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FILE NAME: Goodyear (GY) DATE: 1946 DOC#: GY 103 DOCUMENT DESCRIPTION: Article from Medical Journal - Coexistent Asbestosis & Sarcoidosis , . >- THE AMERICAN JOURNAL ' OF PATHOLOGY Official Publication of The American Associati n of Pathologists and Bacteriologists BOARD OF EDITORS CARL V. WELLER, E ditor-in-Chief MALCOLM H. SOULE, Assistant Editor J. HAROLD AUSTIN TRACY B. MALLORY PAUL R. CANNON SHIELDS WARREN HOWARD T. KARSNER HARRY M. ZIMMERMAN VOLUME XXII (January, March, and May) 1946 ANN ARBOR M ICH IG A N U. S. A. - ase stasis, h er,1 was first described "me; scribed a case in 1914, m tam nntl the case of ce that time, there have apocare f8 approximately 150 n e a t .. ^cisis, is not due whtdly to -^cropsy series asbestosis is on g* -Further,.despite the wide |&ere are cmhpaiStiveiv few s?fi gr& y& s: i9'7" ^ ` -- 7 W o N fa s ^ c s ^ ^ f ro e a ^ o b g ic , a,,d and relatively benign character of tM r b f the " frequency r .. J^*a3ed necropsy reports. "From th T ^ " 0nIy isoIaied only 58 reports of n ecropsh T ^ S Kte?ture ,ere have ` ^ " " " d -d ^ S e r T 30 * '* - * * similarities, and, also* S ^ m o ^ i e ^ V f ^ reDt8em& aPh& * X 5ST2 t,,,>ercu,o,is^ S - L !? sag--rrr^ S JS B p . " -*>* M w fae, a ik/ iS T ? " `f ' * ' * 1" - i l i consiste s a r c M o ,^ t b ^ ^ J ^ m S "s c to present the findings in c,-* a ,, 15 TM Papse of - either pulmonary asbestosis or sarcoidosk ^ ' s,es done at this hospital. m a 861,168 t *8?o mtcrap- ' v, - ; ep. . R epokx of Case the patient was a white maf* , ....... b I WS b^' I943> he ^ d n'o c e r ' i r s S t ^ T 6111 0 ^ ^ e c t o m v So* s x x r 1`^ poeLaad ^ ^ "cs j f S T w Seemed for publication, May 9. o, J E T " * - - Co,,., ,,, *m- mn inifi m'if n~rmyij.i-wigifiijjWiipftiiiWrtjr;i"ip.r-fnmTrT.fimriy --- 494 SKAVXEM AK0 RXTTERKOFF 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 for 23 years, the Iasi 10 years i having been in a supervisory position. During this entire time he had worked in one department in which asbestos pipe was made. There was a slight but appreciable aast hazard associated with the sawing and splitting of the dried asbestos pipe, despite precautionary exhaust ventilation. The total time the patient had snera upon this final operation of sawing was unknown; nor was it learned w heaic: he had been negligent in using the provided respirators. T o the company's knowledge, this was their first case of asbestosis. Physical examination revealed the following findings: Tempera turf. 37 C .; respiration, 22 per minute, arterial blood pressure, 105/70 mm. H g; height, 1 to 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 decomiyansation. Cyanosis and dubbing of the fingers were absent. The liver was barely palpable. Report on the roentgenogram c f the chest (Fig. r) was as follows: " The bony framework is normal. The trachea is in the midline. The hilum shadows are moderately enlarged, bilaterally. One small calcified area is present in each hilum. There are numerous small nodular densities scattered throughout both lung fields, especially throughout the lower Icbos. There is some confluence of these ('entities in the left low tr lobe. Emphysema is present/ Examination of tire blood showed erythrocytes. 5.5 million: leukocytes. 6.0 thousand; 73 per cert neufrocytes, 21 per cent lymphocytes; 5 per cent m onocytes; r per cent erYnoyhiis: sedimentation rase. 26 men. No abnormality was found in the urine. T oe vital (pachy. 2200 cc., was 51 per cent of .normal. Tuberculin inns were not done-. The patient was seen at regular Intelvais and Iris only complaint was increasingly severe exertional dyspnea. A roentgenogram c f the chest 4 mouths 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. A t no time were tbeie evidences of cardiac failure. He died approximately 11 months after the onset cf symptoms, apparently from respiratory failuic A utopsy Findings The necropsy was performed 5 hours after death. Superficially, there wav considerable decrease in the subcutaneous tissues and the body musculature. There was no clubbing of the nail beds or dependent edema. The mediastinum was in the midline. Each lung completely filled its hemithoiax and extended far into the anterior mediastinal space. The domes of the diaphragm, anteriorly, were at the level oi the fourth interspace end 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. Lobatior; was normal. Hemorrhagic fi brinous mak/jag present over the yokcrerivv; nl aspect oi am wit lo w er T h e , P oy/v bound d ie thnria.-aori a.-,/Pari P c . u u .0 ,hn lu n g in COEXISTENT ASBESTOSIS AND SARCOIDOSIS 495 The frontal section of the left lung (Fig. 3) revealed coarse, lacy, tannish brown, hypercrepitant tissue throughout both lobes. Innu merable slightly elevated, grayish green, irregular, firm nodules, 1 to 2 am. in diameter, were present throughout the lung. Thin, radiating, fibrous bands surrounded and connected these nodules. Also, lightly 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 was noted in tie subpleural tissues for a depth of 3 to 3 mm. Generally, these nodules, present in moderate numbers, vvete sepa rated by wide zones cf dry emphysematous lung tissue studded by numerous minute, grayish tubercles. Dissection of the bronchi of the lower lobe disclosed that they were moderately dilated, cylindrical!}-and saccularhc and lined by glistering white mucosa.. In the right lung the same changes were observed as were piesent throughout the left. However, the grayish green, -irregular nodules leaded to he more numerous, larger, and more confluent This was particularly true of the anterior portions cr the lower arid nuclei! lobes, Also, the nodules were connected by thicker grayish alack and graywh white interlacing hands of fibrous tissue. Extending deeply into the lung substance, thickened pleural septa communicate'-5 with the fibrous tissue in and about the clusters of tubercles. Except for more pronounced dilatation and thinning of the mucosa, tire bronchi of the right lung were similar to those of the left. The tracheobronchial lymrh nodes were modeiately enlarged and on section consisted of dense, rubbery, aathracotic centers and thin rims of yellowish white tissue. Calcification was not grossly de monstrable. The embalmed heart weighed 280 gra. and had the following measurements: tricuspid valve, 120 mm.; pulmonary valve, mitral valve, 85 nr a.; aortic valve, 65 mm.; right ventricle wall, ;; to P mm.; left ventricle wail, 15 mm. The greatest transverse cardiac diameter was 13.5 cm. (The estimated normal heart weight on the bSSiS of ,'GCi r length i'6 317 s'S,., plus v minus 4V- ' } j.iie liicuv pid/aortic valve and pnlmonic/aorlic valve raties were 1.84 and r,2.c respectively. (These normally should be \ M and 1.05, respectively.1-') The right ventricle was dilated and its columnar carneae and paullijry musalas were more prominent than usual ITe mural T w cab' were r)i--.. wstwthlr- and tlx- valvular w.doowrscm ww ,canard. CV.; list vis? -VlC-'-u VIC. Sv C.vrrcv. -VI cars cCOC W r i .c v ' v 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 suhp7sural tissues. The intervening lure tissue was moderately emphysematous. Innumerable tubercles were present in the linear and peribronchial fibrotic areas and were present to a lesser extent in me walls of the respiratory bronchioles and the adjacent alveolar walls. Generally, these tubercles were of two types: sarcoidal and foreign body granulomas. The former predominated by approximately ten to one. Tubercles of these types were intimately as sociated and, in addition, many intermediate types were presented. The sarcoidal tubercles (Fig. 4) were free of caseation, cortained no demonstrable organisms and were, for 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 cells 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 cell, with the former predominating, in many of the Langhans' cells .here were numerous small vacuoles, each containing a pink, round body. Other Langhans' cells contained large, clear vacuoles; and, rarely, in those sells containing one large vacuole there was present an " asteroid'' body, an intensely eosinophilic stellate mass. 15 to 20 p is diameter (Fig- S)More frequently, the Langhans' ceils contained 'ound, oval, or suggestively budding, intracytoplasmic bodies of 3cbaurnarmd: 25 to 50 p. in diameter Randy these bodies fmp#*s ""d tr lie nun Ide of danf cells, and some enclosed irregular yellowish material (Figs. 6 and 7). These bodies stained blue with h.-matoxylin and m ferrocvar.ide preparations wer.-. strongly positive for iron. Dr. Leroy U. Gardner,24 who also studied this case, stated that these bodies stained " red with acid fuchsin of van Gieson-Wcigert instead of black like elastic tissue'' * SflidbllliiLl'. J. C'i) i.hi.- naUDT r.f iypip-'Ofl'UlGik: thtnsis fTnlrnd, -ULG iT.D: >.mmmsrb-r M, :'"0 in GGht COEXISTENT ASBESTOSIS AK" SARCOIDOSIS 49? anti that " von Kossa's calcium stain is nega' ive." Re-study or ap propriately stained sections revealed, ns pointed out by Gardner, that the Schaumann bodies did stain red; however, a moderate number also contained calcium in variable degrees, as demonstrated by von Kossa's stain, an occasional g i a n t ceil co-pniaed one or more clefts suggestive of cholesterol crystals. 3 lore frequently, however, doubly retractile, irregular spicules, plaques, and conchoid:' masses were observed in giant cells. These doubly retractile masses were often about, or in, the Sahaumann bodies, particularly the smaller and partially caidiwd forms. The fc>' Jem body tubercles were hidnimilely -demarcated and con - sisted of twiser closely padre i, htdrlsniLclr arranged, large rnonocyuis and one or more foreign bear- giant cells. These tubercles, for the most part, were within the dense zones of fibrosis. Some, however-, were presera in alveoli and respiratory bronchioles. Gulden yellow discoid, verruciform, and incompletely segmented as besi borne:, many of which wore in giant colls worn hbwwed in am'! p ' -: nonuses M'ig. Sj Asbestos borbas. wrigly or in csaAer:; amb in nnw eraie numbers, were pre-ant wau in the devw- fibre-tic area..-' uria, T- and occasionally within alveoli (Fig. ic). Tare Jammated, cJdfiw ! masses. enclosing apparent asbestos bodies ?T':g. rrl are other bodies which appeared to be of the S r atrmaun varen,-, were present in tae linear fibrotic bands. Asbestos bodies were also ancs whered In ana about the sarcoma: tubercles mid in die associated sates Peal giant -'GIs of both varieties, but more frequently in those of foreign body type, Iron preparations dearly demonsP ated die bow: re lonm-, of the as bestos bodies. In many areas it was uithewr to distinguish f e:wwn urn two types of lesions. This was pardcularly :rue tlvougheut the svhplevuai re gion ivla.-;so to fa the lesions and auba-tos bodm- were a o r: ruam oau clustered. and wwhedarj in a deww r ,, r e m e d a ^ n . roaswa of coarse elastic uUaw and fine up ATum. Toe larger bronchi ware u a iim -h ic orb: for slurb: cbm-A, ipr, > matloin The bronchioles a .J :vwsir;n.my To.whioAs. ambedded in dense cmwgen and surrounded by Aibowhs, were anvlarbolv dilated and presented conspicuous focal squamous metaplasia ana woe <te chronic riunvooea 1 .buarw.wwon. In the subpieurr' region.- waeru the a:Tesf'otic fbrosis and the gsawuom.Ww;s rcc lion - m ,-- riuna, in- 408 SKAtftJEM AND EITTERHOFF many contained asbestos bodies and the associated granulomatous reaction. Within the peribronchial fibrous tissue there was a moderate amount of hemosiderin in lu ra rly disposed granules, and fine lipoid droplets. The small pulmonary arteries and arterioles presented slight intimal thickening, and thoe in the subpleurai one /ere surrounded by thick collars of elastic fibers. The Intervening alveoli were m rderately dilated, the capillaries were congested, and there was a slight increase in collagen in the alveolar walls bordering the fibrous masses. Foeally, clusters of alveoli con tained lipoid-laden macrophages. " Heart lesion cells" were infrequent. Sections of the i; leura revealed dense, laminated, and oval fe~ estrated bundles of collagen. Foeally. 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 c '.casionally 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 maaophages were present in the remaining lymphoid tissue. Similar sarcoidal tubercles were present, to a slight degree in the spleen and liver, and to a lesser extent in 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. No asbestos bodies were found. Those in the right ventricular myocardium were associated with considerable fibrosis. The results ei chemical and spectrographic analysis of lung tissue, performed under the d'rectmn of Ur. Leroy U. Gardner,24 are pre sented m Table I. The final niognos.-s acre cinder;,!-- ^'dw-cncrc a-bestesb: ; e.rc.o;dc"-'> O' p o h o .u o v y m b c'cch/o'. -oN ihc h ;e;b no;---; marked, c i a o r c e ;,, an, .,..v i-re.c-.~-.. r r - ; a p e . , ---.-.W _ p . - ~- COEXISTENT ASBESTOSES AND SARCOIDOSIS 499 arteries and arterioles in tlie lungs; marked nodular obliterative pleural fibrosis; focal organizing fibrinous pleuritis; minimal sar coidosis >f the heart, l " ;er. spleen, and kidneys; right ventricular cardiac dilatation and relative right ventricular hypertrophy; acute passive hyperemia of the viscera, slight cirrhosis cf the liver; slight generalised arteriosclerosis; minimal focal chronic adrenalitis mid nephritis; chronic posterior urethritis and interstitial prostatitis. T I Chemical and Spetrotyephk Analysis of Ash 1B?y T'-sue, Approximately 14.1% of Moist Tissue. Ask, 6,/o% of Dry TissueA As oxides 'except CV; rJtcxA.rcsJ ar.e Aym'i C m, Ag, Hg) Pb, Bi. Cdi Mo ] SiOj Fc20 ? AliO, BeO ZaQ MuO CaO MgO BaO SrO TiOj VsOj Cr2Os NiO, CoO NajO KjO AO; Cl CCA Per ccni < n .rs . f) y r . \*7 NoTJu found 0.3c; 0.03 CD02 I. r4 None found None found None fount-. None found 0.27 <0.05 5-44 4 4 -4 ., 8.4.: a.6 i PirSout Total |._ A a K St Ba Ca Ai Me P Si F-: Mrs Ti Cu Ag Sn Cr h-0 Vh Zn m Ft Cl A& eltisents Chemical s-usilyr-ts f AbA'rlFV'g;2, hie 1 M.aiyV, Per cent AJb.-f-VfV-.Cvii .7- Fv' A ; *iii 4 3'2-7 .oO" u found .None found 5, J 0.2 0.7 .O e. 6 0.02 None found O.C.5 None found o, 4.0 1. " ' 0 -'O ; j DO ;oo 75 A 5 .0V A 3 1 G A 4 ;> 1 c D iscussion Clinically, in view oi the significant histoiy of exposure to asbestos, fiie possibility of sarcoidosis was never entertained. In the rapidly progressive, disabling dyspnea, unacconip.nded by dences of enlargement of the light heart or cardiac failure, should hr e aroused suspicion mat there was a couconiaat pulmonary lesion. Ashestosis alone is not usually accompanied by such profound, rapnilv developing, respiratory embarrassment. In ting case, however, rhem were ilo oAloxerai ourucciD '.AA:r:ef --f san-o-Ion-. A 7,0 ubi ,, e g p, ; v vei iecnn-.w ee-w-wur f x ; . .us eed were ..... ,- ; . imp* Soo * SKAVLEM AND' R IT T E R H O F F strate sarcoid lesions and the discovery of asbestos libers in the sputum, with a history of adequate exposure to asbestos fibers and roentgenograpbic evidences of diffuse pulmonary fibrosis. Asbestosis of the degree observed, alone should not have caused death, and sarcoidos;s has generally been regarded as a benign procesr 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 altitude regarding the ultimate outcome." This statement is particu larly true when, as in this case, sarcoidosis complicates pre-existing pulmonary discsse. 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 length," was normal. As determined by 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 caidiac hypertrophy in Higgins' series25 was not usually accompanied by evidences of right ventricular failure. In view of the significant dilatation of the right side of the hf&rt and the slight sclerosis of the pulmonary arterioles, there was, in all probability, some degree of pulmonary hypertension in this case. However,' in ithe 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 by silicotic, tuberculous, sarcoidni, 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-ilruier reflex). In view of the equivocal evidences of hypertrophy of the right heart in this case, mechanical obstruction to the blood flow weald not appear to be the responsible factor but. more likely, because of the diffuse active imrimmatorv process riwouvuoo? the fliPir the tP rinaditotwt reflex -was evtooeraiad. dre-'ornahiy. there was eflriw ;; VP; V'O flip COEXISTENT ASBESTOSIS AND SARCOIDOSIS 501 spiratorv alkalosis or acidosis.. Tissue changes suggestive 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 libers or inclusion bodies, were sometimes seem Is was difficult to determine how much of the fibrosis was due to asbestosis. Morphologically, since the majority, by fax, of the sarcoidal tubercles were without evidences of fibrosis end apparently of rhe seme age, it is suggested that this process was . ..grafted upon an established asbestesis. Further, on the basis of tw idver and Camming"' -G experi mental studies on asbestosis, the marked peribronchiolar fibrosis with sequestrated asbestos bodies, the marked pleural fibrosis and pleural septal fibrosis, and the metaplasia of the bronchiolar epithelium in dicate that the asbestosis was well established and over 700 to Soc days old. D i. Leroy U. Gardner, who kindly examined the iw herFy stated: "In comparison with our other materia! the plgimowd fow hi your case seem to show more fibrosis and less localized ewohov n o. Histologically, tbh- can probably be explained by tb- presence o sarcoid nodules within the asbestotie zones o' reaction. I m old inter that in your case the two conditions developed more or less simul taneously, but that probably the asbestosis was present to some rkg:vv before the sarcoid appeared. This opinion is based upon the occur rence of asbestos fibers and other iron-containing particles in Firinterior of the tubercle-like nodules and in some owes within the. giant cells themselves. The number of asbestos bodies Is smeller thou seen in many c ses." inclusions of rhe Schaumann variety, found only in tie lung, oc curred in 4 per cent of the giant cells. Some of these enclosed goldenyellow, irregular bodies suggesting asbewc.-.-- bodies, bah similar 0 or ganic material previously described vritiiiu such ' , s. Yet them were definite asbestos bodies enclosed by similar dark blue m-vena!, Schaumann inclusions have been described in only 4. per cunt of the reported necropsies on sarcoidosis as summarized by Rubin ami din ner,11 who did not regard these inclusions as >peeM >m ;-ua,od.vs.R, Rich,27 who was impressed by the frequency of Schaiunann inclusioi in sarcoidal lesions and by their absence w unequivocal tuberciboi lesions, noted that Meicbnikoff reported the presence of calcified in clusions hi the bynerruasfic tuberculous lesions of expenmcniaUv I R aw f .V v-rl-j m - Klr-ew 11 waned pop the p a w a , w .o.-bi,.; 502 SKAVLEtt AND RITTERHOFP sarcoidosis. Gardner 24 pointed out that, in his sarcoid material, these bodies, regarded b y many to consist of calcium or deified re. .innate of elastica, do not, by the von Kossa method, contain calcium, but. by the ferroey snide 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, yet all 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 refractile 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 bodies* 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 acid fuchsin, is formed in response to doubly refractile, nonlipoid substance and initially is impregnated by iron and later, in amounts demonstrable by von Kossa's stain, by calcium. Woibaeh,21 in T911, Jadassohn, in 1919," and Friedman,19 in 1944, have described a peculiar intracellular body in cases of sarcoidosis. This body, stellate in shape, varies in size up to 25 /x, generally lies in an intracytoplasmic giant cell vacuole, and stains intensely with acidophilic stains except the central area which is basophilic. Wolhach described them as lying free in tissue spaces, in endothelial leukocytes, and in giant cells. Friedman fotmd such bodies in only 6 to 8 per cent of the giant cells in his case. Both investigators attempted 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 organism, although onehk.noble. IVolbacii rngsiut'.; h as a mm-gc-'.. me om. m-an-rai d i o a u i - r me COEXISTENT ASBESTOSIS AND SAKCOIDOSIS 53 material and decided, that they were not similar to inclusions some times seen in eases e sarcoma. Friedman regarded the.e bodies as nonspecific but highly characteristic of sarcoid lesions. Friedman pro posed that these bodies be called `'asteroids/5 but perhaps it would ho better, eponymically, to call them Wolhach's asteroids. They have been described in 7 cases of sarcoidosis, and never in association with the Schauraarra calcified inclusion body. In the present, case asteroids were present in approximately 1 per cent of the giant cells in the lungs and tracheobronchial lymph nodes.. Definite transition stages of asteroid formation were suggested by the presence of spicules on the pink, eocco.il rap-avaeiiolar, intracytoplasmic bodies, particularly jn those giant ceils in which the small vacuoles were clustered and dis integrating. In addition, an occasional Woibach's asteroid, instead of lying in a large, dear vacuole, was surrounded by agminated ruptured vacuoles. In view of the presence of similar pink, coecoid, intravacuolar bodies, similar asteroids, ana the same suggestive stages of asteroid formation in the giant cells of talcum powder granuloma, so observed in one case in this laboratory, these giant ceil cytoplasmic changes must be regarded as Wolbach originally suggested, nonspecific biochemical cytoplasmic alterations. In addition, such an asteroid is depicted In the giant cells of leprous lesions by Mallory 26 who called them " spicuteted" bodies. No transition stages between Woibacho asteroids and Schaumaim's inclusions were even remotely suggested. The pathogenetic relationships of asbestosis and sarcoidosis are dependent upon the chronologic development of the lesions and Urn nature of the causative agents. Historically and histologic ally, in this case, it is most likely that asbestosis preceded the development of sar coidosis. The predominant localization of the sarcosdal tubercles with in sshestolic ones of fibrosis with attendant morphologic modweation 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 tuberculosis and the pneumoconioses. It must be remembered, though, that even in un complicated sarcoidosis the lesions occur in the framework of the lung, and therefore the morphologic relationships of the 5wo msv bo coincidental. This would be in agreement with those who believe ilwi morphologically sarcoid is not reconcilable with tuberculosis, How ever, to those who regard sarcoidosis as a peculiar form of tubrcuk;si.;. this case then would be one of asbestosis with mperimpwfd v-w - ouk'g Tuberculosis. 504 SK.AVLEM AND RTTTI.RH OFF REFERENCES 1. Gioyae, S. R., and Merewether, E. R. A. Asbestos. Occuparion and H eal'a Supplement. Intern 'tiynal Labour Office, Geneva, iosS. (Cited by Sayers, R. R,. and Dreessen. W . C. Asbestosis. Am. J. Pub. Health, 1939, ag, 205-214.) 2. Murray, M. Cited bv Egbert.5 (Charing Cross Hasp, Gas.. 1000. Also: Departmental Committee on Compensation for Industrial Diseases, .-.-unifies of Evidence. Appendices and Index, 1007. Cd. 3406, p. 127: Report, 1907. Cd. 3495, p. 14-) 3. Fahr, T .. and Feigel. Kristallbildung in der Lunge. Deutsche Wchnschr., 1914, 40, 1548-1549. (Cited by Egbert.5) 4. Cooke, W. E. Pulmonary asbestosis. Brit. M . /., 1927, 2, 1024-'02; M c Donald, S. Histology of pulmonary asbestosis. ibid.., 1927. 2, 1025-2026. (Cited by Egbert.3) 5. Egbert, D. S. Pulmonary asbestosis. Report of a case with ne' >-opsy findings. Ant. Rev. Tuberc., 1935, 3 1, 25-34. 6. Shull. J. R. Asbestosis. A roentgenological review of 71 case- Radiology, 1936, 27, 279-292. 7. Lanza, A. J. Asbestosis. J. A. Pi. A., 1936, 106, 500-309, S. Lynch, K . M . Pulmonary asbestosis. IV . The asbestosis body mod similar objects in the lung. / . A. M . A., 1937, 109, 1974-1978. 9. W iliam s. E. The presence of " curious bodies'' in the lungs of South African goldminers. J. Path. & B a d ., 1939, 48, 475-477. 10. Sutherland, C . L . Tuberculosis in the silica-risk industries. Lancet, 1940. 1, 893-896. 11. Hannesson, H. A case of pulmonary' asbestosis accompanied by pulmonary' tuberculosis. Tubercle, 1971, 22, 40-44. 12. Hoar burger, 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, 19, 797-807. 13. Auerbach, 0 . The pathology of the pneumoconiosis. Quart. Bull.. Sea Viszo Hasp., 1936-37, 2, 3~-7 14. Monthly Labor Review, U.S. Department of Labor, Bureau of Labor Statistics. 1946, 62, p. 153, table 2. 15. Pinner, M. Noncaseattng tuberculosis. An analysis of the literature. Am. Rev. Tuberc., 1938. 37. 600-728. 6. Horton, R., Lincoln, N. S., and Pinner, M. Nncaseating ubercuiosis. Am. Rev. Tuberc., 1939, 3S, 186-203. 17. Rubin, E. H., and Pinner, M. Sarcoidosis. One case report and literature review of autopsled ernes. Am, Rev. Tuberc., 1944, 49, 147 -169. 1.8. Reisuer, D. Beech's sarcoid and systemic sarcmdoAs ( R>snicr-Lueck-.Scnaumann disease): study of 35 cases A n . Kev. Tuberc.. 1944, 49, 289-307 : 437-462. 19. Friedman, M. Fercoidosis of rite spleen. Report of a car., with autopsy ana a study of intracellular " asteroid bodies.1' Am. J. Path.. 9..7, ?o. 621-63;. - C . Kraus, E. J. Sarcoidosis (Eocek-Besnscr Schs.um..nn diarwey a? die cause of a pituitary syndrome. /. Lab. 3- Clin. Med... 1 " \ . 28, jge- 146. 21. Wo'bnch, S. B. A new type of arid inclusion. nw pmesiric. associated with. disseminated grannlem-ions ' cions. /. An a -.-a sc. -m . 24, 37. as. ZcPn P. M. Ilea:; a u r i c , y. The wApa. at T s e n a a m . I:c-:_rt. Arch. a - , COEXISTENT ASBESTOSIS A lii) SARCOIDOSIS s-jer .MW* 505 24. Gardner, L. U. Personal communication. 25. Higgins, G. K . The effect of pulmonary tuberculosis upon the weight of the heart. Am. Rev. Tubera., 1944, 49, 255 -275. 26. Gardner, L. U .; ami Cummings, D. E. Studies on experimental pooomono- koniosit. VI. inhalation of asbestos dust: iis; effect upon primary tuberculous infection, /. Ind-ust. Ilyg. & Toxical., 19315 3, 65-Pj. 27. Rich. A. R. The Pathogenesis of Tuberculosis. C. C. Thomas, Springileid Z: Baltimore, *944, p. 722. la, Jadassohn. Ztir Frage der " Sareoide." dm Lupus pernio uud de= Lupus miliaris in Sombination mit " Acniiis." C c .- B l. /. schtceir. 4erz:`;, ;o ;y , 49, -35458. m. Mallory, F. B. T a P rindp'es of Pathologic Histoicgy, f\ . ;t. P a - f a s Co., Philadelphia & Lande:;, :<)i$T p. 10;. ; Illnriratrons jciUcv J .;;s.r,/^,^ DESCRIPTION OF PLATES P lats 103 Fig. i . Initial roentgenogram of tbe che-t. Fig. 2. PhoUiirncrograph of lung and adherent pleura showing suboleura! septal, peribronchiolar, and marked and focally nodular pleural fibrosis. X avicm `iid '.c^.n U! 0001 v' '[oruiw orai-qdoi.iuun un ppu -*u -;|ij at- pp TpuA\ M W;s Pun^ - - : p|.)i5? 10 jsp n p e a v l;i aip.j - ;): -i Plate icu Fig. 6. Lung. An inclusion of Schaumann encloses an oval yellow bodv, With polarized light, doubly retractile material surrounds this calcified mass. 1 7=5Fig. 7. A giant cel! from the lung with inclusion.-; of Schaumann. X "as. lit: is+H-'i->issiti;-;w .-t,',^ ^ .^r..^^'.^f^l^j^^-r^i'iii#^^ I'l ATE IO" 'TG. S. Luna with tubercies o i>nvX;; body type. TX: c,-:r. r:d ;uX. rolo ho an asbestos bod}' at its periphery. X 160. I'lG. Q- Luny asbestos bodies and cbbters 01 hcntoXdenn-Xdo ntaero- j.- tayes v.ithin an area o fibrosis. X 700.  . # : i **!.,.. . . s , . . . l Y i T t i i T ii ff t i f r i n i m tr nn i f i n r . . . . . . iir iiiit i ii iim i w i M i i r w f c iM iiig i i l i i n r m r r n r - -- I';.ATE IOS i'3G. io. Lung. An asbestos body ;s shown in on alveolus. a 7:;. bos. 11. Lung showing an asbestos hoc1/ encrusted with iron and calcium.