome. J . Lab. Rr Clin. Lied.. i '7 7 28. 40-140, 21. Wolbach, S. B. A new type of end inriusio;., im r - W i v associated with disseminated granuioro'Uons non:-. j . An 22. Z - . P . M. Herat rw rin. :. N - rd :;:,: . Path., T942, W o -'P :. 22 2 P,- : 7c:.P. A nk.  s.'tfpft* - * f -*?& ' s#pr'-\ . rt*?1-*. * C O E X IS T E N T A SB E ST O SIS A N D SARCOIDOSIS 505 Gardner, L . U . Personal com m unication. Higgins, G. K. The effect of pulmonary tuberculosis upon the woight of the heart. Am. Rev. Tuber;:.. 1944, 49, 255 -^75, Gardner, L. U., ami Cummings, D. E. Studies on eaperimr-utal pm\:~tono- koniosit, V L inhalation of asbestos dust: its; eiiect upon primary iu b erceicss infection, I. Indust. Eyg. & Toxicol., 1931, 3, 6}-? t. Rich. A. R. The Pathogenesis of Tuberculosis. C. C. Thomas, Springlleid t: Baltimore, *944, p. 722. Jadassohn. Zur Frage der " Sareoido - pemio und des Lupus m il n s in Kombination m it "Acniiis." C c.-B l. /. sclneei-. 4er-::u:, ;o;y, 4 g, p p 478, Mallory. F. B, T a Priruhpys of Pathologie Histology, y . B. TumCers Cts, Philadelphia & Lnnde:;, y y S , p. to;. [ niurtratrom jvHcxv j DESCRIPTION OF PLATES Plats 103 F ig . . Initial roentgenogram o f the che.-t. Fig. 2. Photomicrograph of lung and adherent pleura showing subpleura! septal, pcrlbronchioiar, and marked and focally nodular pleural fibrosis. X 4. avu'in `id '-c- h Ui m: H -^#***^ * *.-* i pggfli il'ilTiTIJ"i~^~`i 'O P i ATE 107 F tg . 8. Luna with tubercies of XuvXa body type. Too e-rotai ;ua,. rob; has ah asbestos bod}' at its perinhery. X 160. F ig . a. Lucsj shoMfjpg asbestos bodies and c' usiers of hcniobderin-bden ntaeroiXayes svithin an area of fibrosis. X 705.  ;